Anorexia and weight loss Flashcards
What do we mean by weight loss?
Reduction in total body fat/muscle
Body condition rather than weight as other things can affect weight e.g.
* Ascites
* Dehydration
* Masses
Occurs when energy expenditure / calorie loss exceeds intake.
What are the 3 broad possible causes of unwanted weight loss?
- malnutrition: insufficient calories ingested to maintain body condition
- maldigestion: sufficient calories ingested but not being absorbed properly
- malutilisation: sufficient calories ingested and absorbed but not used in the right way
What are reasons for not ingesting enough calories?
diet
- inappropriate
- not enough
Don’t want to eat
- stress/behaviour/psychological/neuro
- appetite suppressed
- nausea
- pain
- pyrexia
Physically can’t eat
- mechanical inability to prehend/swallow/chew
- dental disease/neoplasia/congenital abnormalities
- access to food - can’t bend/stretch/jump
What factors increase and decrease appetite?
Increases
* Empty stomach releases hormone Ghrelin
* Sensory signals (smell, texture, temperature, taste)
* Behavioural cues
* Environmental signals
* Medications (e.g. corticosteroids, phenobarbitone)
* Hypoglycaemia
* And lots more!
Decreases
* Satiety hormones from intestines if food
* Gastric distension
* Leptin from adipocytes
* Insulin
* Inflammatory cytokines
* pyrexia./hyperthermia
* Toxins e.g. uraemia
* Chronic pain
* Stress
* Nausea
* And lots more!
What is masticatory myositis? What are the 2 possible presentations? How is it diagnosed? How is it treated?
Immune mediated inflammatory condition
Inciting cause unknown
Autoantibodies against type 2 muscle fibres
Presentation
Acute phase (can be missed by owner)
* Inflamed masticatory muscles
* Hard to open jaw as painful
Chronic phase
* Fibrosis and atrophy - cannot open mouth (differentiates from Trigeminal Neuritis)
* No pain but anorexia and wt loss
Diagnosis
* Haematology- eosinophilia
* Biochemistry - increased globulins and Creatine Kinase
* Electromyography (EMG)- spontaneous electrical activity
* Biopsy histology- lymphocytic-plasmacytic cellular infiltrates, muscle atrophy, and fibrosis
* Bloods- circulating autoantibodies against type 2M fibres
Treatment
* Best chance of success in acute phase
* Immunosuppressive therapy (prednisolone 2mg/kg)
* Dose gradually tapered over months
* Chronic- attempt to stretch jaw open under GA?
* Recurrence common
What is cricopharyngeal atelectasis? How is it diagnosed? How is it treated?
- Uncommon differential for dysphagia and regurgitation.
- Mostly Springer/ Cocker Spaniels
- Neuromuscular motility disorder causing incomplete/asynchronous relaxation of the upper oesophageal sphincter
- Usually congenital, rarely acquired
- Can cause secondary aspiration pneumonia
Diagnosis- Fluoroscopy
* Cricopharyngeal muscle doesn’t relax
* retention of barium in the caudal pharynx
Treatment- surgery
* Cricopharyngeal myotomy or cricopharyngeal and thyropharyngeal myectomy
* 65% success (less if acquired)
How should you approach a malnutrition case to reach a diagnosis?
History
* Diet- What, how much, how often (bring in bag?)
* Where /with who do they eat (stress?)
* Changes at home (stress?)
* How do they eat/ try to eat? (video?)
* Activity levels/ life stage (anticipated calorie consumption)
* Signs of nausea or pain? Drooling, pawing at mouth
Clinical exam
* Full exam for possible causes of nausea or pain
* Thorough exam of mouth/ jaw/head/neck and ortho exam
* Able to open mouth fully and without pain?
* Offer treats in consult from usual feeding height - observe prehension, mastication and swallow
* Remember to check temperature
Diagnostic tests - depending on history/exam
* Haem/biochem/urinalysis- systemic dx
* Radiographs
* Fluoroscopy- barium swallow
* EMG
* Muscle biopsy
What clinical sign is often associated with maldigestion/malabsorption?
Increased appetite
What are signs and causes of maldigestion?
Stomach
Vomiting /Regurgitation
Common categories
* Neoplastic (e.g. gastric adenocarcinoma)
* Inflammatory (e.g. gastritis, gastric ulceration)
* Infectious (bacterial, viral, protozoal, endoparasites)
* Obstructions (e.g. foreign bodies/ strictures)
* Congenital/traumatic (e.g. hiatal hernia)
What are signs and causes of malabsorption? How are the causes of malabsorption categorised?
Small intestines/ pancreas
* Reduced absorption of fats/proteins/carbohydrates
* Diarrhoea or Increased volume of faeces
* Changes in colour/consistency
* Can also be associated with vomiting
Causes can be considered by location within intestines-
* Luminal (e.g. EPI, Dysbiosis)
* Mucosal (infectious or inflammatory enteropathies, villous atrophy, neoplasia)
* Post mucosal (e.g. lymphangiectasia, vasculitis, portal hypertension)
What approach should you follow when investigating a maldigestion/malabsorption case?
History
* Any vomit/regurgitation (ID which)/diarrhoea/ change in faeces - Characterise- photos?
* Simultaneous changes (e.g. diet- include treats/supplements /scavenging)
* Parasite control- what when and how?
* Health of in contacts/ family
* Evidence of nausea- drooling lip smacking
Clinical exam
* Extra attention to abdominal palpation
* Pain (localise), thickened intestines, masses
* Temperature- look at faeces on thermometer
* Hydration
Diagostic test
* Haematology/Biochemistry ( inc TLI, folate/B12)
* Specific tests for common systemic diseases causing GI signs (e.g. TT4, basal cortisol)
* Faecal exam (possibly culture, microscopy)
* Imaging (ultrasound, fluoroscopy, endoscopy)
* Diet trial
* Biopsy
What are the 2 types of malutilisation? What are examples of each?
