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1429 Cards in this Set

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Primary cause of Aural hematomas?
Scratching and/or shaking of the head
Underlying cause of Aural hematomas?
otitits externa
Makeup of stuff found in aural hematoma?
underlying otitits externa
Aspiration may reveal -serosanguineous fluid
– or may be negative for fluid and filled w/ organized blood clots
Treatment of aurual hematoma?
Surgical drainage is tx to prevent likelihood of rcurrence
Specific type of sx with aural hematoma?
Sx:
Teat cannula
Incisional dranage – S shaped incision on concave surface; more chronic, organized hematomas
Do you do surgery on concave or convex side of ear for hematoma?
concave
Cranial Cruciate Ligament Rupture Etiology?
Progressive degeration w/ age;
Cranial Cruciate Ligament Rupture predisposing factors?
1. Obesity
2. Hormonal (spayed female)
3. Auto Abs? – 50% of jts against Type I & II collagen
4. Excessive slope to tibia
5. Rupture caused by minor exercise or major trauma
Pathogenesis of CCLR?
Cranial medial bundle of CCL becomes partially (8%) or completely ruptured
Normal collagen structure is crimped w/ smooth cells
In CCL, lose crimping & get pyknotic nuclei, fewer in number, ß capillaries
Hx/signalment of dog with CCLR?
Any neutered dog
Large dogs – 5 years
Small dogs – 10 years
Acutely leg carrying lame after minor exercise
Clinical exam tests for CCLR?
1. Positive cranial drawer sign
2. Tibial compression test
Describe how you perform a Positive cranial drawer sign test?
-perform in 15° intervals from full extension to 90° flexion to see if partial tear (will see in flexion but not in extension)
Describe how you perform a Tibial compression test?
-remember to flex the hock, can overcome muscle tension (whereas the drawer can’t) but can’t judge partial tears
Tx for CCLR?
Tx
Conservative:
Good for smaller dogs (< 15 kg)
Restrict for 6-8 wks
Correct obesity
Limited NSAIDs
Name the Sx you can use for CCLR and what you must do before each surgery?
- must clean out ligament fragments before each sx:
1.Intracapsular
2. Extracapsular
3. TPLO
Describe Intracapsular?
– more precise, go inside jt capsule w/ autogenous biceps fasica ‘under & over’ technique, weave under intermeniscal ligament & tack to lateral femoral condyle
Describe extracasular?
– stabilize outside jt capsule by tightening tissues until periarticular fibrosisi can stabilize the jt; good for smaller dogs
Describe TPLO?
– circularly cut proximal tibia and rotate so no longer caudal slope; so don’t need CrCL anymore; arthritis DOES NOT progress
What should you be sure to educate a client about CCLR surgery?
-With chronic instability of stifle, can get DJD and meniscal tears
Drawbacks to extracapsular tx?
Get periarticular fibrosis in 2 months w/ conservative or extracapsular tx
Drawbacks to intracapsular tx?
Must wait 24 wks
Drawbacks to TPLO tx?
6-8 wks, normal in 2-3 mos
****Anatomoy of the Stifle***
****Anatomoy of the Stifle***
Cranial cruciate ligament
Origin?
lateral condyle of femur
Cranial cruciate ligament
inserts on ?
cranial tibia plateau
Cranial cruciate ligament
2 bands?
1. Craniomedial band
2. Caudolateral band
Most taut band and most often injured?
Craniomedial
Taut band in extension?
caudolateral
Function of cranial cruciate ligament?
Prevent cranial drawer
Prevent excessive internal rotation of stifle
Prevent hyperextension of the stifle
Caudal cruciate ligament
Originates on?
medial condyle of the femur
Caudal cruciate ligament
inserts on?
caudal tibia (popilteal notch)
Caudal cruciate ligament
is taut in?
flexion and extension
Caudal cruciate ligament
function?
Function is to limit the cranial drawer
Collateral ligaments
Originate on?
medial and lateral femoral condyles
Collateral ligaments
insert on?
joint capsule, meniscus and tibia
Function of Collateral ligaments ?
-limit valgus and varus movement of stifle
-Become injured in major trauma
6 attachments of Menisci?
– cranial, caudal, lateral, intermenisci, meniscofemoral
What about blood supply to menisci?
Blood supply to outer 10-15% only
Menisci that tends to be torn more?
Medial
Function of menisci?
-a shock absorber, to stabilize and to lubricate
Name the Muscles supporting the knee that will extend the stifle?
quadriceps & long digital extensor
Name the Muscles supporting the knee that will Flex the stifle?
– biceps femoris & caudal thigh muscles or hamstrings (semitendinosisi, semimembranosus, gracillus, superficial digital flexor, gastroc)
Name the various methods for fracture repair?
1. IM pins
2. Full cerclage wires
3. Interlocking nail
4. Bone plates
5. Screws
What should you make sure you do when selecting a pin?
Use one that fills 70% of marrow cavity?
Never IM pin what?
1. radius
2. transverse fracture
Do not retrograde IM pin where?
tibia or distal femur
Use for long oblique fractures?
full cerclage wires
Criteria for using wires?
1. Use minimum of 2 wires
2. Place wire atleast 0.5 cm away from end of fracture line
3. Place wires 1.0 cm apart
4. Place wires against periosteum
5. Place wires perpendicular to long axis of bone
Use for comminuted fractures of humerus, femur, and tibia?
Interlocking nail
Name 3 types of bone plates?
1. Dynamic compression
2. Neutralization
3.Butress
Use a dynamic compression plate when you are repairing what?
Transverse or short oblique fxs in loading position
Use nutralization plate if repairing what?
multiple pieces of a fracture to reduce collapse
Use buttress if repairing what?
missing gap of bone
Use this screw on compact cortical bone?
coritcal screws
Use this screw on softer bone (metaphysis, epiphysis, diaphysis)?
cancellous screws
Provides compression against fx line, over drill hole near cortex?
Lag screw- produce compression
Drill size should be ______ compared to screw?
smaller
Tap should be _______ as compared to screw?
same size
ESF
Type Ia – half pins in one plane; supplement IM pinning; good in humerus or femur
Type Ib – half pins in two planes; good in humerus or femur
Type II – full pins; distal to elbow and knee
Type III – full pins and half pins in another plane; distal to elbow and knee
How many pins can you use?
up to 4 on each side
Maximum size of pin?
Max=20% width of bone
Use what type of profile of pins?
positive profile threaded pins
How do you prevent thermal necrosis while placing pins?
drip saline
What are the reasons you would want to do a bone graft?
1. Nonunions
2. Osteomyelitis
3. Arthrodesis
For:
Osteogenesis
Osteoinduction – major fxn
Osteoconduction
Canine Mammary Cancer is primarily induced via?
1.Hormonal via estrogen and progesterone and progesins and growth hormones
2. Genetic alteration of erB-2 overexpression, p53 mutations & aneuploidy in 50% malignant and 25% benign
DDX of canine mammary cancer?
Pseudopregnancy
Glactorrhea
Mastitis
Inguinal hernia
Obesity
Prevelence of canine mammary cancer?
- 198/100,000 incidence
- 52% of neoplasms of bitch
- Median age is 10-11
- Poodle, spaniels, English setter, Pointers, Fox and Boston terriers
- Least occurrence in Boxer & Chihuahua
- 1% incidence in males
Clinical signs
-Smooth, painless nodule of mammary tissue (pebble like)
-Frequently mulifocal presentation
- Discharge from nipple
- May mimick mastitis
- May excoriate from pendular trauma
- May enlarge during estrus
Median age of canine mammary tumors?
10-11
Least occurence of mammary tumors found in what breed?
Boxer, chihuahua
In general when someone says the lymph channel is blocked what do you think?
Inflammatory Carcinoma-a type of mammary cancer
Pathosphys of inflammatory carcinoma?
-Local lymphatic metastatic obstruction
-Deep lymphatic channels blocked
- Re-routed through dermal lymphatics, Establish growth
-Met to brain causing weird presentations (CNS)
Clinical signs of inflammatory carcinoma?
-Blistery, vesicles, bruising
-Can look like dermatitis
Name the many causes of blocked lymph?
1. If spayed before 1st estrus – has 0.05% risk
2.If spayed before 2nd estrus – 26% risk
3. If spayed at 2.5 years, full risk – 75%
increased risk w/ exogenous pregestins (Megesterol acetate)
4. Estrus promotes tumor by 50-70% b/c of estrogen receptors on tumor
5. Pregnancy, lactation and pseudopregnancy have no effect
6. Homemade diets and red meat diets increase the risk
Name the types of mammary cancer?
1. Inflammatory carcinoma
2. Multifocal disease
Name the 3 types of mammary disease?
1° - epithelial – adenoma/carcinoma
2° - combined organs (mixed)
3° mesenchymal (oma/sarcoma)
% of mammary tumors that are malignant?
50%
What glands are 50% affected in mammary cancer?
Cranial 3 or caudal 2
Which mammary tumors are usually larger?
caudal tumors
How do mammary tumors metastasize?
50% by blood, 50% by lymph
Prognosis of mammary tumors is poor if what?
1.Tumor > 5cm
2. LN involvement
3. Presence of distant metastasis
4. Inflammation of tissues (inflammatory carcinoma)
How do mammary tumors metastasize?
50% by blood, 50% by lymph
Prognosis of mammary tumors is poor if what?
1.Tumor > 5cm
2. LN involvement
3. Presence of distant metastasis
4. Inflammation of tissues (inflammatory carcinoma)
How do you diagnose mammary tumors?
1. Palpation
2. Evaluate for mets
3. Paraneoplastic syndrome
4. Cytology
5. Biopsy
6. Advanced
Metastasis for mammary tumors is primarily to?
