Abdominal, oral, rectal Flashcards

1
Q

What are the different types of shock?

A

Hypovolaemic

Distributive - sepsis, anaphylaxis

Obstructive

Cardiogenic

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2
Q

Signs of hypovolaemic shock

A

Hypovolaemic

o Pale mucous membranes

o Tachycardia (or bradycardia in cats – can maintain a high vagal tone even in severe disease, possibly to increase stroke volume and cardiac output)

o Low temperature

o Weak pulses

o Increased respiratory rate

o Increased CRT

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3
Q

Signs of distributive shock - sepsis

A

Distributive (sepsis, anaphylaxis)

o Red mucous membranes

o Decreased CRT

o Tachycardia

o Pyrexia

o Bounding pulse

o Increased respiratory rat

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4
Q

Signs of obstructive shock

A

Obstructive (compression of blood vessel reducing venous return or cardiac tamponade)

o Pale mucous membranes

o Increased CRT

o Tachycardia

o Low temperature

o Weak pulses

o Increased respiratory rate

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5
Q

Signs of cardiogenic shock

A

Cardiogenic (diseased heart)

o Pale mucous membranes

o Increased CRT

o Tachycardia/bradycardia/arrythmia

o Low temperature

o Weak or asynchronous pulses which may have deficits

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6
Q

POCUS to determine type of shock

A

v Normal left ventricular ejection fraction is 25-40% (classic cardiogenic issue is reduced EF)

v Reducing preload giving less fluid to start with will increase the ejection fraction

v Bounding caudal vena cava = normal preload – used to work out whether hypovolaemia is present

v Right side of heart flapping about = not maintaining volume as can’t expand due to fluid = cardiac tamponade

v Distributive normally caused by an inflammatory process, so go and look for fluid produced by inflammation and then tap it and analyse it to find out where the problem is originating from

o Blood, urine, inflammatory exudate are the main ones in acute abdominal pain

o Also bile and transudates (seen in hepatitis, portal hypertension and especially cancer)

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7
Q

What can cranial abdominal pain indicate?

A

liver, stomach, spleen, pancreas, spine, gallbladder – inflammatory diseases, foreign body, obstruction (pancreatitis with focal peritonitis is extremely painful)

Spine causes abdominal pain everywhere – should always check the spine in cases

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8
Q

What can caudal abdominal pain indicate?

A

uterus, colon, prostate, spine, bladder – prostate is very common, particularly in uncastrated dogs

Spine causes abdominal pain everywhere – should always check the spine in cases

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9
Q

What can dorsal abdominal pain indicate?

A

kidneys, radiating pain from stomach, spleen, spin

Spine causes abdominal pain everywhere – should always check the spine in cases

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10
Q

What can ventral abdominal pain indicate?

A

spleen, intestines, spine, space occupying lesions – gravity dependent fluid so anything producing fluid can cause ventral pain

Spine causes abdominal pain everywhere – should always check the spine in cases

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11
Q

What can cause GDV?

A

Aerophagia (swallowed air)
Eating too fast
Stress/pain – care with patients in practice
Exercise after feeding (oesophagus more open)
Large deep chested dogs – thoracic width:depth ratio (Setters, GSD, Weimaraners, Great Danes, Dobermans, Dachshunds)
Results in gas distension of the stomach and the pylorus twists on the gastric axis and move up
180 degree is the most common, but 360 degrees is also seen – must be some kind of momentum

Don’t really know why

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12
Q

Which way does GDV normally twist?

A

clockwise - 90%

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13
Q

What type of shock can GDV cause?

A

Obstructive - presses on caudal vena cava

Gastric vessel occlusion – necrosis

Spleen often involved – splenic involvement and twisting

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14
Q

How to diagnose GDV?

A

Need to do a right lateral radiograph to diagnose – look for smurf hat

Can tell if the patient is bloated versus GDV if you can’t get the stomach tube down

If you do surgery and find that the stomach is just bloated, you still need to do a gastropexy as likely recurrence

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15
Q

How to fix the obstructive shock of GDV

A

Need to fix the obstructive shock – remove the obstruction

Orogastric or nasogastric tube – orogastric is larger so can decompress it faster
Some GDVs will spontaneously resolve with a nasogastric tube, but much more likely to die

16G or 18G needle or catheter through the stomach – percutaneous
Needle is quicker but can rip the stomach if it moves
Catheter won’t rip the stomach but might get bent = air won’t come out

Give plenty of oxygen therapy
Brain, heart, lungs and kidneys will struggle
Neurological exam

Fluid therapy to help the kidneys

Oxygen therapy for lungs

Heart can get hypoxic damage = arrythmias = ECG

Ventricular tachycardia is the most common finding (stimulated somehow by splenic disease)

Poor stroke volume and filling

Probably results in fibrillation and death if not treated

Treat with lidocaine (sodium channel blocker which slows down the action potential, allowing the SAN time to recapture ventricles) – bolus or CRI

Blood trapped at the back of the body = front of body isn’t getting blood so has a relative hypovolaemia cranially

Bolus fluids IVFT in the cephalic vein

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16
Q

Anaesthetic considerations with GDV

A

Surgery to untwist and decompress the stomach once stabilised
Anaesthesia
Avoid alpha 2 agonists as cause cardiovascular compression
Need to monitor cardiac output (ECG), blood pressure on front end

Can’t breathe properly due to diaphragmatic compression = ventilation-perfusion mismatch made worse by perfusion issues

Capnography
Ventilating patient

Pain relief – methadone premedication
Midazolam premedication or co-induction at the same time as propofol

Co-induction is trying to avoid dysphoria, so in a sick patient you may as well just give it as a premed

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17
Q

Systemic considerations of untwisting GDV

A

Untwisting the stomach results in sudden reperfusion, which can spread a load of toxins from the lysis of necrotic stomach cells back into the bloodstream

Heaps of potassium released = hyperkalaemia – use blood gas machine to measure or look at ECG or give fluids

Length of surgery increases risk of infection – could give prophylactic antibiotics at least during the procedure

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18
Q

Gastropexy

A

Gastropexy

Decompress stomach fully before derotating, even if decompressed before surgery
Prevents ripping off gastric arteries and subsequent haemoabdomen

