227.414 CAMST Summaries FULL.pdf

227.414 CAMST II SA Emergency Medicine.......................... 2 Urogenital Imaging …................................. 35 Anesthesia Acid-Base Balance …........... 5 Urogenital Tract Drugs ….......................... 36 Anesth...

227.414 CAMST II SA Emergency Medicine.......................... 2 Urogenital Imaging …................................. 35 Anesthesia Acid-Base Balance …........... 5 Urogenital Tract Drugs ….......................... 36 Anesthesia of Compromised Patients.. 7 UGT Surgery ….............................................. 37 Fluid Therapy …........................................ 11 Endocrine Medicine …............................... 42 GIT Imaging …........................................... 13 Endocrine Pharmacology …..................... 47 Gastroenterology …................................. 14 Neurology …................................................. 49 GIT Pharmacology ….............................. 20 Neurosurgery …........................................... 56 GIT Surgery............................................. 23 Animal Behavior ….................................... 58 Urogenital Medicine............................. 29 Lecture 1: CPR Immediate CPR increases the chances of survival following cardiac arrest Learning Objectives: Cardiopulmonary resuscitation (CPR) is an emergency procedure 1. Describe aspects of preparedness for CPR consisting of chest compressions often combined with artificial 2. Recognize cardio-pulmonary arrest (CPA) ventilation. 3. Describe basic life support (BLS) technique 4. Review monitoring tools for effective CPR Intubate 5. Underline components of advanced life support CPR is indicated when the patient is immediately (ALS) unresponsive and not breathing alongside chest compressions -Elbows should be locked -Core muscles should be driving force, rather than upper arm muscles Compression frequency of 100-120 bpm + -The patients should be positioned lower than the compressor to allow 10 breathes/min to give etCO2 of >15mm Hg optimal leverage Chest Compressions ***capnography **ECG Both are non-shockable rhythms! The most common arrest "rhythms" in cats + dogs = pulseless electrical activity and asystole Drugs – can go routes other than intracardiac → go IO, IV, IT H: hypovolemia, hypotension, hypothermia, What makes a team best prepared for CPR? preparedness Causes hypoxemia, H+ acidosis, hypoglycemia -designated area ventilation for CPA -well-designed crash cart BLS T: toxins, tension, pneumothorax, tamponade, -regular training thrombosis, trauma -leader for role direction chest compressions  Easy access Designated for stabilization Lecture 2: ER Facility + Preparedness Clear labelling Team-specific Emergency arrangement area Emergency Crash Cart Regular auditing Appropriate equipment Portable, ready for resuscitation, tool Records are drawer/toolbox, clearly labelled, logically essential! organized, frequently audited, strategic placement w/in clinic Necessary equipment Track progress, May require multiples in large clinics drug -adjustable lighting administration, -suction device data collection, Includes ECG, -oxygen source legal obligation capnography, non- -monitoring IV access + emergency drugs: clippers, prep invasive BP, spO2 -crash cart swabs, IV catheters/ports, IO drill, flush, -ultrasound Skill and expertise tape/glue, tourniquets, syringes, needles -exam table -Prioritizing and managing time Drugs: CPR + adrenaline, Fluid therapy -High performance atropine, vasopressin The ideal emergency table – difficult IV Airway: ET tubes, laryngoscope + - adjustable height access, difficult necessities blades, guide wires, forceps, - nonslip intubation, Advanced airway care: ambu-bags - stable thoracocentesis tracheostomy tubes, - incorporated scale -Interventions are feeding tubes, wires, - no electrical interference almost always the suture kits same, regardless of the patient Warming devices: Thoracic intervention: heating pads, Bair thoracocentesis kit, Minimum database (PCV/TP, glucose, -Working effectively