LN, lung
Metastasis for mammary tumors is secndarily to?
Bone, brain, adrenal
What is paraneoplastic syndrome?
Inc IgG, Ca
How do you tell if it should be treated with chemo or radiation?
Need to find cell types with evidence of lymphoid cellular reactivity.
What should you look for in a biopsy of your mammary tumor?
-if benign, then not interpretable
Intravascular growth
Infiltrative v. Expansile v. in situ growth
Name some advance techniques in diagnosing mammary cancer?
1.Degree of nuclear differentiation
2. Malignancy grade
3. Steroid receptor activity
4. S-phase fraction measure of proliferation
5. DNA aneuploidy
6. Number of Ag-stained nuclear organizer regions (Ag/NORs)
Is there any difference in survivial with radical vs conservative treatment of mammary tumors?
no
Goal of surgery with mammary tumors?
a. Remove all neoplastic tissue-usually to abdominal fascia
b. Remove LNs enblock
Contraindications of surgery for mammary tumors?
If its an inflammatory carcinoma.
You can do a nodulectomy of mammary tumor if this criteria is me?
< 1cm
Mastectomy includes what?
Excise portion of gland and margin
A regional mastectomy includes?
Lymphatic/vascular region
Why do you use a regional mastectomy?
If your concerned with overlap
What sections do you remove with a regional mastectomy?
A. 1,2 & 3
B. 4 & 5
What LN do you always need to remove with mammary tumors?
1. Inguinal- it is in the 5th gland
2. Any enlarged glands
Swelling may be seen at what other site with a mammary tumor?
Leg- on same side
What nodes do not have to be removed and are never involved?
axillary
Should you spay while removing mammary tumors?
yes- tumor has estrus receptors
In what cases do you not want to spay while removing tumors?
If you cannot remove all of the tumors
Is chemo very effective with mammary tumors?
not really
What do you want to use if you do treat with chemo?
Doxo, cyclo
What is also helpful in inflammatory carcinoma?
piroxicam
Is radiation helpful in mammary tumors?
Not really, used for inflammatory carcinoma
What is also helpful in inflammatory carcinoma?
piroxicam
Is radiation helpful in mammary tumors?
Not really, used for inflammatory carcinoma
What is an approach to mammary tumor treatment that is similar to effects of chemo but not completely studied?
Biological Response Modifiers
Name exampls of Biological Response modifiers?
a. Levamisole – sheep wormer
b. C. parvum w/ BCG
c. IV BCG
What will reduce circulating estradiol to helpp treat mammary cancer?
LHRH
Tail docking is performed when?
3-5 days old
T or F: Sinus arrythmias are normal in dogs and cats?
False- not normal in cat
Name some of the many causes of sinus bradycardia?
-Increased vagal tone – resting, sleeping, athletism, GI or Resp dz, ocular or carotid manipulation
-Hypothermia
-Hyperkalemia
-Hypothyroidism
-End stage renal dz or hepatic failure
-Neurologic lesions – brain stem, eelvated intracranial prssure
-Drugs or toxicity
Treat bradycardia with what?
1.vagolytic drugs
2. B agonists
3. Pacemaker
Name the vagolytic drugs
glyco, atropine
Name exampes of B agonists?
dobutamine, isoproteranol
Prolonged P-Q =
1st degree AV block
What do you need to rule out with AV block?
wether the arrythmia is due to actual AV block or enhanced vagal tone
How do you rule this out?
Atropine response test
If the response to atropine is normal what does that mean
Block resolves, it is due to enhanced vagal tone
Treatment of 1st degree AV block?
just monitor make sure it doesn't progress
What is 2nd degree AV block?
Intermittent transmission failure- can also be due to increased vagal tone (ART)
What are the 2 types of 2nd degree AV block?
Mobitz I
Mobitz II
Describe mobitz I
Gradual lengthening of PQ until P waves occur without QRS
Describe mobitz II
Constant lengthening of PQ with occassional blocked P waves
Treatment of 2nd degree AV block?
Treat underlying disease
Pacemaker
What is 3rd degree AV block
complete transmission failure and escape rhythm
Which block may be clinically silent especially in cats
3rd AV block
On history/physical what will you have with 3rd degree AV block
exercise intolerance, syncope, signs of R. sided heart failure, jugular pulse, systolic murmur
Describe the escape rhythm in 3rd AV block
ventricular in origin with wide bizarre complexes
Treatment of 3rd degree AV block
pacemaker
What is sick sinus syndrome
irregular discharge of SA node
MC breed of SSS?
Min Schnauzers
SSS associated with what?
fibrous replacement or degeneration of SA nodal tissue.
Causes of degenerated tissue in SSS?
1. Genetics
2. Ischemia
3. Inflammation
Definative therapy off 3rd degree AV block
permanent pacemaker
What is atrial standstill
atrial asystole
What is atrial standstill caused by?
Hyperkalemia
Digitoxin toxicity
Hyperkalemia in AS usually secondary to what?
Urinary obstruction
Hypoadrenocorticism
Treatment for hyperkalemia
Saline, Na bicarb, Ca gluconate
Treatment for digitoxin toxicity
Digoxin immune fab (ovine)- binds digoxin
What is the cause of sinus tachycardia?
Systemic distrubaces relating to body temperatue, blood pressure, exercise, or anxiety
Treatmnet of sinus tach
eliminating cause, vagal maneuver
What drugs can you use to treat sinus tach and what do you have to be aware of before you administer them?
-If no evidence of CHF, then can give
1.digoxin (increases vagal tone via NaK ATPase pump inhibitor),
2. b blockers (slows heart rate)
3. Ca channel blockers (slows heart down)
What are atrial premature depolarizations?
Supraventricular depolarizations that originate somewhere other than the SA node
What is APD's most often associated with?
Atrial muscle stretch or pathology
Treatment of APD's
Dig, B block, Ca channel blocker
What are atrial tach or flutters?
Rapid ectopic depolarization of a non-sinus atrial pacemaker
What do the P waves look like in AT or AF?
-Baseline ‘sawtooth’ P waves
What are causes of AT or AF?
-Same causes as APDs
Treatment of AT or AF?
1. Tx is vagal manuver – ocular presure and/or carotid massage (ventral to ear, caudal to the angle of the jaw) increases vagal tone and may abruptly convert atrial tachycardia or atrial flutter to sinus rhythm by slowing ectopic pacemaker discharge or causing second degree AV block
2. IV chemical intervention:
Esmolol – rapid b blocker to slow sinus rate and cause AV block
Diltiezam – Ca channel blocker to slow heart down
Adenosin – causes acute and transient AV blocker
Describe A. Fib?
Rapid supraventricular rhythm w/ no organized atrial depolarizaiton
A. Fib occurs most commonly with what?
Occurs w/ significant atrial muscle pathology (stretch or fibrosis)
Commonly seen w/ dilated cardiomyopathy in large breed dogs
Pathognumonic of A. Fib on ECG?
No P waves
Treatment A. Fib?
No P waves will be present on ECG
Therapy w/ Diltiazem or Qunidine
Long term w/ digoxin (CHF) and b blockers or Ca blockers added if digoxin alone does not control heart rate
Describe VPCs/ V tach (> 3 VPCs)?
Ectopic depolarizations that originate from any location in the ventricle
VPCs/ V tach (> 3 VPCs) caused by?
-Caused by severe caridac or systemic dz
-Incomplete ventricular filling and an abnormal sequence of contraction
VPCs/ V tach (> 3 VPCs) result in?
-Incomplete ventricular filling and an abnormal sequence of contraction associated w/ VPCs results in decrease stroke volume for that contraction
-Causes “V on T’ phenomenon
Emergency therapy of VPCs/ V tach (> 3 VPCs)?
Emergency therapy – lidocaine, Procainamide, or DC cardioconersion (synchronous defibrillation)
Carnasal tooth abscess occur at what tooth?
Upper PM4 and lower M1
What is significant about the above teeth?
These have triple roots
Abscesses usually involve what part of tooth?
the periapical/apical portion of the tooth (collagen fibers around the cementum of the tooth root)
Tooth abcesses can be caused by what?
periodontal dz, foreign body or a fx tooth
External drainage of abcessed tooth will be seen where?
below the medial canthus of the eye or into the nose
What will you see on dental rads with a n abcessed tooth?
Dental radiographs will reveal periapical lucency
Treatment of an abcessed tooth?
- root canal, or extraction of affected tooch
-Abs prior to endodontics or extraction to resolve acute signs and continue 2 weeks after procedure
-Apply chlorhexidine daily until inflammation has resolved
*** Acute Pancreatitis***
***Acute Pancreatitis***
Signalment
-Middle aged, fat, female dogs
-‘garbage eaters’
-‘sick’; depressed
- V+/D+
- Painful abdomen, tucked up abdomen
- DIC
- Sudden death
Tests you can run?
Amylase, Lipase, Hyperlipidemia, Hypocalcemia, TLI
MOA of amylase
Hydrolizes 1,4 glucodidic linkages of CHO leading to di and mono saccardies
In health amylase comes from where?
intestine and liver
What is best measurement of amylase?
-Colormetric amyloclastic assay is best by measuring presence of amylase by the disappearance of starch substrates
Do you collect serum or plasma to measure amylase and why?
serum- amylase requires Ca
Half life of amylase
12-48 hrs- will peak here this many hours post onset
Is amylase a reliable measurement for pancreatitis in cats?
No- cats do not get an increase (they actually get a decreased amylase b/c of an inhibitor secreted)
Causes of increased amylase:
1. Pancreatitis – 3 to 4 times the reference
2. pancreatic duct blockage
3. renal dz – many theories, may be b/c amylase has a renal tubular epithelial origin
4. intestinal obstruction
MOA of lipase?