Many different approaches
Don’t do tube gastropexies as these increase risk of infection
Belt loops use serosa and create a kind of triple layer, but is more difficult with no clear benefit

Incisional gastropexy is the best option
Incision into the serosa of pylorus of stomach (don’t penetrate stomach lumen) and deep into the abdominal wall
Stitch them together
Some bleeding and inflammation creates an adhesion, creating scar tissue which keeps the stomach in a normal position

If the spleen is black then remove it, if purple it’ll probably be fine, but if in doubt it’s always safer to take it out, especially if twisted (don’t untwist before you remove it so no toxins are released)

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19
Q

Post op GDV care

A

Post-operative care

o Monitor electrolytes, lactate and keep the ECG on for at least 24-48 hours as can go into ventricular tachycardia or atrial fibrillation at any time after

o Methadone

o Lidocaine for the next 24 hours – excellent pain relief as well as helping ventricular tachycardia

o Best not to send them home straight away as still a risk of sudden death

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20
Q

Septic causes of peritonitis

A

GI perforation
- Foreign body ingestion – scavenger, vomiting, pain

Haematogenous
- Distributive shock

Extenal penetrating injury
- Obvious

Iatrogenic
- Recent surgery – e.g. swabs left in
- Pain, distributive shock, vomiting

Ascending urinary tract infection
- Reduced urine volume, stranguria, increased frequency of urination
- Pain
- Haematuria
- More likely in male dogs with prostatitis

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21
Q

Aseptic causes of peritonitis

A

Pain Vomiting PUPD

Splenic abscess (uncommon)
Hepatitis
Nephritis
Cholangitis
Pancreatitis – enzyme release

Bile
- Super painful
- History of chronic disease (weight loss, inappetance, etc.)
- Jaundice if ruptured due to an obstruction

Haemoabdomen
Urine
Stomach contents – gastric perforation
- Foreign body or gastric ulcer
- Super painful at first when the foreign body/ulcer is eroding, then lack of pain when it ruptures and then super painful again as peritonitis develops
- Vomiting, anorexia

Aseptic causes are fluid which contains no bacteria but will still illicit an inflammatory response (e.g. not chyle because this doesn’t stimulate the immune system)

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22
Q

POCUS for peritonitis

A

Look for triangles/shapes with angles to demonstrate free fluid
Circular things on ultrasound = organs/blood vessels

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23
Q

What to do with tap of free fluid in peritonitis

A

Gross colour

· Low glucose and high lactate

o If bacteria present then they are respiring anaerobically = use up glucose and produce lots of lactate

o Glucose 1mmol/L or lower supports sepsis

o Lactate 2mmol/L or higher supports sepsis

· Smear cytology – back-up as takes time away from patient; look for intracellular bacteria

· If you can’t reach fluid due to lack of volume then stick some more fluid inside = diagnostic peritoneal lavage

o 22ml/kg of warm saline into abdomen, then shake the animal and take a sample

o Expect glucose and lactate to be lower than normal in that sample = not diagnostic tests in this case

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24
Q

Treatment of peritonitis

A

Treatment – source control

· Depends on the source

· Can remove the fluid and/or fix/remove the source of the fluid

· Enzyme leakage = place a drain to constantly remove them if the source can’t be resolved +/- lavage

o Until patient is fixed and a lot better

· Don’t give antibiotics if an aseptic cause

· In sepsis they need antibiotics immediately – risk of death increases 7-10x for every hour you wait to give antibiotics

o Though if you can do source control well you may not need antibiotics, but you have to be brave

o Could avoid giving antibiotics at first and only give once culture and sensitivity has come back with evil stuff/patient is getting worse

o Could give lots of antibiotics and then see what culture and sensitivity comes back as

o Septic process:

§ Amoxicillin clavulanate

§ Optional metronidazole

§ Fluoroquinolone

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25
Q

What to do if haemoabdomen

A

POCUS!!

Tap fluid and analyse

· Red fluid could be a serosanguinous fluid and not always pure blood

· Don’t diagnose on whether or not it clots as haemoabdomen will be using up all the clotting factors and platelets to stop the bleeding

· Use PCV to differentiate (PCV of 2-3% will still look like blood)

o Compare to animal’s blood PCV

o Serosanguinous fluid will always be significantly lower than blood PCV

o Fluid PCV higher than blood PCV = semi-acute issue as the animal has an acute bleed a few hours ago and has probably stopped bleeding

o Fluid PCV lower than blood PCV = chronic issue (e.g. cancer) as has bled a while ago and now haemosiderophages (differentiated macrophages) start to eat up the blood + inflammation and fluid leakage into the area = dropped PCV

o Fluid PCV same as blood PCV = acute haemoabdomen

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26
Q

Causes of haemoabdomen

A

Neoplastic bleed
Trauma - blunt, pointy
Coagulopathy
Aneurysms
Splenic rupture secondary to neoplasia more than splenic trauma

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27
Q

Neoplastic haemoabdomen

A

Blood pressure and lactate to measure perfusion

o Poor perfusion = fluids and transfusion?

§ Autotransfusion will seed the neoplasia everywhere, but evidence in humans suggests that metastatic rates are low, so could still do them

§ Donor whole blood

§ Packed red blood cells fixes short term – could combine with fresh frozen plasma to get everything you need

o Surgery to remove the mass or chemo/radiotherapy or euthanasia if unremovable

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28
Q

Trauma haemoabdomen

A

Blunt
Bleeding from many places so avoid surgery if at all possible
RTAs most common cause
Acute issue = can quickly die
Blood pressure and lactate to measure perfusion
Poor perfusion = fluids and transfusion
Whole blood
Packed red blood cells combined with plasma
Tranexamic acid
Antifibrinolytic that prevents or reduces bleeding by impairing fibrin dissolution

Pointy
Measure blood pressure and lactate to look for poor perfusion
Poor perfusion = fluids and transfusion
Whole blood
Packed red blood cells and plasma
Tranexamic acid
Surgery