**Abnormal nutrient handling **
- protein losing nephropathies
- diabetes mellitus
- liver disease
Increased demand for nutrients
- neoplasia
- hyperthyroidism
- infection
- cardiac cachexia
- parasites
Usually systemically unwell
What approach should we follow when investigating malutilisation?
History
* Parasite control- what when and how
* Changes to drinking or urinating
* Vomiting/diarrhoea
* coughing/sneezing/ respiratory effort
* Changes to activity levels- decreased or increased
* Behaviour changes
* Appetite
Clinical exam
* Thorough cardiac exam- HR, murmurs, dysrhythmias, pulses, CRT
* Respiratory assessment- MM colour, resp rate and effort, resp sounds, dullness?
* Abdominal palpation- pain, masses, thickened intestines, organomegaly
* Palpate LNs and check for goitre
* Check temperature
Diagnostic tests
* Haematology- anaemia? Evidence of inflammation/infection?
* Biochemistry- Liver/ kidney parameters, Ca2+
* Urinalysis (dipstick and USG, UPCR?)
* Specific tests (TT4, fructosamine)
* X-ray/ultrasound/ echo
What approach should you follow when investigating anorexia linked to loss of appetite? What are common causes?
- Signs of systemic disease on history or clinical exam?
- Particularly note drooling, pyrexia, pain
- Consider haematology/biochem/ urinalysis
- Imaging as indicated
- Consider antiemetic trial for possible nausea?
Common causes
* Renal/ Hepatic dx (toxin accumulation)
* Any inflammatory /infectious process causing pyrexia
* Neoplasia
What approach should you follow when investigating anorexia linked to reluctance to eat? What are common causes?
- Instigating factors- stress full event?
- Changes around feeding- location, bowl, other animals, diet?
- General changes at home- new pets, building work etc
- Tempt to eat in other locations/ with other foods and monitor or improvement
- Consider consulting behaviourist
Common causes
* Association of food with nausea/pain/ stressful event e.g. hospitalisation
* Stressors e.g. other pets, building work etc
* Change to less palatable diet e.g. prescription renal diet
What approach should you follow when investigating anorexia linked to the mechanical inability to eat? What are common causes?
- On exam able to open and close mouth normally?
- Tongue and oral soft tissues appear normal?
- Pain in neck/mouth/limbs
- When does eat any issues chewing/swallowing/choking/drinking- video?
- Better with wet vs dry food or fed at a different height?
- Any sign of dental/oral pharyngeal disease/ pain – may need sedate/GA to fully assess
- Often imaging for investigation (dental rads/ x-ray)
- Consider pain relief trial?
Common causes
* Dental disease
* Gingivostomatitis
* Oral/pharyngeal/oesophageal masses
What are treatment options for anorexia?
- Treat underlying condition
- Tempt to eat (beware of causing food aversions)
- Appetite stimulants (e.g. mirtazapine)
- Antiemetics if nausea (e.g. maropitant)
- Analgesia if painful conditions
- Minimise stress
What is hepatic lipidosis? What clinical signs are associated? How is it diagnosed? How is it treated? What is the prognosis?
- Mostly cats if rapid weight loss due to absolute/relative calorie deficit
- Increased risk if high BCS
- Peripheral fat mobilization exceeds livers capacity to redistribute or use it.
- Excess fat deposited in hepatocytes causing liver failure
**Clinical signs **
* Hepatomegaly
* Jaundice
* Lethargy
* Vomiting/diarrhoea
* Ileus
* Hypersalivation
* Pallor
* Neck ventroflexion,
* Coagulopathies
Diagnostic tests (changes in addition to those from underlying diseases)
* Biochem-Increased ALT, ALP, AST
* Haem- nonregen anemia, poikilocytosis, increased Heinz bodies
* Coags – possibly prolonged PT and APPT
* low vit K- check and supplement before FNA or feeding tube
* Ultrasound- hepatomegaly- homogeneous hyperechoic parenchyma
* Liver FNA- significant vacuolar distention of hepatocytes
Treatment
* IVFT- 0.9% NaCL NOT Hartmann’s (cannot metabolise lactate)
* Suppliment K+, phosphate and B12 according to biochem results
* Start feeding slowly- high protein low carb diet (tube feeding)
* Consider antiemetics- maropitant
Prognosis- >80% recovery if treatment started early
What is refeeding syndrome? What clinical signs are associated? How can it be treated? How can it be prevented?
- If patient fed too much/too quickly after prolonged anorexia.
- Starvation causes electrolyte depletion (notably Mg2+ and K+)
- Insulin released by pancreas when refeeding implemented
- K+ and glucose co-transported into cells so serum K+ drops- hypokalaemia
- Body responds so sudden reintroduction of carbohydrates by making lots of ADP and ATP- uses lots of phosphorus- hypophosphatemia
Clinical signs- seen within 5 days of refeeding
* cervical ventroflexion,
* severe muscle weakness
* acute red blood cell lysis
* respiratory failure
Treatment
* Immediately reduce feeding 50% and lower carb diet and increase slowly over 4-6 days
* Check electrolyte levels and give Potassium Phosphate CRI as needed
* May need Magnesium Sulphate too or hypoK+ may be refractory
* Monitor electrolytes and glucose q4-6hrs and adjust accordingly
* Monitor PCV closely for hypophosphatemia induced haemolytic anaemia- transfusion if needed
* ECG- heart rate and rhythm
Prevention
* Reintroduce feeding slowly
* Max speed- 1/3rd RER on day one , 2/3rd day two, all day three
* Monitor K+, Mg2+ and phosphorus at least daily and supplement as needed.