Hydrolyzes TGs to form LCFA
Most reliable test between amylase and lipase?
Lipase
Lipase is more reliable because of what?
More reliable test than amylase b/c the pancreas is the principal source of lipase; lack of hyperlipasemia can rule out acute pancreatitis
Causes of increase lipase:
-pancreatitis – 2 times the reference
-Renal dz
-Liver dz
-Corticosteroids
-Simple abdominal exploratory
Why do you have hyperlipidemia with pancreatitis?
-Inhibitor of lipoprotein lipase is released from necrotic pancrease
*** Acute Pancreatitis***
***Acute Pancreatitis***
Signalment
-Middle aged, fat, female dogs
-‘garbage eaters’
-‘sick’; depressed
- V+/D+
- Painful abdomen, tucked up abdomen
- DIC
- Sudden death
Tests you can run?
Amylase, Lipase, Hyperlipidemia, Hypocalcemia, TLI
MOA of amylase
Hydrolizes 1,4 glucodidic linkages of CHO leading to di and mono saccardies
In health amylase comes from where?
intestine and liver
What is best measurement of amylase?
-Colormetric amyloclastic assay is best by measuring presence of amylase by the disappearance of starch substrates
Do you collect serum or plasma to measure amylase and why?
serum- amylase requires Ca
Half life of amylase
12-48 hrs- will peak here this many hours post onset
Is amylase a reliable measurement for pancreatitis in cats?
No- cats do not get an increase (they actually get a decreased amylase b/c of an inhibitor secreted)
Causes of increased amylase:
1. Pancreatitis – 3 to 4 times the reference
2. pancreatic duct blockage
3. renal dz – many theories, may be b/c amylase has a renal tubular epithelial origin
4. intestinal obstruction
MOA of lipase?
Hydrolyzes TGs to form LCFA
Most reliable test between amylase and lipase?
Lipase
Lipase is more reliable because of what?
More reliable test than amylase b/c the pancreas is the principal source of lipase; lack of hyperlipasemia can rule out acute pancreatitis
Causes of increase lipase:
-pancreatitis – 2 times the reference
-Renal dz
-Liver dz
-Corticosteroids
-Simple abdominal exploratory
Why do you have hyperlipidemia with pancreatitis?
-Inhibitor of lipoprotein lipase is released from necrotic pancrease
What else may you see hyperlipidemia with other than pancreatitis?
Hypothyroidism
May also see an inc in these with hyperlipidemia?
May also see inc cholesterol and LDLs
Other things you will see with pancreatitis?
hyperglycemia – if DM
peritoneal efusion
prerenal azotemia – V+ and D+
inc HCT – dehydration
inflammatory leukogram with toxic changes – if severe
DIC
Hypocalcemia seen with pancreatitis due to what?
due to saponification formation of Ca salts and Na / K; seen as fat necrosis microscopically, look like chalk like deposits grossly
TLI mechanism of action?
When amylase and lipase are not dx, can use the TLI. Trypsinogen is produced in the pancreas and released into the small intestine via the pancreatic duct. Trypsinogen is activated in the intestine by enterokinase and alkaline pH. In pancreatitis, inflammation allows trysinogen and trypsin to leak into the blood. In severe cases, trypsin is attached to an inhibitor, alpha 2 macroglobulin or alpha 1 antiprotease.
Treatment of pancreatitis?
Tx
-Fluid and electrolyte balance
-20 MEQ KCL per liter of fluids
-Antiemetics can be used for 24-48 hours if V+ is severe – Chlorpromazine; Metoclopramide (Reglan)
-Steroids only for shock
-NPO
-Gradually introduce a high CHO diet (rice, pasta) and
-reduce fat in diet
-NPO again if V+ recurs
-Discourage feeding scraps
-Pain relief w/ Butorphanol (Torbugesic) or Meperidine (Demerol)
-Ab use is NOT recommended b/c bacteria do not play a primary role in pancreatitis – but can be used in toxic or septic situations
-If severe, NPO for up to TWO weeks after cessation of V+ (May need a J tube)
Pathophys of jaundice
Caused by high bilirubin (> 2 mg/dl)
BR comes from RBCs, unconjugated BR is transported in plasma bound to albumin
Liver takes up BR and conjugates it w/ glucoronic acid
Conjugated BR then goes through the biliary system and expelled in to the intestines where it is converted by flora to urobilinogen
Hyperbilirubinemia (Jaundice) is caused by:
1. Prehepatic
2. Primary hepatic
3. Post hepatic
Describe the 3 types of jaundice?
1. Prehepatic - Excessive BR production
2. Primary hepatic - Imparied processing of BR by hepatocytes
3. Post hepatic - Interference w/ BR excretion
Prehepatic causes
a. Hemolytic disorders
b. Sudden onset, resp and caridac abnormalities
c. Will see severe anemia, spherocytes and Heinz bodies
d. DIC
e. Immune mediated dz – drugs, SLE
f. Infectious – Felv, HTW, erlichiosis, lepto
g. Oxidative injury – toxins to RBCs (zinc and copper
Hepatic causes?
a. Abnormal uptake, conjugation or secretion of BR by hepatocytes
b. Hepatomegally, ascites, PU/PD
c. High ALT and ALP, low albumin and BUN
d. Shock
e. DIC
f. Infectious agents – viral, bacterial or mycotic
g. Neoplasia
h. Drugs – anticonvulsants, acetaminophen, adrogens and thiacetarsamide
i. Chlangitis
j. Cirrhosis
k. Chronic active hepatitis
h. Fleine hepatic lipidosis
i. Hepatic necorisis
j. Infiltrative dzs
Posthepatic causes
a. Chronic or recurrent bouts of pancreatitis, abdominal pain or masses
b. High ALT, ALP
c. Cholecytsittis
d. Cholangitis
e. Biliary neoplasia
f. Intraluminal bile duct occlusion
g. Pancreatitc dz
h. Ruptured biliary tract
What is the Diazo reaction?
Direct bilirubin assay that assesses direct and total bilirubin in serum
Treatment of hepatic jaundice?
A. Encephalopathy – Lactulose – inhibits fxn of urase producing bacteria, speeds intestinal transport and alters gut pH to decrease absorption of ammonia
B. Metronidazole – kills urease-rpoducing bacteria in the gut
C. Lasix – ascites
D. Spironolactone – ascites
E. Antiemetics – metoclopramide or low dose phenothiazines for intractable V+
F. Histamine blockers –
G. Cimetidine to reduce ulcers
Define Diabetes Mellitus?
Inadequate insulin available for normal fxn of cells in liver, fat and muscle
Diabetes Mellitus is due to what?
1. Degenerative changes of b cells of the islets
2. Reduced effectiveness of insulin due to antiinsulin Abs or inactive complexes
3. Immune-mediated islet cytotoxicity
4. Excessive hormone secretion by endocrine neoplasms in other organs
Signalment of Diabetes Mellitus?
Female, small breed dogs (but can happen to any gender or breed)
Diabetes Mellitus
1. Relapsing pancreatitis (exocrine) spreads to endocrine portion of pancrease destroying islets & replacing w/ fibrosis. Remaining pancreas is firm & nodular w/ scattered areas of hemorrhage and necrosis
2.Infiltration of amyloid, glycogen & collagen
3. Idiopathic atrophy of pancrease in young dogs
4. Acute pancreatitis w/ necrosis and hemorrhage
5. Aplasia or hypoplasia of islets
6. Viral infection
What breed is Diabetes Mellitus an autosomal recessive inheritence?
Keeshond
What species has amyloid depositions in islets throughout pancreas?
cats
What does the above cause?
changing of a & b cells
What else do cats have contributing to DM?
-Cats can also have hydropic degeneration of a & b cells; cytoplasm of b cells is expanded by massive accumulation of glycogen b/c of long term insulin resistance
Clinical signs of DM?
1. PU - from inability of renal tubular epithelium to concentrate urine effectively against osmotic graident of glucose in glomerular filtrate (hyperglycemia)
2. PD – fluid loss
3. Polyphagia w/ wt loss
4. Bilateral cataracts – lenticular opacites due to sorbitol pathway used to metabolize excess glucose that diffuses into the lens
5. Weakness
6. Recurrent infections – impaired chemotactic, phagocytic & microbiocidal fxns and adherence of segs causing cystitis, prostatitis, bronchopneumonia, & dermatitis
7. Hepatomegally – fatty change from increased fat mobilization to the liver; hepatocytes are also injured by ketonemia, may have regenerative hyperplasia and fibrosis
8. Chronic renal dz, blindness & gangrene – microangiopathy w/ basement membrane thickening
What gets enlarged with heartworm disease?
1. Main pulmonary artery segment enlargement
2. Lobar arterial enlargement and tortuosity
3. Large right heart
Type of lung pattern seen with heartworms?
alveolar or interstitial
Pathophysiology of heartworms?
1. Microfillaria are L1 and may circulate in a host for up to 2 years after being released from a gravid female
2. MF are ingested by a mosquito and molt to L3 (infective stage)
3. L3 migrate to proboscis of mostquito and are depostied on the skin and enter the host after the mostquito bites the dog
4. L3 molt to L4 & L5
5. L5 reach circulation by penetrating veins
6. Adult worms may survive up to 8 years
What other 2 syndromes are seen with heartworms and describe it?
1. Caval syndrome – displacement of worms to the right atrium, tricuspid valve, caudal vena cava or hepatic veins causing pulmonary hypertension
2. Glomerulonephritis – immune complexes containing worm antigen in glomerular basement membrane
DX of heartworms?
A. 20-75% do not have circulating MF b/c too early, host hypersensitivty, unisex infection, chemophrophylactis (monthly tx) or infertile heartworms
B. ELISA – detects antibody to D immitis antigen
C. False positives are common – retest
Treatment of adult HW?