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29
Q

Coagulopathy haemoabdomen

A

Iatrogenic causes most common
Warfarin ingestion
IMHA
Von Willebrand’s – Dobermans
Measure blood pressure and lactate to look at perfusion
If perfusion is poor then give fluids and transfusion
§ Autotransfusion is the best idea alongside plasma – contains micro-aggregates
Then fresh frozen plasma as contains clotting factors
Then packed red blood cells
The whole blood (last option)

Avoid surgery as much as possible

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30
Q

What to do with uroabdomen

A

Diagnosis:
POCUS!!
Put bubbles into fluid into bladder and radiograph – if bubbles are outside the bladder on ultrasound then there is a bladder leak/rupture
Or above with other contrast media on radiograph

Tap fluid and analyse
Urea is a freely moving solute, so won’t see any difference in uroabdomen compared to normal
Creatinine >2x blood = uroabdomen
Potassium >1.4x blood = uroabdomen
Electrolytes – blood gas analysis
Hyperkalaemia assessed via ECG – bradycardia or atrial standstill if really bad
Glucose upregulates sodium/potassium pumps = want to upregulate this to get potassium back into the cells
Want to get glucose into cells = give insulin (care with hypoglycaemia so add in glucose) or feed the patient or give a glucose bolus (if pancreas works)
Or give biocarbonates
Or give a beta-2 agonist like salbutamol
Give Hartmann’s fluid – ultimate option as is acidic

Source control

· Urinary catheter into a ruptured bladder can help the patient remove fluid and reduce inflammation for a couple of days before surgery (or even resolvement)

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31
Q

Ascites - clinical signs and prognosis

A

Clinical signs
Dependent on underlying cause
The obvious – abdominal distension
Some discomfort
Dyspnoea – either from pressure on diaphragm, or if also have pleural effusion
Lethargy
O’s may report weight gain, difficulty getting up/lying down
Other signs depending on underlying cause (e.g. V/D – liver disease, coughing/syncope – CHF etc.)

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32
Q

ddx for ascites

A

Organomegaly - splenomegaly, hepatomegaly
Abdominal mass
Pregnancy
Bladder distension
Obesity
Gastric distension

All these cause abdominal distension without effusion

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33
Q

Identifying ascites

A

History - past and recent
Clinical exam - whole animal!
Ballottement
Ultrasound

Sample it
- Abdominocentesis
- blind or US guided

Gross appearance and smell - septic - opaque and foul smelling
Cellularity - number and type - good quality smears
Protein content - total protein on refractometer
Or send to lab

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34
Q

Exudate vs transudate

A

Total Nucleated Cell Count
Exudates are fluids, CELLS, or other cellular substances that are slowly discharged from BLOOD VESSELS usually from inflamed tissues

Transudates are fluids that pass through a membrane or squeeze through tissue or into the EXTRACELLULAR SPACE of TISSUE

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35
Q

Causes of transudate - protein poor - ascites fluid

A

Altered fluid dynamics
Hypoalbuminaemia will cause this
Decrease in plasam colloid oncotic pressure

ddx
- PLE
- PLN
- Hepatic failure - hypoalbuminaemia or pre-hepatic portal hypertension

Biochem, urinalysis and US

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36
Q

Causes of protein rich transudate - ascites fluids

A

Caused by
increased hydraulic pressure within blood and or lymphatic circulation - usually lungs or liver
Protein leaks from permeable capillaries, ascites develops when resorbative capacity of regional lymphatics is overwhelmed
TP is more important - transudates will irritate mesothelium - inflammation and increased TNCC - total nucleated cell count

ddx
- cardiovascular disease
- chronic liver disease - post hepatic portal hypertension
- neoplasia
- thrombosis - rare

investigations
- US
- Radiography - thoracic - neoplasia and heart disease
- Biochem - after imaging

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37
Q

Causes of exudate ascites fluid

A

Caused by
- Inflammatory process - chemotactants and vasoactive substances attract inflammatory cells and cause increased vascular permeability
- High TNCC - neutrophils and other phagocytic/inflammatory cells
- Can be septic or non septic
- If septic - bacteria, fungi or mycoplasma

Septic ddx
- Penetrating wound
- Surgical complications
- Rupture of infected lesion
- Bacteraemia

Investigations
- Abdominocentesis
- Appearance/smell of fluid
- Cytology - numerous degenerate neutrophils +- intracellular bacteria - diagnostic
- C&S
- lactate and glucose levels in fluid - bacteria use up glucose and produce lactate

Non septic ddx
- Neoplasia
- Uroperitoneum
- Bile peritonitis
- FIP

Investigations
- Abdominocentesis
- Appearance of fluid
- Cytology - non degenerate neutrophils, abscence of bacteria
- Fluid analysis - high urea, creatinine, potassium in fluid if uroperitoneum
Biochem
US

38
Q

Lymphatic compromise - ascites

A

Rare - more commonly chylothorax
Chylous or non chylous
Obstruction or destruction of lymphatics
Leakage of lymph and lipids

ddx
Cardiac disease
Hepatic disease
Neoplasia
Steatitis

Appearance - milky
Cytology - small lymphocytes irritation - neutrophils and macrophages
Triglyceride higher than serum, cholesterol lower
US
Biochem

39
Q

Haemorrhagic ascites

A

ddx
surgical and non surgical trauma
haemostatic defects
neoplasia

investigation
PCV and TP of fluid
Presence of platelets
Cytology
US

39
Q

Haemorrhagic ascites

A

ddx
surgical and non surgical trauma
haemostatic defects
neoplasia

investigation
PCV and TP of fluid
Presence of platelets
Cytology
US

40
Q

Clinical signs of FIP

A

Depends on organ/s affected.
In all cats with nonspecific clinical signs, such as chronic weight loss or fever of unknown origin resistant to antibiotic treatment or recurrent in nature, FIP should be on the list of differential diagnoses.

Disease generally becomes apparent from a few weeks to 2 yr after the mutation has occurred. Cats are at greatest risk of developing FIP in the first 6–18 mo after infection with FCoV; the risk decreases to ~4% at 36 mo after infection.

