Abdominal, oral, rectal Flashcards

Question

What to do if haemoabdomen

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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)

Answer 7

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.)

Answer 8

Organomegaly - splenomegaly, hepatomegaly Abdominal mass Pregnancy Bladder distension Obesity Gastric distension All these cause abdominal distension without effusion

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

ddx surgical and non surgical trauma haemostatic defects neoplasia investigation PCV and TP of fluid Presence of platelets Cytology US

Answer 16

ddx surgical and non surgical trauma haemostatic defects neoplasia investigation PCV and TP of fluid Presence of platelets Cytology US

Answer 17

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.

Answer 18

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

Answer 19

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

Answer 20

* 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

Answer 21

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

Answer 22

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

Answer 23

* 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

Answer 24

* 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

Answer 25

* 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

Answer 26

* 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

Answer 27

* 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

Answer 28

* 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

Answer 29

* 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

Answer 30

* 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!

Answer 31

* 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 (?)

Answer 32

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

Answer 33

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

Answer 34

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...

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

* Umbilical* Inguinal* Incisional* Diaphragmatic* Perineal* Pericardio-peritoneal* Hiatal

Answer 40

* 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

Answer 41

* 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

Answer 42

* 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

Answer 43

* 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

Answer 44

* 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

Answer 45

* 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

Answer 46

* 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

Answer 47

* 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

Answer 48

* 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

Answer 49

* 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

Answer 50

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

Answer 51

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

Answer 52

*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

Answer 53

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)

Answer 54

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

Answer 55

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 -*Nausea*Pyrexia/inflammation*Pain*Stress Increased appetite and weight loss - diabetes mellitus, hyperthyroid, neoplasia, cardiac cachexia, PLN, chronic GI disease, intestinal parasites

Answer 56

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 indicated*Consider 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

Answer 57

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

Answer 58

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

Answer 59

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

Answer 60

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

Answer 61

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)

Answer 62

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

Answer 63

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!

Answer 64

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

Answer 65

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

Answer 66

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

Abdominal, oral, rectal Flashcards

(90 cards)