Place in Class I (subclinical dz), Class II (moderative dz), Class III (severe dz)
A. Immiticide – Two melarsonmine injections in lumbar muscle either 24 hours apart (Classes I & II) or 30 days apart (Class III)
2. Caparsolate – thiacetarsamide;
3. Surgical extraction of heartworms
Treatment of microfilaria?
1. Ivermectin – watch in collies
2. Milbemycin oxime
Monthly prophylaxis of HW?
1. Ivermectin (Heartgard)
2. Milbemycin oxime (Sentinel, Interceptor)
3. Diethylcarbamzine citrat (DEC) – daily administration) contraindicated if MF are present
4. ProHeart 6
What is pseudocyesis?
pseudopregnancy
Define pseudopregnancy.
Physical and behavioral condition simulating pregnancy athat occurs in a nonpregnancy bitch
Why is psudopregnancy so indistinguishable from pregnancy?
Serum progesterone is indistringuishable from pregnant bitches and at the end of diestrus will have a decrease in PG and increase in prolactin, inducing peripartuent behavior
When is pseudopregnancy most prevalent?
Signs may be observed in bitches after OVH in diestrus b/c removal of ovaries simulates parturition w/ a rapid drop in P4
What are cs of pseudopregnancy?
a.Mammary gland development
b. Aggression, lethargy
c. Wt gain from overfeeding b/c owners think bitch is pregnant
d. Nesting , mothering inanimate objects, anorexia, restlessness
e. Lactation – normal or brownish watery fluid
pseudopregnancy sequela
Mastitis in engorged mammary glands is possible sequela
Drug causing signs of pseudopregnancy?
Progestognes may cause signs of pseudocyeisis and milk production may occur when drug is discontinued
Treatment options for pseudopregnancy?
Milbolerone (Chequeâ drops)is needed only for marked behaviroal changes
Cheque drops are used to prevent estrus (used 30 days prior to proestrus)
Future of normal estrous with pseudopregnancy
There is no association w/ dimishished fertility in future estrous cycles
What is dermatomycosis aka?
Dermatophytosis- ringworm
Etiology of dermatophytosis in dog/cat?
Microsporum canis, gypseum, Trichophyton mentagrophytes
Special about M. canis in cats?
M canis can infect cats, especially those w/ long hair w/ inapparent or sublinical infection – important source of zoonotic infection
Classic ringworm lesion?
– foal alopecia w/ follicular papules at perfiphery w/ scale and crust
Diagnosis of ringworm
1. Culture other pets w/ new toothbrush for asymptomatic carriers
2. Can also examine on KOH – not as reliable as culturing
3. Wood’s light CANNOT be used alone to r/o dermatophyte b/c only M canis shows up and only 50% of the time
What is only type of ringworm that may show up on woods lamp?
M. Canis
Topical treatment of ringworm
Ketoconazole, Miconazole, Enilconazole, Lime sulfur, Clotrimazole, Imidazole
Systemic tx of ringworm.
griseofulvin, ketoconazole or itraconazole (most effective)
Careful with griseofulvin why?
a. Enhanced by giving w/ a fatty meal (not water soluble)
b. May cause V+, D+, anorexia, bone marrow suppression in cats
c. Teratogenic – avoided in first 2/3 of pregnancy
Sign birth is about to occur?
Drop in body temp <99- birth will occur in less than 24 hrs
Normal interval b/t pups?
Not longer than 1 hr apart
Causes of dystocia
a. Uterine inertia – primary or secondary after prolonged efforts to deliver fetus
b. Small litter size fails to initiate labor
c. Prolonged gestation - >70 days from 1st breeding, >66 days from LH surge, > 60 days from diestrus
c. Myometrial exhaustion
d. Hypocalcemia/hypoglycemia
e. Uterine torsion
f. Vaginal masses – hyperplasia, strictures or bands
g. Oversized head
h. Malpresentation
i. Lack of lubrication
j. Fetal anomalies
Owner should call vet if what?
1. Prolonged gestation > 70 days from first breeding date
2. Has been in Stage I for over 24 hours (drop in temp, nesting, panting, trembling, inappetence, V+)
3. Has been in Stage II (visible contractions) for >1hour without fetal expulsion
4. Has been in Stage III (expulsion of placental membranes) for > 4 hours w/ fetuses remaining
5. Abnormal degree of pain or depression
6. Excessive hemorrhage or malordorous vaginal discharge
7. Uteroverdine – green-black vaginal discharge
Name the 3 stages of parturition?
I.Drop in temp, nesting, panting
II. Visable contraction, fetal expulsion
III. Expulsion of fetal membranes
What is the gestation of a dog?
- 65 days after LH surge
- 63 days after ovulation
- 57 days after beginning of diestrus
How do you detect LH surge?
Progesterone assay
This property of progesterone is unique to the bitch.
Dramatic inc in Prog prior to LH surge and ovulation caused by preovulatory leutinization of the follicle
What do you measure to predict ovulation?
progesterone
Name some properties of progesterone?
A. Amt in late anestrus/early proestrus – 1.0 ug/ml
B. LH surge – 2-3 ug/ml (Heath recommends 2.1 – 2.9)
C. Ovulation – 3-8 ug/ml
D. Maximum 20 days (between days 15-30) after LH peak – 15-80 ug/ml
E. A pregnant bitch may have a 2nd progesterone peak as well as a less dramatic decline during the 4th to 5th week of gestation
F. Fluctuations of serum progesterone are seen a daily basis
Therefore, diagnosis of pregancy using progesterone is not useful.
What do you use to tell if a bitch is at term?
Progesterone < 2= she is
Name things you would do in a preg check of a dog?
A. Vital signs
B. Abdominal palpation – uterine tone, presence of fetuses
C. Vaginal exam for fetuses, vaginal/pelvic tone, vaginal discharge
D. Vaginoscopic evaluation – direct visualization of cervix
E. Mammary glands for colostrum
F. Abdominal U/S for fetal viability
G. Radiography for litter size or remaining fetuses – obstructing canal
h. Progesterone level - < 2 means she is at term
Ca and glucose levels
Treatment of canine dystocia?
A. C section if parturition date is not known or if there is an obstruction
B. Oxytocin once obstruction is ruled out
C. Give one shot of oxytocin and observe for 30 minutes
D. Digitally feather the dorsal vaginal wall to stimulate reflex contractions
E. Encourage bitch to urinate and efecate if necessary
F. Offer water and food
G. IV 10% Ca gluconate 2-10 mL in 5% dextrose and water over a 10 minute interval
H. Repeat oxytocin injection
I. Failure of oxytocin to stimulate vaginal delivery w/in 1-4 ours should be followed by a C section
Collapsed trachea is usually in what direction?
dorsoventral
What is the definition of a collapsed trachea?
Prolapse of dorsal membrane into the trachea
MC breed with collapsed trachea?
Small dog dz
2 sites of collapsed trachea?
1. Cervical (extrathoracic) 2. Intrathoracic – expiration
Which site wil cause inspiratory stridor and what does it involve?
Cervical (extrathoracic) – cough or airway obstruction on inspiration
Which site wil cause expiratory stridor?
Intrathoracic
What is the history found with collapsed trachea?
Goose honk cough; elicited by excitement
Treatment of collapsed trachea?
A. Steroids
B. Bronchodilators – Theophyllin, Terbultaline, Albuterol
C. Cough suppressants – must r/o infectious processes – butorphanol, hdrocodone
D. Wt loss
E. Harness for leash walking
Avoid environmental stress of heat or humidity
F. Avoid excitement
G. Sx ring prostheses
Cystic endometrial hyperplasia aka?
Pyometra
What is the bad apple in pyometra causing this?
progesterone
Why would progesterone be being produced?
Produced during diestrus
What are the effects of progesterone?
a. promotes accumulation of uterine secretions
b. stimulates endometrial hyperplasia
c. inhibites local leukocyte responses to infection
d. Along w/ estrogen which dilates the cervix, allowing E coli to ascend to the uterus and enhances stimulatory effects of progesterone
e. Megestrol acetate (or another progestin) and pseudopregnancy can cause Progesterone effects
Signs of pyometra?
a. Infertility
b. Older animals
4-10 weeks after estrus
c. Open cervix w/ sanguinopurulent vaginal discharge
d. May have ADR and PU/PD systemic signs
e. May have no vaginal discharge if cervix is closed
f. Abdominal enlargement
V+, dehysration, Azotemia, shock, collapse, coma
Dx of pyometra
a. Purulent vulvar discharge
b. Enlarged, soft, doughy uterus\
c. May have inc WBC
d. Nonregenerative anemia
e. Azotemia
f. May be confused w/ UTI b/c may have pyuria and bacteriuia
g. Don’t cysto these guys b/c may rupture uterus
X rays and U/S may see
Tx of pyometra?
a. Fluid therapy
b. BS Abs – TMS or Enrogloxacin
g. PGF2a (Lutalyse only b/c natural and less potent) if owner wants to salvage dog for breeding; not recommended if dog is critically ill; may rupture the uterus
3 types of pneumonia?
Bronchiolar, lobar, interstitial
Common causes of pneumonia
a. Strept, Staph
b. E coli, Proeus, Pasteurella multocida
c. Bordetella
d. Pseudomonas
e. Actinomyces, Nocardia (anaerobes)
f. Bacteroides,
g. Fusobacterium (anaerobes)
h. Clostridium (anaerobe)
MC mode of transmission of pneumonia?
inhalation
Classic on x-rays with pneumonia?
air bronchogram
DX of pneumonia?
TTW, BAL for culture
TX pneumonia?