FCoV infection can cause a transient and clinically mild diarrhea and/or vomiting due to replication of FCoV in enterocytes. Kittens infected with FCoV may have a history of stunted growth or upper respiratory tract signs. Occasionally, the virus may cause severe diarrhea with weight loss, which may be unresponsive to treatment and continue for months. However, most FCoV-infected cats do not show clinical signs.

41
Q

Common diseases of the rectum and anus

A

Anal sac disease
* Anal furunculosis
* Anal adenomas
* Other peri-anal neoplasia
* Rectal prolapse
* Rectal stricture
* Rectal neoplasia

42
Q

Anal sac disease

A

Scent glands
* Located at 4 and 8 O’clock in between external and internal anal sphincters
* Discharge through ducts at defaecation
* Unless soft stools
* Abnormal content:
* Large volume
* Blood stained
* Smell permeates the entire practice

  • Impaction or abscessation
  • Due to a change in consistency of secretion or interference with normal duct emptying; e.g., diarrhoea, diet, tapeworm, seborrhoea (scaly skin), oestrus, scar tissue
  • Remember neoplasia and bites in cats
  • Clinically, perineal irritation “scooting”
  • Impaction/infection very readily diagnosed on palpation
  • Manual expression of the gland
  • Inspissated content may need irrigation
  • Blood tinged material/pus requires lavage and packing with local antibiotic – cow mastitis tubes/ear drops normally under GA
  • Culture
43
Q

When to perform anal sacculectomy

A
  • Indications* Recurrent impaction* Neoplasia* On occasion, an additional component of the treatment for to perianal fistula (anal furunculosis)

Delay surgery if recently ruptured abscess

Closed - fill and dissect around it - remove without entering lumen of sac
Open - open up wall of sac itself - higher risk of contamination and more difficult

44
Q

Complications of anal sacculectomy

A
  • Bilateral surgery perfectly acceptable as one procedure
  • Complications
  • Draining sinus (some gland left)
  • Infection
  • Dehiscence
  • Tenesmus
  • Faecal incontinence
45
Q

Define tenesmus

A

Tenesmus is the feeling that you need to pass stools, even though your bowels are already empty. It may involve straining, pain, and cramping.

46
Q

What is anal furunculosis

A
  • Suppurative, progressive, deep ulcerating tracts in the perianal tissues
  • Can be very difficult to manage
  • GSD,but any breed including crossbreeds
  • Low tail carriage
  • +++ density of apocrine glands in perineum
  • Immunological theory

End up as craters feeding in towards the rectum
Progresses and is really debilitating -very expensive to treat and so is worth talking about euthanasia on first presentation

Cyclosporin (“Atopica”) for 12 weeks will resolve 60% but 70% of these will recur in 4 to 17 months
* Very expensive, many £100’s
* Can have multiple adverse effects; e.g., v+/d+, coat changes, nephrotoxicity or hepatotoxicity, gingival hyperplasia

  • Hypoallergenic diet and immunosuppressive doses of prednisolone
  • Only helped in 1/3 of very mild cases
  • Based on theory that there is an association between IBD and fistulae
  • If a failure to respond to cyclosporin then check no anal sac involvement
  • If there is, then the dog will require an anal sacculectomy
47
Q

Perianal adenoma

A
  • Perianal sebaceous gland adenoma
  • Third most common tumour in male dog
  • Hairless area of anal ring most common location, can see at tail base, prepuce and ventrum
  • Must differentiate from malignant adenocarcinomas
  • Biopsy
  • Testosterone dependent benign masses
  • Normally seen in older patients
  • Cats have no perianal glands
  • Slow growing
  • Rare in castrated dogs and should resolve with castration
  • 0.5 to 3cm diameter
  • Can ulcerate
  • Rarely adherent to surrounding structures
48
Q

Anal adenocarcinoma

A
  • Malignant lesion of perianal sebaceous glands
  • Occur in same areas as adenomas
  • Can diffusely infiltrate anal areas
  • Often adherent to deeper tissues
  • Rapidly growing
  • Clinical signs of dyschezia and pain
  • 13% have signs of sublumbar lymph nodeenlargement on presentation
  • Rare to metastasize to other organs
  • Do not respond to castration
  • Aggressive surgical removal with adequate margins is indicated
  • Adjunctive radiotherapy but rarely curative
  • Regional lymph node excision
  • Poor prognosis due to local recurrence and metastasis
  • Distant metastasis can take many years to develop, repeat palliative local surgeries justified
49
Q

Anal sac adenocarcinoma

A
  • Generally older female dogs (over 10 years)
  • Small discrete nodules in wall of either sac
  • Paraneoplastic syndrome often accompanies
  • Tumour secretes PTH-like substance
  • Hypercalcaemia causes pu/pd, depression, weakness, weight loss
  • Aggressive, 50% metastasised at presentation
  • Prolonged hypercalcaemia can produce irreversible renal damage
  • Diagnosis based on
  • Palpation
  • Biochemical findings
  • Abdominal/thoracic radiographs
  • Abdominal/thoracic CT scans
  • Ultrasound of sublumbar lymph nodes
  • Treat hypercalaemia prior to surgery
  • Treatment
  • Excision of primary mass
  • Metastectomy
  • Adjunctive chemotherapy
50
Q

Rectal prolapse

A
  • Associated with endoparasites/enteritis in young animals and tumours or perineal hernias in middle aged/older animals
  • Incomplete prolapse - mucosa only
  • Complete prolapse - all layers of rectal wall in entire circumference
  • Few mm to many cm
  • Everted tissue is oedematous, excoriated and can be bleeding
  • Dogs and cats, especially Manx* Recent straining; e.g., perineal surgery, constipation, urinary tract infection, dystocia, etc.* No specific lab tests or diagnostics needed other than for underlying condition
  • Ensure not intussusception - put in finger and see whether it will return to normal anatomy
  • Barium meal and radiography will diagnose intususception
  • Acute presentation
  • Lavage
  • Lubricate
  • Reduce and place purse string suture
  • Non-reducible or severely traumatised
  • Amputation
  • Recurrent
  • Colopexy - anchors rectum to the body wall
51
Q