as a huggers, fluid pericardiocentesis kit, chest Emergency azostick) team heaters, water- drain kit, Finochietto rib lab Coagulation testing (PT, aPTT) filled gloves spreader, open chest CPR CBC/biochemistry + lactate, blood gas analyzers, electrolytes, creatinine Lecture 3: Triage and Stabilization Vital organ systems = triage respiratory, cardiovascular, + Short clinical examination to assess vital organ unstable nervous systems systems and determine if the patient is stable. stable Phone triage Triage -allows vet to prepare categories awkward -identify if animal needs to come in -transport instructions Neurological triage away - Mentation Circulation - Posture HR – tachycardia, bradycardia, arrhythmia - PLRs Oxygen therapy Pulse quality – bounding, weak, irregular, paradoxical, normal - Motor reflexes POCUS MM color: pink > icteric > hyperemic > pale > white > grey/muddy - Withdrawal Stabilize > cyanotic reflex CRT: 1-2s; delayed or accelerated C at: 140-200 bpm respiratory - Deep pain Dog: 6 0-120 bpm distress response Low-stress Sedation + handling analgesia balance of diagnostics Horizontal Approach and therapy Basic Triage Exam hypotension - Initial treatment - Mentation 6 perfusion parameters without diagnosis - Respiratory effort + rate - Large amount ✓ CRT - Pulse rate + quality of information ✓ HR - MM color - CRT required ✓ Mentation Feline - Treatment of most ✓ MM color - + anything obvious shock probable ✓ Pulse quality triad - Clinical intuition ✓ Temperature (pattern recognition) - Risk/benefit ratio bradycardia hypothermia Lecture 4: Acid-Base Balance 1 End tidal CO2 (etCO2) is ≈ alveoli most of The deeper the anesthesia, the more CO2 that will be the time → will required for the normally be very hypothalamus to notice Hyperventilation works similar to by ↓CO2, so less arterial (PaCO2) dilution occurs, allowing ↑O2 This pathway is use capnography to give suppressed w/ an estimate of anesthesia, resulting in PaCO2 hypoventilation ***if issues w/ O2 are suspected, this indicates diffusion is compromised as PaO 2 ≈ 5x FiO2 CO2 is much more diffusible than >40 mmHg PaCO2 = hypoventilation O2 → CO2 may not be affected, but Q Hypoxemia = 90% saturation, or PaO2 = < 60 mmHg Fixed acids are removed In-line Zone 2 via kidneys → = w/ heart; V = Q metabolic acidosis Low V-Q = low ventilation Below the CO2 is removed via respiration → = Zone 3 + high perfusion heart; V < Q respiratory acidosis High V -Q = high ventilation + low In areas of local hypoxia, vasoconstriction perfusion For a metabolic problem, the respiratory system can occurs (reflex), so zone 3 doesn't exist and Under anesthesia, the compensate BUT the metabolic system cannot compensate zone 2 is the majority zones are flipped, and the effectively for a respiratory problem reflex is absent, leading V-Q Mismatch to... Lecture 5: Acid-Base Balance 2 Strong base NaCl + H2O → NaOH + HCl Strong acid CO2+ H2O → H2CO3 → HCO3- + H+ Carbonic acid The problem w/ Bicarb... - indictor of metabolic imbalance, as opposed to CO2 which gives only pulmonary indicator → however, not independent from respiratory - any increase in HCO3 results in an alkalosis Modern systems instead have... - HCO3 is not an independent factor, and is directly related to CO2 → if CO2 ↑, HCO3- ↑ >24 mmol/L = alkalosis Base excess (BE) In acute respiratory disorders, a ΔCO2 of 10 = ΔHCO3- of 1 12hrs Hyperadrenocorticism = Cushing's ↑BG = osmotic diuresis = hypovolemia + dehydration Care required w/ nerve blocks to avoid ↑responsiveness to catecholamines → hyperT → Administer fast- damage/trauma check liver + kidney function acting insulin Diabetic ketoacidosis – cells produce ketones; severe Dehydration (inhibit ADH) + hypovolemia risk = electrolyte imbalances occur hypoT can result Risk of hypoventilation + hypothermia Stabilize ketoacidosis via blood gas analysis Dex medetomidine, medetomidine, Recommend: well-managed before Sx, check + k etamine all help to release hydration before pre-med, discontinue ACE- Low dose of acepromazine ↓ afterload glucose Low dose propofol → vasodilation inhibitors before Sx, get baseline BP + HR, avoid NSAIDs (synergistic w/ GCC) Mitral regurgitation: endocardiosis of LAV MR valve; aim to ↓afterload + ↑contractility Avoid α-2 agonists → massive Cushing's Tx (tril ostane/mitotatane) for systole vasoconstriction Hypoadrenocorticism = Addison's inhibit production of glucocorticoids Px prone to dehydration, azotemia, hypoT, hypoV whose stress response combats P imobendan ↑contractility so should be shock → stabilize before Sx dominant vagal tone (maintains continued vasoconstriction + BP) during Sx → Dilated Cardiomyopathy: heart is Arrhythmias due to ↑[K+], give Ca2+ IV to stabilize give d ex amethasone DCM flaccid, ↓contractility so ↓SV = CO Same management as MR/MVD myocardium, insulin to send K+ IC (need to also give maintained by ↑HR = avoid bradycardia glucose) If HypoT develops, d obutamine Hyperthyroidism + ↑contractility = β-1 receptors, (+) inotrope = ↑contractility + HR Limit stress w/ CHILL protocol @ home, low-stress handling Often w/ HCM, hyperT, CKD, Hypertrophic Cardiomyopathy: ↓CO, LA HCM arrhythmias; can have enlargement = diastolic dysfunction (filling) α-2 agonists ↓HR = beneficial Hypothyroidism hypoventilation + hypovolemia of LV = avoid tachycardia Acepromazine contraindicated Obesity + muscle weakness = hypoventilation → = hypoT as preload is necessary bradycardia + hypoT Recommend: well-managed CO = HR x SV Often have laryngeal paralysis + megaesophagus before Sx, limit stress, meds SV = preload, contractility, = ↑risk for reflux + aspiration pneumonia can continue (β-blockers, afterload Slower metabolism of drugs = use ↓[pre-med] diuretics, thyroid drugs); stop DO2 = CO + ACE-inhibitors 24hr prior Recommend: well-managed, use short-acting + CaO2 reversible drugs, preoxygenate (prepare for IPPV), give ***Patients w/ suspected cardiac H+ inhibitors (omeprazole) & extubate w/ cuff ½ Ketamine not disease identified via history, recommended – CaO2 = [Hg] x SaO2 physical exam + diagnostics deflated, address bradycardia + hypoT tachycardia + renal metabolism Lecture 10: Fluid Therapy 1 Osmole = solute that dissociates in solution to form one mole of particles COP – proteins are (-), attracting Na+ = retains H2O w/in IVF Moves from low osmole to high osmole = osmolarity Tonicity = comparison of osmolarity in two solutions w/ cell membranes In normal BP COP circumstances, Small pores w/in the endothelium Cellular membrane is very tight – regardless of the only allows water to move freely; value, all the BP > COP which allows O2, only allow tiny proteins + glucose, etc. to reach cells electrolytes to freely pass ions require pumps osmolarities should be around the same Osmolarity of IVF and ISF should be the same as electrolytes can pass through the endothelium hypotonic isotonic hypertonic H2O will shift into ISF, but cannot enter IVF (glycocalyx) and will Fluid will initially ↑ECF, but you gave lower If you add isotonic solution into the ECF, the enter lymphatics → re-enter circulation @ cd vena cava osmolarity → ECF osmolarity ↓ osmolarity will not Δ, meaning water will not Water shifts towards higher osmolarity = H2O move = just ↑ECF volume The solution enters ECF and ↑ the osmolarity; water moves into ICF until equilibrium is reached again shifts from low to high = H2O moves from ICF to ECF Will ↑ the IVF space = ↑BV Removes fluid from cells (cellular edema) Hypotonic fluids will ↑the volume of ICF To ↑BP or in cases of hemorrhage Na+ can be excreted in the kidney, and eventually ↓osmolarity of IVF to reach equilibrium Lecture 11: Fluid Therapy 2 - osmolarity ≈ isotonic LRS - more electrolytes (like plasma), lactate acts as buffer - lactate metabolized, consumes H+ = alkaline effect → will not cause acidosis (O2 is present) Crystalloids Composed of small - calcium important for contractility + vagal tone – will be chelated by molecules that readily citrate in blood products = use separate IV lines to avoid precipitation pass b/w IVF + ISF Distribute between IVF Normal Saline + ISF proportionately Indications = hypochloremic Complications