1. Abs are primary therapy based on C & S
2. Nebulize via mask, closed cage or intubation
3. Humdify enclosed area – bathroom
4. Coupage – therapeutic percussion to stimulate coughing and secretion clearance
5. Brochodilators for small
Do not use what with pneumonia?
expectorants
*** Sertoli cell tumors***
*** Sertoli cell tumors***
They line what?
Line seminiferous tubles, releases sperm and digests the cytoplasmic droplet
May cause what
A sertoli cell tumor may cause feminizeing syndrom and bone marrow suppression b/c releases estrogen
Look like what
Frim, white, lobulated
Can invade and metastasize to what?
spermatic cord and metastasize to the internal iliac LN
Produce what
1/3 will produce estrogen
Malignant neoplasia increased 13.6 times in what?
cryptorchid
MC breed
boxer, weimer, shelties
TX
orchi of both testes
What are the side effects of estrogen production by Sertoli cell tumor
-Feminization
-Gynecomastia
-Nonregenerative anemia
-Granulocytopenia
-Trhombocytopenia
-Hypothyroidism
-Alopecia
-Hyperplasia
-Squamous metaplasia of the acini of the prostate gland
-Adenomyosis of epididymis
What is the definition of glaucoma
-Elevation in IOP (>15-30 mmHg) caused by abnormal aqueous drainage
-Iridocorneal angle and ciliary cleft is closed or collapsed
Causes of glaucoma
1. Inherited as autosomal recessive in beagle
2. Anterior uveitis
3. Aqueous flare
4. Synechia
5. Lens luxation
6. Tumors
7. Rubeosis iridis – fibrovascular membranses
8. Melanocytosis
DX of glaucoma
Tono

1. Schiotz – indentation performed under topical anesthesia
2. Applantation tonometry – expensive but more accurate and verstaile
2 groups of those with glaucoma
1. potentially visual
2. Blins
Tx of glaucoma
a. Hyperosmotic agents that dehydrate the vitreous – Mannitorl, Glycerin
b. Carbonic anhydrase inhibitors – decrease aqueous production – Dichlorphenamide, Methazolamide, Acetazolaminde
c. Topical autonomic agents – Pilocarpine, Timolol, (b blocker)
What is the mc cutaneous tumor of a dog?
mast cell sarcoma
What is a mast cell sarcoma?
Granules containing histamine and heparin arise from tissue mast cells in the dermis
MC breeds with above?
9 year old Boxers, Bostons, Labs, Beagles, Schnauzers
mast cell sarcoma aka?
“The Great Pretender”
Can wax and wane
MC cs of mast cell sarcoma?
a. Edema from degranulation
b. GI ulcers – histamine acts on H2 receptors in parietal cells to inc HCL
c. V+
d. D+
e. Melena
f. Lifethreatening hypotension from prostaglandins
g. Coagulation abnormalities form heparin release
h. Often solitary
i. Well differentiated usually present for 6+ months
j. Slowly growing
h. Undifferntiated – rapidly growing
MC areas of mast cell sarcoma?
a. skin 50-60%
b. Visceral
c. Nasopharynx
d. Salivary gland
e. Larynx
f. Oral cavity
Metastatic rate of mast cell sarcoma?
55-96% for undifferentiated tumors to regional LNs spleen, liver, liver, bone marrow, peripheral blood
If you get mast cells on an aspirate what should you do?
1. bloodwork
2. 3 view rads
3. abdomen U/S
4. aspirates of spleen and liver
4. bone marrow aspirate
5. buffy coat smear
Treatment of mast cell sarcoma?
Aggressive Surgical excision
A. 3 cm margins in diameter of tumor
B. Treat all the same surgically
Prognosis of mast cell sarcoma?
A. If complete, surgery usually curative for grade I, often for Grade II, and rarely for grade III.
B. If incomplete excision, then re-excise and irradiate (2 year control rate of 85-95%
C. Grade is best predictor of outcome
D. Stage – lower is better
E. Location – peripreprutial, sublingual, perianal, oral, mucocutabeous are more likely to be undifferntiaed (55-95% of mets)
F. Bone marrow has grave prognosis
G. Growth rate – slower growing are usually benign
You will have a worse prognosis with MCS if what?
1. systemic illness
2. older animals
3. breed – Boxers have well differentiated tumors
4. Sex – males have shorter survivial
5. High AgNOR count
6. High PCNA count
7. Aneupleidy
Best predictor of outcome of MCS?
Grade
Name the grades?
A. Grade I – 80-90% long term survivial w/ excision (<10% mets)
B. Grade II – 60-75% long term control (20-50% mets)

C. Grade III – die w/in 6 months (90% mets)
***Heatstroke***
***Heatstroke***
Define classic Heatstroke
Non exertional occurs to confinement in overheated enclosure
Define exertional Heatstroke
Muscular activity, animals with predisposing factors
Thermoregulation in the dog is controlled by what?
hypothalamus
Describe pathophys of thermoregulation?
-Hypothalamus has a ‘set point’ that acts as a trigger to activate physiologic processes to maintian normal temperature
-Afferent signals originating throughout the body (skin, viscera, CNS) detect temperature of circulating blood and converge in the caudal hypothalamus
-Warm blood crosses the posterior hypothalamus and activates the panting center in the dog
-With excessive hyperthermia, the thermoregulatory fxn weaknes, and the cooling mechanisms are diminished
Excessive hyperthermia causes thermal injury to cells via:
A. Cellular necrosis through B. denaturization of proteins
C. Inactivation of enzyme sytems
D. Destruction of cell membrane lipids
E Alteration of mitochondrial fxn
F MODS – multiple organ systems are affected
Hypothermia cs?
1. Shivering
2. Increased voluntary activity
3. Increased cataecholamine secretion
4. Cutaneous vasoconstriction
5. Postural changes
6. Piloerection
7. Increase in thyroxine production
Hyperthermia cs
1. Cutaneous vasodilation
2. Increased respiration
3. Panting
4. Anorexia
5. Sweating – dogs can’t sweat, however
Heatstroke temps
A. >105°
B. Upper lethal body temp (ULBT) is 109°
C. Temps > 106° can cause permanent damage
CS of heatstroke?
a. Rectal temp > 106
b. Excessive panting
c. Hypersalivation
d. Seizures, coma,
e. disorientation – poor prognosis
f. Petechial
g. hemorrhages/ecchymosisi
h.Melena
Predisposing factors to heatstroke?
a. Brachycephalic breeds
b. Laryngeal paralysis – change in bark recently
c. Underlying cardiovascular dz – Lasix will decrease hydration
d. Environment/lack of water
e. Obesity
f. Geriatric
g. Haircoat
h. Hyperthyroidism
Clin path of heatstroke
A.Polycythemia – HCT up to 85%
B. Azotemia – pre-renal
C. Myoglobinuria and casts
D. Hypoproteinemia - due to GI loss (poor prognosis)
E Elevated liver ezymes – ALT, SAP, BR
F. INC CPK – muscle
G. Hypoglycemia
H. Prolonged clotting tests
I. Elevated FDPs
J. Decreased fibrinogen
K. Thrombocytopenia
L. DIC – above 3 present
M. INC Na
N.INC K
O. DEC P
P. DEC Ca
Q. Respiratory alkalosis and metabolic acidosis
Treatment of heatstroke
1. DO NOT give ice bath – may actually cause hypothermia
2. Let owner begin cooling at home or on way to hospital
Obtain MDB – PCV, TX, AZO, 3. Glucose and USG
4. Give shock doses of IV fluids
5. Give BS Abs
6. Cool water enemas may interfere with taking temperatures
7. Put ice pack in axillary region
8. Correct hypoglycemia with 9. 2.5% dextrose
10. Protect the GI tract with carafate or ranitidine
11. Tx for DIC with heparainized saline
12. Correct electrolytes and acid base distrubance if not corrected by fluids
13. Monitor for arrhythmias – lidocain
14. Urine output
15. Neurologic status – mannitol, diazepam
16. Steroids? – may prevent cerebral edema and stabilize membranes (Solu-Delta-Cortef and Dexamethasone)
Key to successful tx of heatstroke
most non survivors die in 24 hrs
What is enostosis?
Panosteitis
Panosteitis aka
AKA Eosinophilic panosteitis (rare finding), Enostosis
Panosteitis etiology?
Very common profound lameness in large breed dogs (esp the GSD), especially in the ulna at nutrient foramen (jxn at proximal 1/3 with distal 2/3)
Proposed causes of Panosteitis?
1. *no bacterial, viral or parasite has been found despite the rare fidning of eosinophilia
2. vascular abnormalites
3. allergies
4. metabolic
5. hyperestrinism
6. parasite migration
7. autoimmune dz
8. stress
Panosteitis affects what part of body and what breed?