Rectal stricture

A
  • Normally occur secondary to proctatitis chronic anal sacculitis, penetrating FB’s or as complication of anorectal surgery* Clinically cause dyschezia, constipation and tenesmus* Diagnosed by digital rectal exam* Contrast radiography/colonoscopy are difficult as superficially located* Deep biopsy differentiates from neoplasia
  • Superficial strictures treated by bougienage (well lubricated finger/blunt instrument)* This may need to be repeated at regular intervals for many days* Corticosteroids then for 2-3 weeks* Extensive strictures require resection by, for example, rectal pull-through
52
Q

Rectal polyps

A
  • Benign, adenomatous polyps* Male and female equally affected* Mean age 7 years* Sessile, raised or pedunculated* Single or multiple* Cause unknown
  • Clinically* Blood/mucus in faeces* Tenesmus can occur* Polyp can occasionally prolapse from anus* Secondary rectal prolapse can occur
  • Treatment* Small pedunculated masses can be removed from distal rectum with electrocautery, or excision and suture placement* Larger polyps may need intestinal resection
53
Q

Rectal adenocarcinoma

A
  • Infiltrative, ulcerative or proliferative* Invades rectal wall causing fibrosis and stricture* Clinically cause tenesmus, dyschezia, weight loss and lethargy with advanced malignancy* Diagnose on palpation, radiography, ultrasound, endoscopy/proctoscopy
  • Three sites* Colorectal junction and cranial 1/3 rectum* Middle 1/3 rectum* Caudal 1/3 rectum and anal canal
  • Surgery* Colorectal resection and anastomosis +/- ischial pubic flap osteotomy* Dorsal perineal approach* Rectal pull-through* Consider and discuss continence with owners!
54
Q

Atresia ani

A
  • Uncommon, can be associated with recto-vaginal or recto-urethral fistulae* Secondary megacolon* Neonate with absent anus* Tenesmus and bulging of perineum* Diagnosis confirmed by radiography* Treatment involves creation of an anus by excision of skin and terminal rectal mucosa and careful suturing* Subtotal colectomy (?)
55
Q

Define dyschezia

A

Difficult or painful defaecation +/- blood(haematochezia)

Colonic impaction - bones/tumour
Perineal hernia and rectal diverticulum
Rectal strictureAnal neoplasia
Severe prostatomegaly - presses on the colon
Obstipation - when severe constipation makes defecation impossible or nearly impossible

I.e mainly lesions near the anal region

56
Q

Define tenesmus

A

Excessive straining to pass stools

Colitis - frequently passing soft stools covered in mucus +/- blood
Bone ingestion
Rectal/anal tumours
Post operatively following perineal surgery
Prostatomegaly
Can lead to rectal prolapse

57
Q

Define constipation

A

Infrequent or difficult passage of stools associated with retention of faeces within the rectum and colon

Few truly constipated dogs
We feed, exercise and water them so lack of exercise, water, fibre,etc. should not happen
A lot have tenesmus and dyschezia however
Eat bones
Pelvic fractures
Rectal/Anal tumours
But these dogs have tenesmus and dyschezia normally…

58
Q

Colitis

A

Tenesmus
Soft stools
Mucus in stool
Fresh blood
Generally well animal
Could be your first case in practice on day one…
Metronidazole, sulphasalazine, high fibre feed, occasionally steroids

59
Q

Feline idiopathic megacolon

A

Feline idiopathic megacolon - true cause of constipation in cats

Soapy water enemas and lubricant
If enemas aren’t achieving much then have to head to surgery to remove the entire colon

RECURRENT CONSTIPATION
Dilation of colonRecurrent constipation and hypomotility of colon
1) idiopathic
2) pelvic #
3) sacral spinal deformity
4) aganglionosis to colon??
Permanent loss of colonic structure and function
1.5 x length of 7th lumbar vertebra
Laxatives, enemas, high fibre feed ~~~~~~subtotal colectomy

60
Q

What history questions for anal conditions

Clinical exam

Investigation

A

When did it start?
What is he/she passing?
Is there any mucus/blood?
Any change in diet or access to bones/fb?
Are they eating?
Any vomiting?
Any trauma?
Any weight loss?
Any excessive licking of perineum or scooting?

Assess demeanour and hydration
Start at nose and examine to tail
Assess abdomen for any palpable gas or faecal excess - colon palpable in dorsocaudal abdomen
Check temperature
RECTAL EXAM - cats likely to require sedation/GA (turn finger upwards to the spine to check the sublumbar lymph nodes)

Rectal exam
Abdominal x-ray +/- contrast (barium enema)
Ultrasound
Colonoscopy
CT
Blood work - hydration, Tp, anaemia, wbcc, electrolytes
Urinalysis - some owners assume constipation when the animal is actually straining to urinate (especially cats with cystitis)

Cause-dependent
Laxatives - lactulose, liquid paraffin, micro-enema (useful for neurological causes)

High fibre or low residue diets
Metronidazole/sulphasalazine
ENEMA - micro vs soapy water
Surgery - perineal herniorrhaphy- anal sacculectomy - neoplasia- subtotal colectomy- rectal pull through
Pelvic fracture repair

61
Q

Hernia vs rupture

A

Hernia - * A protrusion of an organ or part of an organ through a defect in the wall of the anatomical area in which it normally lies.* Generally consists of a hernial ring and sac

Rupture - normally no ring or sac

62
Q

Hernia locations

A
  • Umbilical* Inguinal* Incisional* Diaphragmatic* Perineal* Pericardio-peritoneal* Hiatal
63
Q

How to reduce hernia

A
  • Some are non-reducible
  • Directly incise over site
  • Ensure adequate exposure
  • Try to use atraumatic technique
  • Breakdown adhesions

Check viability of herniated tissues especially if strangulated hernia
* Resect non viable tissue before returning to abdominal cavity

  • Direct opposition if possible
  • Know anatomy to ensure holding strength
  • Don’t compromise vasculature
  • Use sufficiently strong suture material; e.g., polydioxanone, polypropylene, etc.* Monofilament to avoid sinus formation
  • Use muscle flap; e.g., internal obturator for perineal hernia
  • Polypropylene mesh if necessary
  • Well tolerated, allows capillary and granulation tissue in growth
  • Strict asepsis
  • Omentum - new blood vessels, cells, etc
  • Eliminate dead space, drains if necessary
64
Q