to compartment space alkalosis, hypercalcemia Dilution: anemia, hypoproteinemia, coagulopathy (5:15) = give 3 -4x Edema: ↓COP as ↓[albumin] = edema vol ume l ost for IVF Acidifying effect: giving a lot of NaCl will ↑Cl in plasma; HCO3 Potentially pulmonary edema and Cl are exchanged together, Acetated Polyionic Solutions so ↑Cl = ↓HCO3 and pH eventually drops Hypertonic saline Plasma-lyte A No cellular edema, anti- Liver metabolizes lactate, but every cell Responders – will see large ↑BP inflammatory, ↑SV, ↑CO, ↑BP, ↓SVR has capacity for acetate (esp. muscle) = good choice for hepatic-compromised Short duration, no balanced patients If you give a small amount electrolytes, hemodilution No calcium = same line as blood products and they're located at the Bolus causes vasodilation = ↓BP plateau of the curve and Contraindications: there's no response, then hypernatremia/hyperosmolarity, cardiac Reason why we don't use it commonly → only their preload was already dysfunction, dehydration, uncontrolled indicated for hepatic dysfunction sufficient = non-responders hemorrhage, coagulopathies Cannot inject pure H2O as osmosis causes entry to erythrocytes = RBC lysis Ongoing fluid losses 1mL/kg/hr 5% Dextrose (D5W) Fluid Therapy Rapidly metabolized into water (proportionately), as Pre-existing fluid deficit glucose is metabolized to CO2 + H2O Peri-anesthetic fluid rate = Proportions – only 5% stays in IVF Maintenance requirement 2-5mL/kg/hr Lecture 12: GIT Imaging 1. Describe using Roentgen signs 2. Make an interpretation – signalment, history, rad description + ranked DDx "Given the patients signalment, history, and radiographic findings..." Roentgen signs (6) As cending, transverse, descending colon Correct position, contain normal location, number, size, shape, opacity, margins R ight k idney tucked in amounts of gas + feces caudate fossa of liver Transverse = immed. caudal to stomach Intestinal populations = areas Lef t k idney is more mobile of small intestine that have Des cending = down left abdominal wall R ectum contains Caudal es op hagus – not Past pelvic inlet = rectum normal amounts of different width/height normally seen gas + formed feces Stomach contains normal amounts of gas + fluid Des cending Pyl orus R HS – gas w/ LLR d uodenum runs Fun d us LHS – gas w/ RLR down RHS of abdomen Liver separates stomach from diaphragm Mention RPS, Check serosal detail w/ f alciform f at MSK system, Small intestine - "long + lazy" caudal thorax Urinary bl adder Contains fluid, gas + ingesta Check distension, radiopaque ventral to colon +/- cd. VC U reters not foreign material, plication, Spl een in ventral image normally seen atypical positioning, ileus *do not usually see feline spleen in DV C ecum – corkscrew Normally has more gas Do not mistake colon for pathologically distended small intestine Rare to see in cats Positive contrast enema is a quick way to see if Usually right of midline it's in the colon or SI – or use an ultrasound  - didn't ask the right questions; poor Lecture 13: Gastroenterology 1 Alters diagnostic approach Majority of history-taking errors in clinical - failure to correctly define the problem practice are due - failure to discriminate between symptoms Vomiting must be to a small # of - inadequate/incorrect reasoning Affects risk of aspiration differentiated causes - all result in in adequate investigation of from regurgitation! DDx pneumonia Changes DDx's vomiting Regurgitation = passive action of ingesta w/in esophagus moving out - centrally controlled + coordinated act via reverse peristalsis - see 'retching' prior → synchronous abdominal -no abdominal contractions contractions -no nausea, but hypersalivation (ptyalism) = not a useful measure - associated w/ signs of nausea (lip-licking, -bile staining unlikely to differentiate hypersalivation, depression, ++ swallowing, Presenting problems -food has not reached the stomach → pathology is w/in esophagus vocalization) Bil e staining ✓ Vomiting nearly always - can be immediately after eating, hrs later, or on an ✓ Regurgitation indicates