Long bones of large breeds
Order of pathogenesis of Panosteitis
1. Death of adipose tissue in bone marrow
2. Osteoblasts & fibroblasts infiltrate the medullary canal, endosteum and periosteum
3. Osteoclasts infiltrate
4. Eosinophils are rare
5. Occur in 90 days
6. Rare to occur twice in same bone
Signalment of Panosteitis
1. Young, Male, GSD
2. Females are more prone during estrus
3. Sudden onset that gets worse over first few day
4. VERY PAINFUL
PE of panosteitis
1. Nonweight-bearing to subtle, depending on time of presentation
2. May be depressed, reluctant to walk
3. Temp is usually normal
4. Deep palpation of affected bone cause a very painful response, especially over nutrient forament area
4. Be sure not to compress a muscle or nerve – gives a false positive
panosteitis rads
1. Lags behind clinical stages by a week
2. NO releationship bet severity of dz and rads
3. Initial –
a. inc opacity medulary canal at the metaphyseal diaphyseal jxn (area of nutrient foramen)
b. Loss of trabecular pattern or granular appearance
c. Difficulty distingusing the cortex from the metaphysis
4. Middle phase –
a. patchy densities rather than completely filling the medullary canal
b. Fine trabeculae of normal bone usually replaced w/ fewer, coarser trabeculae
c. Smooth periosteal new bone may be observed
5. Late phase –
a. Medullary canal opacity regresses
b. Coarse rabecular pattern remains
c. Roughened endosteal surface and periosteal new bone return toward normal
d. Epiphysis is never affected
Tx of panosteitis
Self limiting inflammatory dz of medullary cavity of long bones
Tx is unnecessary or limited to good nursing care
Pain meds of NSAIDs or corticosteroids may be given
panosteitis
Repeated clinical episodes occur often
Can last from a week to 9 months
Avoid stress
Hemangiosarcoma seen most commonly in what?
older (8-13), male GSD, Goldens and Labs
Hemangiosarcoma seen in cats at what age
9 yr DSH
Hemangiosarcoma of dog primary site
spleen
Hemangiosarcoma in dog can also occur in
right atrium, skin, pericardium, liver, lung, kidneys, oral cavity, muscle, bone, bladder and peritoneum
Hemangiosarcoma occurence in cats
50% occur in liver, spleen or mesentaery
50% SQ, thorax or nasal cavity
Are hemangio tumors solitary or multiple?
both
Describe a hemangiosarcoma
a. Often contain areas of necrosis
b. Poorly circumbscribed, nonencapsulated, adherent to organs
c. Rupture and hemorrhage are common
CS of splenic hemangio in dogs?
a. Weakness
b. Abdominal distension – hemoabdomen
c. Tachycardia and tachypnea
d. Anemia
e. History of weakness w/ recovery w/in hours to days
f. Sudden death w/ acute blood loss
If right atrium involvement with splenic hemangio (25%), then what?
a. Pericardial effusion
b. Muffled heart sounds
c. Arrythmias
d. Right heart failure
e. Pericardiocentesis – emergency
Metastatic tendancy of splenic hemangio
1. Highly metastatic - >80% have mets at dx
2. Liver, omentum, mesentery, lungs & brain
Presumptive dx of hemangio
1. Establish presumptive dx
2. PCV
3. Abdominocentesis – hemoabdomen (don’t base on this, only 2/3 have cancer)
Tx of splenic hemangio
a. Stabilize
b. Shock therapy
c. Restore fluid volume
d. Blood products if needed
e. Compression bandage to control hemorrhage
f. CXR before sx
g. Sx – splenectomy
Life expectancy with splenic hemangio
a. 3-4 months w/ sx alone
b. 6 months w/ chemotherapy (doxorubincin) along w/ sx
What is a cutaneous hemangio?
A. Solar induced cancer of endothelial cells of the skin
B. Confined to the dermis
C. Predilection for light haired skin
D. Excision
E. Good prognosis w/ excision
What is a Subcutaneous hemangio?
A. Endothelial cells of SQ blood vessels
Extends below dermis into the SQ tissue
B. Highly invasive
C. Highly metastatic
D. Similar to hemangiosarcoma
E. 6 month survival w/ surgery
What does regurgitation look like?
Tubular, caused by esophageal disease
1st step to do in diagnosing vomiting?
– Differentiate between Dysphagia v. Regurgitation v. Vomiting
Defne dysphagia
drooling, ptyalism, exaggerated swallowing movements, multiple attempts at swallowing, head an neck is extended, drops food, may see respiratory signs
Define regurgitation
same signs as above but food comes back up, may be delayed up to hours, may be tubular form; caused by esophageal disease; may see respiratory
Define vomiting
– neural reflex initiated by CTZ, forceful; expulsion of ingesta outward, nausea (prodomal signs), restlessness, hypersalivation, aspiration rarely occurs
Name the 5 phases of swallowing
a.Oral – voluntary prehension and bolus of food into the oropharynx
b.Pharyngeal – contraction of pharyngeal muscles & movement to the crycopharyngeal sphincter; inhibition of respiration
c.Crycopharyngeal – relaxes crycopharyngeal sphincter and moves along bolus
d.Esophageal – closes crycopharyngeal sphincter and initiates 1° and 2° peristaltic waves, releaxes esophageal sphincter
e.Gastroesophageal phase – relaxes LES as bolus approaches and rapidly closes LES after bolus passes
Nerves involved in swallowing
V (facial, motor),
VII (trigeminal, sensory), IX (glossopharyngeal),
X (vagus),
XII (hypoglossal)
Diseases of the pharynx:
a. RABIES
b. Obstructive disease of brachycephalics
c. Pharyngeal mucocele
d. Nasopharygneal polyp
e. Foreign body
f. Neoplasia/granuloma
g. Neuromuscular dysphagia - central lesion in the brainstem, peripheral neuropathy (botulism, tetanus, polyradiculoneuritis, tick paralysis), Myasthenia gravis
h. Hypothyroidism
i. Pharyngitis
j. Abscess
k. Trauma
Regurgitation is usually indicative of what?
esophageal disease
What is esophagus made of in dog
striate m
In cat esophagus is made of?
striated-proximal 2/3
Smooth- distal 1/3
Esophagus innervated by?
vagus
Where is the defect in the esophagus usually.
· During the esophageal phase of swallowing (see above) sensory receptors stimulate nucleus solitarius – a defect here may be responsible for idiopathic instances
Diseases of the esophagus include?
a. Esophagitis
b. Spirocirca lupi
c. Foreign body
d. Vascular ring anomaly
e. Stricture (sx, foreign body, trauma, caustic agents, esophagitits
f. Extraluminal obstruction –
g. Hiatal hernia -
h. Diverticulum
i. Bronchial esophagial fistula
j. Megaesophagus
k. Toxins, caustic agents
l. Neoplasia
Describe Vascular ring anomaly?
– Persistent right aortic arch, double aortic arch, anomalous left subclavian artery, aberrant right subclavian artery
Describe possible causes of Stricture of esophagus?
-sx, foreign body, trauma, caustic agents, esophagitits
Extraluminal obstruction of esophagusm can be due to?
– mediastinal mass, thryoid tumors, SqCC, foreign body abscess, fungal granuloma, heart base tumors, thymomas, hialar lymphadenopathy
Diverticulum of esophagus can be due to?
pulsion, traction
List possible causes of MG
-Congenital, acquired, idiopathic
-Myasthenia gravis
-Hypoadrenocorticism
-Hypothyroidism
-Systemic lupus or other immune-mediated dz
-Toxin – lead, thallium, cholinesterase inhibitors such as Atropine or glycopyrollate
-Peripheral neuropathy – botulism, tetanus, polyradiculoneuritis, tick paralysis
-Canine distemper
-Polymyositis – toxoplasmosis, neosporum
-Thymoma
-Dysauromia
Neoplasia of esophagus?
Sarcomas, SqCC, osteosarcoma, fibrosarcoma, carcinoma, leiomyomas
Sarcomas in esophagus usually from what?
S. lupi
Diagnosis of regurg?
1. PE and history
2. Neuro exam
3. Survey films
4. Esophagram
5. Fluoroscopy
6. Endoscopy
7. Esophageal manometry
Tx of regurg?
Metochlopramide (Reglanâ) stimulates distal esophageal peristalsis
Anticholinergics (Atropineâ) decreases LES pressure
Calcium channel blocker (Nifedipineâ) decreases LES pressure
Vomiting controlled by?
CTZ of medulla
3 areas vomiting can come from?
Pylorus, Prox duodenum, distal small intestine
If vomiting comes from pylorus then what?
-H+ are loss and induces a metabolic alkalosis
If vomiting comes from Prox duodenum then what?
then water and electrolytes are lost
If vomiting comes from distal small intestine then what?
, then loss of bicarb, and acidosis can occur
DDX of vomiting
1.Enteritis – Non-specific acute gastritis
2.Gastritis
3.Diet
4.Parasites – young animals
5.Gastric or intestinal obstruction
6.Pancreatitis
7. Liver dz
8. Hypoadrenocorotism
9. Hypercalcemia
10. Uremia
11. DKA
a. diabetic ketoacidosis;
12. Hyperthyroidism
13. Feline heart worm dz
14. Colitis
15. Gastrinoma –
16. Gastric/duodenal ulcers
17. Neoplasia – gastric, intestinal, liver, pancreas
18. Chronic renal failure – uremic toxins Ý serum gastrin which irritates the stomach
19. Parvo
MOA of pancreatitis causing vomiting?
– trypsinogen (along with phospholipase A, elastase, lipase and colipase) is activated causing autodigestion of pancreas
MOA of liver diasese causing vomiting?
nitrogenous waste productes causes GI ulceration
MOA of addisons causing vomiting
glucocorticoid deficiency increases V+
MOA of DKA causing vomiting
- insulin resistance b/c inc in diabetogenic hormones (epinephrin, glucagon, cortisol, growth hormone, FFAs, AA, metabolic aciodsis
b. This stimulates lipolysis which induces a ketogenesis and gluconeogenesis causing a hyperglycemia
MOA of CRF causing vomiting?
-uremic toxins in serum gastrin which irritates the stomach
Chronic vomiting in cat=
heartworms
What is Zollinger-Ellison syndrome?
Gastrinoma
Good antiemetic for parvo?