Umbilical hernia

A
  • Generally young
  • Usually congenital due to failed embryogenesis
  • Thought to be inherited
  • True hernias lined by peritoneal sac
  • Can see in association with cryptorchid dogs
  • Clinically soft, painless swelling at umbilicus
  • May be vomiting/abdominal pain if strangulation of bowel
  • Normally contain fat/omentum, occasionally intestine
  • Check diaphragm and heart
  • Radiography not normally necessary
  • Diagnose on palpation
  • Can resolve spontaneously, or be corrected at neutering
  • Repair by reducing, incise over hernia, excise sac and repair muscle edges
  • Don’t debride margins
  • Close with synthetic, absorbable, monofilament suture; e.g., polydioxanone
65
Q

Incisional hernia

A
  • Surgical closure of body cavity fails
  • Generally linea alba which fails
  • Normally within 7 days
  • Can be chronic

Day 5 is weakest point for wound healing

  • Generally surgeon to blame
  • Incorrect technique* Incorrect suture material/pattern
  • Entrapped fat between wound edges
  • Infection
  • Steroid therapy/cushingoid patient - poor healing
  • Poor post-op care
  • Oedema, inflammation and serosanguinous fluid often pre-empt
  • Soft painless swelling
  • Palpable defect
  • Exposed viscera
  • Commonly obvious but in some cases ultrasound might be useful
  • Similar with x-rays and advanced imaging
  • Repair asap
  • Evisceration is an acute abdominal emergency
  • Lavage and resect nonviable tissues/anastomose bowel if necessary
  • Re-open and repair entire wound
  • Only debride edges if infection or are non viable
  • Suture EXTERNAL SHEATH OF RECTUS ABDOMINIS (strongest holding layer)
  • Ensure monofilament suture, long lasting and appropriate size
  • Chronic hernias often more difficult due to adhesions
66
Q

Traumatic abdominal rupture

A
  • Caused by blunt trauma/bite
  • Flank
  • Prepubic
  • Prepubic tendons can rupture associated with pelvic fracture
  • Can be easy to miss
  • Use same hernia repair principles
  • Contaminated wounds e.g. bites, lots of lavage and avoid mesh
  • Identify free edge of abdominal wall and reattach to cranial pelvic brim if prepubic tendon rupture
  • Prognosis relates to organs involved
67
Q

Inguinal hernia

A
  • Due to congenital inguinal ring abnormality or trauma
  • Intestine, bladder or uterus can enter subcutaneous space
  • Can be associated with obesity/pregnancy
  • Thought to probably be inherited => recommend neutering

Scrotal hernia is rare form (can be traumatic) or post castration in small mammals with large inguinal rings and open methods

Inguinal hernia
* Non traumatic inguinal hernias mainly seen in intact female middle aged dogs or under 2-year-old male dogs
* Small breeds e.g. Cairn/WHWT
* Non-painful inguinal swelling
* Painful if incarcerated contents
* Omentum is most common content

68
Q

Inguinal hernia

A
  • Due to congenital inguinal ring abnormality or trauma
  • Intestine, bladder or uterus can enter subcutaneous space
  • Can be associated with obesity/pregnancy
  • Thought to probably be inherited => recommend neutering

Scrotal hernia is rare form (can be traumatic) or post castration in small mammals with large inguinal rings and open methods

Inguinal hernia
* Non traumatic inguinal hernias mainly seen in intact female middle aged dogs or under 2-year-old male dogs
* Small breeds e.g. Cairn/WHWT
* Non-painful inguinal swelling
* Painful if incarcerated contents
* Omentum is most common content

69
Q

Diaphragmatic rupture

A
  • Relatively common presentation following RTAs
  • Can be congenital (hernia)
  • Results from including abdominal pressure with open glottis
  • Tear in diaphragm allows abdominal content to move into thorax
  • Muscular portion of diaphragm most commonly affected as weakest point
  • Radial or circumferential tears
  • Tears usually occur along the fibre orientation of the muscles (i.e., radial tears) or at their attachment to the ribs (i.e., circumferential tears)

Clinical signs
* Normally present shortly after trauma shocked
* Pale/cyanotic
* Tachypnoeic/dyspnoeic
* Tachycardic
* Occasional cardiac arrythmias
* Hydrothorax

  • Can be chronic injury with respiratory/GI clinical signs
  • Exercise intolerance
  • Dyspnoea
  • Vomiting
  • Weight loss
  • Etc.
  • Occasionally incidental finding
  • Radiography
  • Loss of diaphragmatic line
  • Loss of cardiac silhouette
  • Presence of gas filled structure in thorax
  • Atelectasis
  • Displaced abdominal organs
  • Water soluble contrast into abdomen
  • Ultrasonography, esp. in chronic case

Treatment
* OXYGEN
* IVFT and warm up
* Higher mortality if surgery performed less than 24 hours following injury (also greater than 1-year-old)
* If acute gastric distension you need to operate a.s.a.p.
* Prophylactic antibiotics due to toxin release from organ strangulation
* ECG

70
Q

Perineal hernia

A
  • Not uncommon
  • Can be spectacular
  • Bulging perineal area
  • Faecal tenesmus/dysuria
  • Normally entire older male
  • Occasionally in bitch/cat
  • Cause
  • Progressive weakening of pelvic diaphragm
  • Hormonal influence
  • Tenesmus
  • Congenital/acquired weakness
  • Colitis/prostatomegaly

Pelvic diaphragm
* Levator ani, coccygeus and external anal sphincter muscles provide lateral support to the anus
* Disruption to this causes rectal enlargement, faecal impaction and tenesmus
* Can be bilateral
* Pelvic fat, peritoneal fat, prostate and bladder can herniate

  • Reducible perineal swelling* On rectal, absence of pelvic diaphragm* Always check for bilateral disease* Assess sphincter tone - chronic cases can remain incontinent* Ultrasound hernia/contrast urethrography will highlight bladder
  • Bladder retroflexion– Emergency– Stranguria– Hyperkalaemia– Azotaemia– Avascular necrosis
  • Cystocentesis through perineum if bladder retroflexed and cannot pass urethral catheter* IVFT (check K+levels if urinary obstruction)* Herniorrhaphy