empty stomach ✓ Abdominal pain vomiting so how digested the food is does not matter! ✓ Tenesmus ✓ Dyschezia Fecal color: from bile pigments + diet ✓ Hematochezia Diarrhea - complete biliary obstruction → pale (acholic) -color - ↑motility = ↓time for bacterial degradation = lighter color (green, yellow); usually associated w/ ✓ Constipation softer feces ✓ Flatulence -frequency Blood in feces: oxidized or fresh ✓ Hypersalivation -consistency - upper GIT (above ileum) = oxidized blood, mel ena = black/dark blood ✓ Weight loss -blood - lower GIT (below ileum) = fresh blood, hematochezia = bright red ✓ Altered appetite Diseases where there's abnormal absorption +/- digestion = steatorrhea = grey/bulky ✓ Fecal incontinence ✓ Depression ✓ Lethargy, anemia ✓ Shock Danger signs → necessitate more than symptomatic Tx Includes evidence of shock, +++ dehydration/weight loss/weakness, +++ depression/persistent anorexia, abdominal pain/distension/masses/effusions, Cannot use vomiting, jaundice/pale/congested MM, pyrexia, v. frequent vomiting/diarrhea, large chronicity, dehydration, or severity of associated volume malodorous vomiting, delayed gastric emptying, hematemesis, signs to distinguish b/w melena/dysentery, regurgitation, chronicity them!  Investigate Compare glucose for Lecture 14: Gastroenterology 2 altered GI peristalsis the fluid! septic peritonitis acute gastroenteritis/enterocolitis/colitis shock - many causes + toxins "acute - manage symptomatically unless danger signs are seen vomiting diarrhea abdomen" - careful PE w/ detailed abdominal palpation - imaging + systemic screening → look for extra-GIT fever diseases that cause 2o V/D dyspnea anorexia - other 2o consequences = electrolyte imbalances, dehydration, azotemia 7 F's – fat, fluid, food, fetus, feces, flatus, foreign object, f*cking big organ - rule out acute parasitism w/ fecal sample - rule out ARF → novel protein or hydrolyzed diet Symptomatic Tx: anti-emetic (maropitant +/- ondansetron), 25% RER w/ source of fermentable fiber, +/- H+ inhibitor Maropitant is 1st- (omeprazole) & gastric protectant (sucralfate) line, as works for ***Have owner watch for development of danger signs 24hrs ***oral antibiotics have no place in the management of uncomplicated gastroenteritis*** On d ansetron good for mucosal damage The use of probiotics currently have little evidence for maropitant → + ondansetron → + metoclopramide Severe mucosal damage – anything greater than a small effect in acute diarrhea; however, unlike ABs there's no harm in adding them CPV enteritis Therapeutic goals: estimate bacteria cost (establish level of care), Fluid should contain electrolytes, glucose, & amino establish effective tissue acids - translocation of bacteria through perfusion, dehydration + Importance of enteral mucosal wall + ↓WBCs due to viral - restore perfusion parameters rapidly ongoing losses, electrolyte nutrition invasion → activation of - replace deficit + main + losses over ~12 hrs; reassess imbalances +/- acid-base fluid - feed gut ASAP endothelium, neutrophils + main + losses problems, intractable therapy - aggressively control macrophages - loss of electrolytes + fluids → often hypokalemic vomiting, septicemia, gastric vomiting to allow - majority of CPV deaths as result of - usually acidotic, but can be alkalotic acid-induced disease, feeding gram(-) sepsis - use LRS & K+ empirically (max rate 0.5mmol/kg/hr) nutrition, fecal microbial - feed ~25% of RER in - significant disturbance in - if K+ is not improving, consider concurrent Mg2+ transplant small, frequent meals microflora Kill the bacteria that have deficiency → treat w/ 0.75 MgCl mEq/kg/day CRI - consider placement of passed the mucosa – so give in IV line NE tube parenteral, not PO dose → BS analgesia – amoxicillin/clav + enrofloxacin Acid-base balances will often self-resolve once intermittent dose of (short duration) fluid therapy is administered methadone  Observe the animal Lecture 15: Gastroenterology 3 ***always distinguish b/w vomiting & regurgitation*** Physical exam eating/drinking -oral/pharyngeal -neck palpation 1. Pharyngeal plain lateral -neurological exam -thoracic auscultation 2. Cervical + thoracic radiography 3. Barium contrast Important to check for aspiration pneumonia Alveolar pattern in ventral area (right middle lung lobe), w/ regurgitation = aspiration pneumonia esophageal stricture Circumferential band of fibrotic esophagitis bands IBD dysphagia + Presents 1-3 weeks after 'event' esophagus function - - neoplasia regurgitation causes - transport bolus to - lymphangiectasia stomach - hepatic disease esophageal FB - prevention of reflux - chronic gastritis megaesophagus via normal tone of LE - GI ulcers Failure of esophageal peristalsis Chronic cases have risk of - pyloric hypertrophy pseudomediastinum, and/or sphincter Congenital, NM, trauma, pneumothorax, pyothorax, perforation - intussusception metabolic, idiopathic acquired of esophagus Defects include CN defects, polyneuropathies, NM dysfunction; FB Circumferential damage can result in common for acute presentation; stricture @ site of prior damage; s tricture f ormation pain + inflammation can lead to ileus = abnormality/difficulty swallowing dysphagia Oral phase: prehension, bolus formation - difficulty prehending, modified eating behavior Extra-GIT Pharyngeal/cricopharyngeal phase: initial gag/swallow - CKD - outstretched/flexed neck - Hyperthyroidism - repeated swallowing - Pancreatitis Acid reflux is silent, but is the - immediate regurg; oral/nasal - Hepatitis most common cause of esophageal damage Esophageal/gastroesophageal phase: transit, LES, 2o peristalsis Primary-GIT - repeated swallowing - AFR - cough + gag; regurgitation Consider signalment + history - IBD - Parasitism  En d oparasitism: demonstrate their absence; low #'s, Lecture 16: Gastroenterology 4 fecal float of 3 samples or IDEXX fecal PCR panels Chronic diarrhea (manual Trichuris needed) - consider relevance as many are ubiquitous PE – BCS, hydration, AFR : perform 2 week food trial w/ History: signalment, MM, thyroid gland No novel/hydrolyzed protein and highly fermentable duration, severity, (cats), careful fiber + high digestibility variability, SI vs LI, abdominal palpation, localizing inciting causes, full rectal exam signs Sys temic d isease s creening: CBC, serum biochem, dietary history, urinalysis, T4 (older cats), serum B12, basal cortisol (Addison's) - rule out extra-GIT disease, diagnostic associated signs Abdominal palpation checks for PLE's include clues for GIT disease, 2o sequelae pain, masses (intussusception, FB, lymphangiectasia, neoplasia), fluid, organomegaly, infectious, structural, bowel thickening EP I rul ed out: pancreatic acinar atrophy (dogs), neoplasia, IBD, chronic pancreatitis (cats) If localizing signs w/ pain, organomegaly, mass, FB, endoparasites, GI hemorrhage dilation consider fecal transplant abdominal imaging Imaging: plain radiograph, US, contrast radiograph; partial obstruction, masses lymphadenopathy, intestinal thickening, extra-GIT disease Exocrine Pancreatic Insufficiency Pancreatic acinar atrophy or chronic pancreatitis Biopsy: required for IBD, lymphangiectasia, diffuse + Inflammatory Bowel Disease Diagnosis: feline TLI (overseas), canine TLI testing focal neoplasia → endoscopic or laparotomy Triad of genetics, microflora, & environment/diet Tx: enzyme replacement; empirical starting dose, then adjust Loss of tolerance to microflora + dietary antigens = based on response Endoscopic Laparotomy polyclonal globulin response (+) less invasive, direct (+) sample other Disruption of normal bowel structure, function, motility + visualization, multiple organs/abdominal exploration, dysbiosis → malabsorption, abnormal motility biopsies, usually mucosal (-) equipment, GIT only, retrieval/excision, full Present w/ diarrhea, vomiting, weight loss (poor BCS), duodenum/prox jejunum thickness sample malnutrition Osmotic – maldigestion, malabsorption, only, mucosa only, small (-) invasive, small # of To Dx IBD, an exhaustive search for all potential causes reduced SA, low digestibility biopsies, dehiscence risk, sample must be completed