Ondansetron is a good choice
List the antiemetics?
a.Chlorpromazine (thorazineâ)
b.Prochlorpromazine
c.Metochlopramide (Regland)
d.Butorphanol
e.Ondansetron – good for Parvo
BAD MOP
List antacids
a.H2 blockers (Cimetidien, Ranitindin, Famotidien
b.Proton pump inhibitor – Omeprazole
List GI protectants?
a.Sucralfate
b.Misoprostel – PGE analog, good for NSAID –induced ulcers
List treatment in general for vomiting
-Fluids (Ringers for acidosis, Saline for alkalosis)
-NPO, then water and bland diet
-Remove offending agent
-antiemetics
-Antaacids
-AB
-Cytoprotectants
Do not use what with vomiting
atropine- paralyzes gut, causes ileus
Otitis media often occurs due to what?
occurs as an extension of otitis externa through a ruptured tympanic membrane
Watch out for damage to what
CN 8
What produces wax?
· Cerumen (aprocrine) glands in external ear canal produces wax
What is underlying disease of otitis externa/media?
a.excessive moisture (swimming)
b.improper cleaning solutions
c.parasites – otodectes cynotis, Demodex, Sarcoptes and Notoedres, Otobius megini
d.allergies
e.Foreign bodies – grass awns
f.obstruction – neoplasia, polyps, cerumen gland hyperplasia, accumulationof hair
g.Keratinization disorders – seobrrhea, increased cerumen produciton
CS of otitis media/externa
a.Ear pain
b.Redness, swelling
c.Scaling and exudation
d.Malodor
e.Head tilt – vestibular signs
If media/interna is infected than what may happen?
-nerve damage facial nerve (CN 7) to ophthalmic branch causing lack of tear production and parasympathetic branch causing gastrointestinal signs via ipislateral rostral 2/3 of tongue
-V+ and nausea
-Horners syndrome and anisocoria and/or protrusion of third eyelid
-Tympanic membrane is gray, dull, opaque and bulging indicating middle ear exudate
-Pain on opening mouth
-Corneal ulcer b/c can’t blink eye
What is the relationship between large dogs and small dogs with hydration
Not a linear relationship
The larger the animal, the less proportionally they need in calories and water
What is maintenance fluids for small animals
66 ml/kg
However, as the previous question states, may be too much for large dogs
What is surgical hydration infusion for small animals
11-22 ml/kg/hr
What is BER
Basal (resting) Energy requirement – usually 12 hours after feeding, following sleep and a thermoneurtral condition
BER = 30 x Kgbw + 70
BER = 70 x Kgbw0.75
Second one is much more accurate
What is MER
Maintenance (daily) energy requirement
Adds needs for moderate activity of gathering food
MER (dog) = 1.8 x BER
MER (cat) = 1.4 x BER
What is TER
Total Energy Requirement
Includes ‘life factors’
TER (hospitalized) = BER x Illness factor
TER (at home) = MER x Illness factor
What is the illness factor for sepsis
1.2
Why try to feed the least calories
Cost
Which life factor is the highest
Sledding
Peak lactation
What is important to remember when feeding a kitten
Stomach has very small volume so must increase the density of the food
What is a neutraceutical
Potential, rather than established benefit
Ex: Herbs, vitamins, immunomodulators, performance enhancers, chondroprotecive agents
What are the special amino acid requirements for dogs and cats
Dogs need:
Arginine
Glutamine – enterocyte health via chyme coating
Butyrate – bacterial fermentation for fiber
Linoieic and alpha linoleic acid – fats
Eicosapentaenoic

Cats – Taurine
What are the energy comparisons of protein, fat and CHO
Protein – 4 Kcal/gm
Fat – 9 Kcal/g
CHO – 4 Kcal/g
What are the protein requirements for dogs and cats
Dogs = 4g/kg/day
Cats = 6 g/kg/day
What is the ideal BCS for small animals
3/5
True tapeworm
eucestoda
false tapeworm
cotyloda
Name some general characteristics about tapeworms?
·Hermaphroditic
·Always endoparasites
·Adults always in GI tract
·Lack alimentary tract –take food via absorption through body wall
·Great variety in size
Armed tapeworm?

·
– if has hooks or rostellum (retractable nose which may be covered with backward facing hooklets
Unarmed tapeworm?
if scolex used to anchor the adult tapeworm in place of small intestine
germinal region from which rest of body will develop in
tapeworm?
neck
What is the strobila of a tapeworm?
segments called proglottids, each contain both female and male repro organs
In a tapeworm which is part more developed?
proglottids: as they grow futher from scolex, the more mature and developed the scolex gets.
Mature proglottids of tapeworm found where?
middle in chain, contain mature, fully functioning repro organs ‘teenagers’
Gravid proglotids are where?
– most distal, farthest away from neck, contain degenerated, non-functioning (atrophied) repro organs. Only organ left is uterus distended with eggs. Some become detached as it is passed out of the feces.
Internal organ system of a tapeworm?
1.Tegument – outer covering, feeding or absorptive structure, lacks a digestive tract
2. Muscular system
3. Excretory system
4. Nervous system
5. Repro system – hermaphroditic
Life cycle of a tapeworm?
1.Adult - within intestine of definitive host
2.Eggs – proglottids containing eggs are voided in feces of definitive host
3.Metacestode – when ingested by suitable intermediate host, LARVAL TAPEWORM; egg hatches, metacestode migrates to extraintestinal site within intermediate host.
4.Definitive host igests intermediate host containing metacestode stage. Scolex excyst or evaginates and attaches to mucosa of the small intestine. Scolex grows a neck, neck grows the strobila containing proglottids = Adult tapeworm.
Developmental stages of a tapeworm?
1.Egg – oncasphere, growth ball fuly embryonated; 3 pr. Of hooklets; embryophore (covering); igested by immediate host; penetrates intestinal wall & migrates to extraintestin
2.Metacestode – immediate host; many types!
·Cystecercoid
·Cystecercus
·Coenurus
·Hydated cyst
·Misc metacestode stages (explained later)
Cystecercoid
– single scolex; NOT invaginated into itself in a tiny fluid-filled cavity; ‘right side out’ scolex; usually invertebrates such as mites or fleas
Cystecercus
– single scolex; invaginated into itself in a large, fluid-filled cavity; ‘Inside out’ scolex; vertebrates such as ruminants, rabbits & mice
Coenurus
– Large, fluid-filled cavity with many invaginated scolices; multi-headed cystecercus
Hydated cyst
– Large, fluid-filled cavity; develops other cysts called ‘brood capsules’, brood capsules contain protoscolices
Horse tapes have the following in common with small animal tapes?
1.Scolex don’t have rostellum or hooks so unarmed
2.Squatty body
3.Oncosphere has 3 coverings; Innermost membrane called Pyriform Apparatus
4.Large animal GI tract is definitive host
Only exception of above?
Dipylidium caninum – double pored tapeworm does not possess 1-4 above
Describe Taenia type tapes?
·Usually large
·Usually have proglottids thant are ‘slim-jim’
·Usually armed
·Single-pored-only one pore per proglottid
·Typical taenid type egg- embryophore is brown with striated appearance, on inside of egg are SIX tiny hooklets
What are the metacestode stages of taenia?
1. Cysticercus
2. Strobilocercus
3. Coenurus
4. Hydatid Cyst
Importtant about MOST LARVAL METACESTODES ?
WILL BE MORE PATHOGENIC TO INTERMEDIATE HOST THAN ADULT TAPEWORMS ARE TO DEFINITIVE HOST !!!!!
Describe lifecycle of a false tape?
·Bothria - narrow grooves on scolex (true has scolex with 4 suckers)
·One set of male and female repro organs per proglottid, usually in center
·Produce operculated eggs – release ciliated hexacanth embryo
·2 intermediate hosts
·First intermediate host is Crustacean for metacestode stage Procercoid
Second intermediate host is fish or frog for the metacestode
‘double pored tapeworm’
Dipylidium caninum
Species infected with Dipylidium caninum
dogs, cats, humans
Location of Dipylidium caninum
Small intestine
Gross appearance of Dipylidium caninum-description?
Armed, 4 scolexes, 3-4 rows of hooks, 2 sets of male & female repro organs, an individual gravid proglottid resembles seed of cucumber, ea filled with 100s – 1000s of egg packets Each egg packet is filled with 20-30 hexacanth embryos.
Dipylidium caninum feed on what?
larval fleas
Dipylidium caninum is transmitted how?
•the eggs. Eggs igested by larval fleas; eggs develop to infective cysicercoid stage. Host Adult in host; gravid proglottids break from the chain and voided in feces; Proglo rupture, release egg packets, which rupture & disseminating is infected by igesting cyticercoid . Cysticercoid release the scolex, scolex attaches.
Infective stage of Dipylidium caninum to flea?
cysticercoid
Infective stage of Dipylidium caninum to dog, cat, human?
egg
Dipylidium caninum effects to human, dog, cat?
Not very harmful; constipation, D+, Pot-bellied, unthrifty; cause host to ‘scoot’, Gravids can crawl all over the place before releasing eggs.
Dx Dipylidium caninum
visual
Is Dipylidium caninum zoonotic
yes
‘double pored tapeworm’
Dipylidium caninum
Species infected with Dipylidium caninum
dogs, cats, humans
Location of Dipylidium caninum
Small intestine
Gross appearance of Dipylidium caninum-description?
Armed, 4 scolexes, 3-4 rows of hooks, 2 sets of male & female repro organs, an individual gravid proglottid resembles seed of cucumber, ea filled with 100s – 1000s of egg packets Each egg packet is filled with 20-30 hexacanth embryos.
Dipylidium caninum feed on what?
larval fleas
Dipylidium caninum is transmitted how?
•the eggs. Eggs igested by larval fleas; eggs develop to infective cysicercoid stage. Host Adult in host; gravid proglottids break from the chain and voided in feces; Proglo rupture, release egg packets, which rupture & disseminating is infected by igesting cyticercoid . Cysticercoid release the scolex, scolex attaches.