Complications
* Faecal incontinence* Suture placement - hit sciatic nerve* Duration of problem* Urinary problems* Infection* Rectal prolapse* Sciatic nerve entrapment* Recurrence - castration

71
Q

Hiatal hernia

A
  • Brachycephalic breeds (English bulldog, French bulldog, pug, etc.), Shar pei* Congenital defect* Clinically very similar to oesophagitis* Regurgitation* Hypersalivation* Visceral discomfort* Normally thin

A hiatal herniaoccurs when the upper part of your stomach bulges through the diaphragm

  • Radiography* Soft tissue opacity in dorso-caudal thorax adjacent to diaphragm* Fluoroscopy* Endoscopy

Tx oesophagitis* Antacid* Sucralfate* Prokinetic* Antibiotic (if aspiration)

  • Surgery* Ventral midline coeliotomy* Reduce hernia at oesophageal hiatus and close* Pexy oesophagus to diaphragm* Pexy stomach to body wall
72
Q

PPDH - peritoneopericardial diaphragmatic hernia

A
  • Congenital communication between pericardial sac and abdomen* Faulty development of septum transversum* Often cardiac/sternal deformity in association* Can be asymptomatic* GI or respiratory signs e.g. v+/d+, anorexia weight loss, wheezing, dyspnoea* Weimaraner, Cocker spaniel
  • Radiography* Enlarged cardiac silhouette* Dorsally displaced trachea* Gas opacities in pericardial sac* Ultrasound* Contrast radiography
  • Ventral midline coeliotomy* Incise sternum if necessary* Reduce viscera* Suture diaphragm * No need to separately close pericardium
73
Q

3 broad causes of weight loss

A

Malnutrition - insufficient calories ingested to maintain body condition
Maldigestion/malabsorption - sufficient calories ingested but not absorbed properly
Malutilisation - Sufficient calories ingested and absorbed nut not used in right way

74
Q

Causes of malnutrition

A

Diet - inappropriate or not enough
Physically cant eat - cant access or mechanical inability to chew, prehend, swallow
Dont want to eat - stress, behaviour, appetite, nausea, pain

75
Q

Masticatory myositis

A

*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 as these can open their mouths
*No pain but anorexia and weight 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 fibresTreatment

*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?
*Often poor prognosis by this stage
*Recurrence common

76
Q

Cricopharyngeal atelectasis

A

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)

77
Q

Maldigestion/malabsorption

A

Almost always associated with signs of GI disease
Presenting GI signs can be similar to some
Malutilisation causes
Appetite often increased (if not associated with nausea)

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)

Malabsorption (small intestines/pancreas)
*Reduced absorption of fats/proteins/carbohydrates
*Diarrhoea or increased volume of faeces
*Changes in colour/consistency, particularly in EPI (fat in faeces)
*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)

Remember -some common systemic diseases can cause GI signs which can be severe enough to cause malabsorption or maldigestion without pathology of the gastrointestinal tract. Common examples include Hyperthyroidism in cats Hypoadrenocorticism (Addison’s disease) in dogs

78
Q

Malutilisation

A

Abnormal nutrient handling
- PLN
- Diabetes mellitus
- Liver disease

Increased demand for nutrients
- Neoplasia
- Hyperthyroidism
- Infection
- Cardiac cachexia
- Parasites

Usually systemically unwell with systemic signs beyond weight loss

As caloric demand not being met, diseases causing weight loss often result increased appetite unless underlying disease process also causes appetite to be overridden by negative factors, commonly -NauseaPyrexia/inflammationPainStress

Increased appetite and weight loss - diabetes mellitus, hyperthyroid, neoplasia, cardiac cachexia, PLN, chronic GI disease, intestinal parasites

79
Q

Anorexia

A

Not eating at all
Hyporexia - not eating enough for normal maintenence

Loss of appetite, reluctance to eat and/or mechanical inability to eat

Loss of appetite
*Signs of systemic disease on history or clinical exam?
*Particularly note drooling, pyrexia, pain
*Consider haematology/biochemistry/urinalysis
Imaging as indicatedConsider antiemetic trial for possible nausea?

Common causes
- Renal/hepatic disease - toxin accumulation
- Any inflammatory/infectious process causing pyrexia
- Neoplasia

Reluctance to eat
*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

Mechanical inability to eat
*On exam able to open and close mouth normally?
*Tongue and oral soft tissues appear normal?
*Pain in neck/mouth/limbs
*When does eating cause 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 radiographs/ x-ray)
*Consider pain relief trial?
Rule out systemic causes first…

Common causes
Dental disease
*Gingivostomatitis
*Oral/pharyngeal/oesophageal masses

Treatment
*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

80
Q

Hepatic lipidosis

A

Mostly cats if rapid weight loss due to calorie defecit
Increased risk if high BCS
Peripheral fat mobilisation exceeds liver capacity to redistribute or use - deposited in hepatocytes - liver failure

Clinical signs
- Hepatomegaly
- Jaundice
- Lethargy
- Vomiting/diarrhoea
- Ileus
- Hypersalivation
- Pallor
- Neck ventroflexin - hypokalaemia
- Coagulopathies

Diagnostic tests (changes in addition to those from underlying diseases)
*Biochemistry -increased ALT, ALP, AST
*Haematology -nonregenerative anaemia, poikilocytosis, increased Heinz bodies
*Coagulopathies –possibly prolonged PT and APPT
*Low vitamin 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)
*Supplement K+, phosphate and B12 according to biochemresults
*Start feeding slowly -high protein low carb diet (tube feeding)
*Consider antiemetics -maropitant
Prognosis->80% recovery if treatment started early

81
Q

Refeeding syndrome

A

Focus on Refeeding syndrome

*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 = severe hypokalaemia
*Body responds to 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
*Maxspeed-1/3rdRER on day one , 2/3rdday two, all day three
*Monitor K+, Mg2+ and phosphorus at least daily and supplement as needed