Motility - ↑/↓ 2o to cannot visualize mucosa Tx: dietary management essential +/- immunosuppression inflammation or Check serum B12 in all cases Permeability – diarrhea abnormal sensation inflammation, congestion, Dx of IBD requires: ulceration, cellular Secretory – Diet w/ n-3 PUFA, antioxidants, high 1. chronic clinical signs inflammation, ↑membrane pump digestibility, fermentable fiber source, 2. histological description consistent apoptosis novel protein w/ IBD activity 3. absence of an inciting cause  urolithiasis Lecture 17: Gastroenterology 5 anorexia abdominal distension vomiting (diarrhea unusual) +/- Hepatic PS Shunt hematemesis, melena PU/PD Sin gle extrahepatic P S shunt Hepatic Disease – small breeds ascites Diagnosis hepatomegaly or Sin gle intrahepatic PS shunt inappetence microhepatica – large/giant breeds 1. Patient assessment See poor growth + post- icterus 2. Initial lab assessment (CBC, jaundice stunted depression (hepatic prandial signs of hepatic biochem, urinalysis) growth encephalopathy) - nausea, encephalopathy hypersalivation Bile acids – pre is normal, 3. Expanded lab assessment (bile acids, coag profile, NH3) post ↑ Tx of choice = surgically Bile acids do not 4. Hepatic imaging PIVKAs can be measured in occlude vessels, but can quantify hepatic 5. Hepatic biopsy plasma → if patient would respond manage medically if the damage to vitamin K supplementation If you suspect severe hepatic causes of liver disease owner cannot afford it fibrosis, or hepatic sorosis → not - cholangitis suitable for biopsy / cholangiohepatitis (cats) - chronic hepatitis (dogs) - neoplasia US is the tool of choice for general support = maintain hydration, electrolyte + acid-base, - hepatic lipidosis imaging the liver nutritional support, anti-emesis, gut protectants - portosystemic shunts - acute toxic hepatitis / hepatopathy hepatic encephalopathy Lactulose = fermented by - drug induced Cholangitis / Cholangiohepatitis hepatopathy - ↓ NH3 from dietary protein Two forms – l ymphoplasmacytic, suppurative bacteria, ↓pH; laxative effect; - ↓ bacterial production of NH3 modifies microbiome to ↓ NH3 - bile duct obstruction Dx : w/ ↑bilirubin, +/- ALP/ALT; US non-specific; definitive Dx w/ biopsy - Prevent intestinal absorption Lymp hoplasmacytic: chronic, vague history, I-M – often w/ IBD + pancreatitis; Tx w/ bacteria - Prevent muscle catabolism steroids + nutritional support Suppurative: acute, fever, hepatic pain, neutrophilic peri-portal infiltrate, presumed ascending biliary infection; Tx w/ ABs (non-O2, gram(-)) + nutritional support Feline Hepatic Lipidosis Develops acutely when cats cannot export lipids to be Regenerative processes delivered to the liver Canine Chronic Hepatitis release enzymes – high Cat cannot assemble phospholipid droplets and lipid Poor BCS, mild-severe jaundice, may develop ascites, frequently small liver [ALP]/[ALT] w/ recovery proteins, so fat accumulates w/in the liver Serum bile acids show damage (elevation), US unremarkable, biopsy shows hepatic Dx : w/ unremarkable CBC, ↑ALP, ALT + AST activity, ↑total degeneration + necrosis bilirubin; bilirubinuria precedes jaundice C auses: breed idiopathic (Doberman), copper storage (WHWT, Dalmation, Doberman), Severe hepatocellular damage + cholestasis drug toxicities (carprofen, pentobarb) Tx : correct dehydration, electrolyte alterations, hepatic - cop per: ↓dietary copper, address toxicity w/in liver; requires 1g of tissue biopsy for encephalopathy → forced enteral nutrition = cornerstone [Cu] of therapy Give sulfur AA, SAMe, K+, vit K Lecture 18: Gastroenterology 6 Triglycerides → Pancreatitis Suddenly introduce a high-fat diet when 1. ↑ chylomicrons in haven't been feeding it – set them up for pancreatic capillaries high fat intolerance 2. Hyperchylomicronemia ↑ viscosity + impairs perfusion C C K = most important p ancreatic 3. TG hydrolyzed by s ecretion mediator Anything that causes ↑ pancreatic lipase in - produces Ca2+ release from IC store chylomicrons can cause - triggers zymogen granule exocytosis endothelium greater production