82
Q

Resting energy requirements calculation - RER

A

30(BW kg) + 70
If between 2 and 45 kg

83
Q

Weight gain

A

Exercise, growth, pregnancy

Pathological increased lean mass
Neoplasia
Hyperplasia
Inflammation
Cysts/abscesses
Organomegaly - disease/iatrogenic
Fluid retention - hypervolaemia, oedema, third space, ascites, pleural effusion, pericardial effusion

Overfeeding, reduced exercise (possible pathology), predispositions (neutering, age, breed, owner)
Increased appetite - systemic disease - normal calorific demand (hyperadrenocorticism), higher calorie demand - acromegaly, insulinoma
Iatrogenic - glucocorticoids
Behavioural
Hypothyroid

84
Q

Insulinoma

A

Functional neuroendocrine tumour of pancreas
B cells of islets of Langerhans
*Secretes multiple hormones including somatostatin, glucagon, gastrin, pancreatic polypeptide, IGF1 and serotonin and INSULIN.
*Excessive insulin - low blood glucose- clinical signs

Clinical signs
*Increased appetite and weight gain (BCS)
*Weakness, ataxia, collapse, seizures
*Particularly after exercise/fasting OR feeding (stimulates insulin release)
*Glucose admin improves signs

Diagnosis -bloods
Demonstrate hypoglycaemia (BG <3mmol/l) while clinical signs, which resolve with glucose admin
*History clinical exam and routine bloods –
*Exclude other causes of hypoglycaemia (e.g. sepsis, liver failure, Addison’s, toxin ingestion, etc.)
*Increased suspicion if
*Increased insulin:glucose (not sens or spec)
*Low fructosmaine

Diagnosis-imaging
*Ultrasound and x-ray chest and abdomen
*Looking for mass or mets
*50-75% insulinomas visible on ultrasound
*Dual-phase CT angiography may be the best, but still can miss some as so small

Surgery
*Excisional biopsy treatment of choice
*Even with mets can reduce clinical signs
*Care to correct bloodglucose before/during GA
*Nodulectomy or partial pancreatectomy
*Possible post op complications
*Pancreatitis, persistent hypoglycaemia (incomplete removal/mets), DM, hyperglycaemia (B cell atrophy)

85
Q

T3 T4 actions

A

Increase basal metabolic rate
Affect protein synthesis
Regulate long bone growth and neural maturation
Increase sensitivity to catecholamines
Regulate protein, fat, carb metabolism
Stimulate heat generation
Stimulate vitamin metabolism

86
Q

Hypothyroid

A

Primary in most cases
- Idiopathic thyroid atrophy
- Immune mediated lymphocytic thyroiditis
Secondary
- Space occupying mass in pituitary destroying pituitary thyrotrophs

Congenital
- Abnormal thyroid gland development
- Dyshormonogenesis of thyroid hormone
- Abnormal TSH production

Iatrogenic - cats - following excessive treatment for hyperthyroid

Signalment
*Middle aged to old
Mostly large breed (including Golden Retrievers, Dobermans, Dachshunds, Cocker Spaniels…)Increased risk if female neutered?

Clinical signs Very variable! Easy to attribute to normal aging
*Demeanour - dull, lethargic, exercise intolerant
*BCS - weight gain without increased appetite, obesity
*Temp - hypothermia, heat seeking behaviour
*Skin/coat - dry, +++ shedding, slow hair regrowth
*Symmetrical alopecia of trunk/thighs/tail/neck, hyperpigmentation
*Occasionally secondary pyoderma and pruritis
*Tragic facial expression (myxoedema - increased GAGs in skin make facial folds more pronounced)
*Neuro - increased risk of peripheral neuropathies/ megaoesophagus, vestibular disease, etc., myxoedema coma (rare!)
*(Signs associated with tumour possible if 2ndary)
*CVS - hypotension, bradycardia
*Repro issues/failure

Congenital
Rare abnormality of puppies and kittens.
Signs include:*Disproportionate dwarfism
*Dullness, lethargy and impaired mental development
*Goitre (enlarged thyroid gland due to thyroid really trying)
*Epiphyseal dysgenesis (underdeveloped growth plates in long bones), short vertebral bodies, and delayed growth plate closure (increased fracture risk)
*Retained puppy coat
*Poorappetite
*Constipation
*Delayed dental eruption
*Neuromuscular signs including tremors, proprioceptive deficits, exaggerated spinal reflexes
Diagnosis and treatment as for adult form

Routine bloods:
*Haematology -normocytic, normochromic, nonregenerative anaemia (50%)
*Biochemistry -hypercholesterolemia (80%) triglycerides, alkaline phosphatase and CK

Definitive diagnosis
Compatible signs + LOW Total T4/Free T4 and NORMAL-HIGHTSH
If equivocal further testing possible (scintigraphy, TSH stim) but not widely available.
If still unsure consider treatment trial?

Treatment
*Levothyroxine -0.02-0.04mg/kg SID or divided BID-With or without food -be consistent-Lifelong treatment

Lots of nonthyroidal illness and certain drugs can lead to low serum thyroid hormone measurements in dogs and cats which do NOT have thyroid disease. This is a phenomenon termed sick euthyroid.
Many of these conditions have signs similar to hypothyroidism and some of the clinical signs can even improve after levothyroxine administration despite not being truly hypothyroid!
These cases will usually have LOW Total T4/ Free T4 and LOW/NORMAL TSHT4 and TSH testing is vital for accurate diagnosis!

87
Q

What makes up the periodontium

A

Alveolar bonePeriodontal ligament (PDL)CementumGingiva

Act as a seal between tooth and gumsPeriodontal ligament fibres -shock absorbing fibres from alveolar bone to cementum and root

88
Q

How is gingivitis scored?

A

G0 - G3
- On tendancy to bleed
Periodontal probe
Gingival inflammation
Erythema
Swelling/oedema
Bleeding

G0 = no gingivitis
G1 = limited gingivitis but no bleeding
G2 = small mounts of delayed bleeding
G3 = bleeding almost as soon as you touch it with the probe

89
Q

Periodontitis

A

Attachment loss pattern
- periodontal pocket
- Gingival recession
- furcation involvement - f0-f3 - lost bone between teeth
- Mobilitu - m0-m3