w/ gastric pancreatitis - 4. FA > albumin → clump feeding vs parenteral together as micelles, acting Prevalence of as a detergent → Acute Pancreatitis Proximity to stomach → gastritis hyperlipidemia in endothelium damage + fusion of granules min i schnauzers inflammation w/ lysozymes = Attached to is very high 5. Endothelial + acinar cell (~50%) activation → descending damage, ischemia, edema autodigestion of duodenum → Proximity to ascending/ small bowel transverse/ descending reduced clearance of pancreatic tissue enteritis colon → large bowel active zymogens = ↓ enzyme secretion diarrhea + colitis autodigestion continues also involved *** not much correlation between severity of Checking for arrhythmias, the disease and enzymes levels → enzymes ↑ w/ 1o stabilization w/out Dx pulmonary edema, abnormal repair Present w/ plenty of Key principles of Mangement BP or albumin, electrolytes, 'danger signs' → start w/ Maintain adequate tissue perfusion : ↑removal of activated enzymes, avoid glucose, azotemia systemic screening Diagnostic Findings dehydration or fluid-overload, ↓ free radical damage w/ antioxidants, O2 delivery Correct electrolyte or acid-base: multi-drug emesis Tx w/ analgesia Clinical signs: vomiting, cranial abdominal Control emesis : aggressive → maropitant, + ondansetron, + CRI of metoclopramide cPLi pain, weakness, dehydration, fever, diarrhea Manage pain: as for acute GI disease l ip ase f PLi (small or large), hematochezia or melena Supportive nutrition : enteral ASAP – stimulate pancreas to avoid zymogen Dx Co-morbidities: jaundice, colitis, diabetes, accumulation w/in cell → basal metabolism = enzymes still being produced, regardless testing if eating; multiple benefits of feeding the gut – use 25% of RER w/ highly digestible fat +/- rads, US, shock, DIC amyl ase restrictive diet FNA/cytology Clinical path: variable; inflammatory FFP / colloids: fresh frozen plasma if DIC; limited evidence of efficacy leukogram, ↓ platelets (coag cascade Gastric protection: H+ pump inhibitors (omeprazole) indicated +/- sucralfate activated), pre-renal or renal azotemia, Severity: paroxysmal or sustained ventricular Monitoring: cardiac, respiratory, intestinal integrity, vascular, etc. tachycardia, pneumonia or ARDS, hematochezia, reactive hepatopathy w/ ↑ bilirubin, ↓ +/- surgical debridement melena or regurgitation, no enteral food for >3 albumin (↑ permeability) days, SAP 180 mmHg & [serum albumin] > In most of the patients, nasoesophageal tube is good enough as 18g/L don't want to put under GA to place esophageal tube Lecture 19: GIT Pharmacology 1 Opioids decrease peristalsis → decrease motility, allowing ↑water resorption Only give ABs when the mucosa has been invaded! Tx: fluids! Protective to some extent diarrhea (like vomiting) Be cautious using motility reducers – can allow pathogenic bacteria to vomiting remain in GIT ABs are not usually common problems indicated Goal: maintain fluid and - vomiting acid-base balance - diarrhea Anti-emetics indicated when - ulcers vomiting is no longer anti-emetics - ileus productive Phenothiazines – - colic Protective reflex to remove perchlorphenazine - constipation toxins from stomach – helpful Dopamine antagonists – - bloat in certain instances BE x blood volume = HCO3 metaclopramide, (mmol) required → give ½ dose, droperidol check, then ½ dose if required 5HT3 antagonists – ondansetron Fluids NK1 antagonists - Oral is best but requires intact reflexes and the animal not vomiting maropitant SQ not useful as peripheral perfusion is impaired IV best bet, but difficult w/ flat animals – may require cutting down to the vein then suturing a catheter in Standard isotonic fluid = Hartmann's (LRS) - has low [K+] so may require addition w/ KCl; dilute KCl (not just added to fluid line) to avoid arrhythmias → know K status before administering Know acid-base status – get blood gas analysis w/ BE → acidotic (-BE) or addition of glucose in fluids can alkalotic (+BE) make transport of Na+ faster  Lecture 20: GIT Pharmacology 2 Drug options work of different areas of the