Infective stage of Dipylidium caninum to flea?
cysticercoid
Infective stage of Dipylidium caninum to dog, cat, human?
egg
Dipylidium caninum effects to human, dog, cat?
Not very harmful; constipation, D+, Pot-bellied, unthrifty; cause host to ‘scoot’, Gravids can crawl all over the place before releasing eggs.
Dx Dipylidium caninum
visual
Is Dipylidium caninum zoonotic
yes
Mesocestoides tetrathyridum tapeworm affects who?
amphibians, birds, rats,humans dogs and cats
Location of Mesocestoides tetrathyridum
SI
Odd about Mesocestoides tetrathyridum?
infected can also be intermediate host
Mesocestoides tetrathyridum lifecycle
-2 metacestode stages Cysticercoid in grain mites,
intermediate hostMesocestoides tetrathyridum
Cysticercoid in grain mites
Mesocestoides tetrathyridum body made of what?
4 suckers and Unarmed
Mesocestoides tetrathyridum egg appearance.
Lack striated embryo
Mesocestoides tetrathyridum gross appearance outside of body
look like snow or grits
Mesocestoides tetrathyridum lifecycle
Adult found in sm intest of def host. Eggs passed on to environment and are ingested by the 1st imm host, coprophagous (feces-eating) mites. Cystercercoids develop. 2nd imm host ingests & tretrathyridum form and multiply asexually by longitudinal splitting.
Mesocestoides tetrathyridum causes what in humans
D+ in humans
Prevention of Mesocestoides tetrathyridum
Prevent dogs and cats from roaming
Broad fish tapeworm
Diphyllobothrium latum
Species affected by Diphyllobothrium latum
Dog, cat, polar bear in great lakes
Diphyllobothrium latum location
SI
Diphyllobothrium latum pathogneumonic lesion
1. Longest tapeworm.
2. ‘Rosette Effect’ – on gravid proglottids,
3. Operculated eggs
Diphyllobothrium latum lifecycle?
-Adult has wide host range in small intestine, eggs contact water and hatch. Produced cilia-coated hexacanth “Coracidium’ 1st host eats and it develops into Procercoid stage. 2nd host ingests & it becomes a Plercercoid stage. Def host eats
Diphyllobothrium latum effects on its host
This tapeworm absormbs a large amt of B-12 from the gut. Lack of this vit produces pernicious anemia
Diphyllobothrium latum prevention
cook and freeze fish thoroughly
zipper tapeworm’
Spirometra mansonoides
Spirometra mansonoides affects what species?
dog and cats- SI
Spirometra mansonoides egg
operculated
Spirometra mansonoides unique because
-CYCLOPS
Spirometra mansonoides intermediate
crustacean, frog, rat, water snake
Spirometra mansonoides
-Same as above, only another name for Plercercoid is Sparganum If humans drink water containing the cyclops w/ procercoid, the sparganum will develop in musculature of human, If human eats the musculature of 2nd host contianing sparganum, it will migrate to musculature of human
When flesh of frogs, rats or water snakes are used for poultice, can develop sparganum in SQ.
Spargana in humans can migrate SQ.
FF, can be mistaken for fluke eg
Broad fish tapeworm
Diphyllobothrium latum
Species affected by Diphyllobothrium latum
Dog, cat, polar bear in great lakes
Diphyllobothrium latum location
SI
Diphyllobothrium latum pathogneumonic lesion
1. Longest tapeworm.
2. ‘Rosette Effect’ – on gravid proglottids,
3. Operculated eggs
Diphyllobothrium latum lifecycle?
-Adult has wide host range in small intestine, eggs contact water and hatch. Produced cilia-coated hexacanth “Coracidium’ 1st host eats and it develops into Procercoid stage. 2nd host ingests & it becomes a Plercercoid stage. Def host eats
Diphyllobothrium latum effects on its host
This tapeworm absormbs a large amt of B-12 from the gut. Lack of this vit produces pernicious anemia
Diphyllobothrium latum prevention
cook and freeze fish thoroughly
zipper tapeworm’
Spirometra mansonoides
Spirometra mansonoides affects what species?
dog and cats- SI
Spirometra mansonoides egg
operculated
Spirometra mansonoides unique because
-CYCLOPS
Spirometra mansonoides intermediate
crustacean, frog, rat, water snake
Spirometra mansonoides
-Same as above, only another name for Plercercoid is Sparganum If humans drink water containing the cyclops w/ procercoid, the sparganum will develop in musculature of human, If human eats the musculature of 2nd host contianing sparganum, it will migrate to musculature of human
When flesh of frogs, rats or water snakes are used for poultice, can develop sparganum in SQ.
Spargana in humans can migrate SQ.
FF, can be mistaken for fluke eg
Broad fish tapeworm
Diphyllobothrium latum
Species affected by Diphyllobothrium latum
Dog, cat, polar bear in great lakes
Diphyllobothrium latum location
SI
Diphyllobothrium latum pathogneumonic lesion
1. Longest tapeworm.
2. ‘Rosette Effect’ – on gravid proglottids,
3. Operculated eggs
Diphyllobothrium latum lifecycle?
-Adult has wide host range in small intestine, eggs contact water and hatch. Produced cilia-coated hexacanth “Coracidium’ 1st host eats and it develops into Procercoid stage. 2nd host ingests & it becomes a Plercercoid stage. Def host eats
Diphyllobothrium latum effects on its host
This tapeworm absormbs a large amt of B-12 from the gut. Lack of this vit produces pernicious anemia
Diphyllobothrium latum prevention
cook and freeze fish thoroughly
zipper tapeworm’
Spirometra mansonoides
Spirometra mansonoides affects what species?
dog and cats- SI
Spirometra mansonoides egg
operculated
Spirometra mansonoides unique because
-CYCLOPS
Spirometra mansonoides intermediate
crustacean, frog, rat, water snake
Spirometra mansonoides
-Same as above, only another name for Plercercoid is Sparganum If humans drink water containing the cyclops w/ procercoid, the sparganum will develop in musculature of human, If human eats the musculature of 2nd host contianing sparganum, it will migrate to musculature of human
When flesh of frogs, rats or water snakes are used for poultice, can develop sparganum in SQ.
Spargana in humans can migrate SQ.
FF, can be mistaken for fluke eg
Broad fish tapeworm
Diphyllobothrium latum
Species affected by Diphyllobothrium latum
Dog, cat, polar bear in great lakes
Diphyllobothrium latum location
SI
Diphyllobothrium latum pathogneumonic lesion
1. Longest tapeworm.
2. ‘Rosette Effect’ – on gravid proglottids,
3. Operculated eggs
Diphyllobothrium latum lifecycle?
-Adult has wide host range in small intestine, eggs contact water and hatch. Produced cilia-coated hexacanth “Coracidium’ 1st host eats and it develops into Procercoid stage. 2nd host ingests & it becomes a Plercercoid stage. Def host eats
Diphyllobothrium latum effects on its host
This tapeworm absormbs a large amt of B-12 from the gut. Lack of this vit produces pernicious anemia
Diphyllobothrium latum prevention
cook and freeze fish thoroughly
zipper tapeworm’
Spirometra mansonoides
Spirometra mansonoides affects what species?
dog and cats- SI
Spirometra mansonoides egg
operculated
Spirometra mansonoides unique because
-CYCLOPS
Spirometra mansonoides intermediate
crustacean, frog, rat, water snake
Spirometra mansonoides lifecycle
-Same as above, only another name for Plercercoid is Sparganum If humans drink water containing the cyclops w/ procercoid, the sparganum will develop in musculature of human, If human eats the musculature of 2nd host contianing sparganum, it will migrate to musculature of human
When flesh of frogs, rats or water snakes are used for poultice, can develop sparganum in SQ.
Spargana in humans can migrate SQ.
FF, can be mistaken for fluke eg
Shock therapy with crystalloid fluid: (no head trauma or pulmonary edema)
Dog – 90 mL/kg/hour
Cat – 60 mL/kg/hour
Blood transfusion (PCV < 20%)
20 ml/kg fresh whole blood
15-30 ml/kg Oxyglobin
Shock therapy for head trauma or pulmonary contusions:
Hypertonic saline + Hetastarch or dextran
Total dose = 5 ml/kg
Draw up 1/3 volume as 23% saline, 2/3 as colloid
Small volume resusitation:
5ml/kg IV hetastarch or dextran
Repeat every 5-10 minutes until HR, pulses and color improves
***Crystalloids***
***Crystalloids***
Rate
run very fast
Frequency
Doesn’t stay in vascular space, so need to give 3-4 times what they have lost
Avoid if
Avoid in animals w/ interstitial edema:
1. head trauma
2. pulmonary contusions
3. hypoproteinemia
Lactated ringers
Buffered pH of about 7.4 which is good for acidosis
The lactate in Lactated ringers is converted to bicarb for acidosis
Latate is metbolized in the liver and has calcium
Normalsol R
Buffered pH of about 7.4 which is good for acidosis
The acetate in normalsol R is converted to bicarb for acidosis
Acetate is metabolized in the muscle and has magnesium
0.9% NaCl
Not buffered
5% Dextrose in water
Hypotonic solution
Don’t use in shock
Causes lysis of RBCs
0.45% NaCl
Hypotonic solution
Na overload
Don’t use in shock, heart failure, or pulmonary edema
Good for maintenance fluids (Add 20 mEq/L of K+)
What fluids contain large amounts of albumin?
colloids
What does albumin serve to do in colloids
-retention of fluid in the vascular space
-Increases oncotic pressure b/c are not filtered in the glomerulus
What volume of colloids do you need to give to restore circulation?
3. Give smaller volume to restore circulation:
a.20 mL/kg/day
b.10 mL/kg/day
Indications of colloids
4. Indications:
a. Hypoproteinemia
b. 3rd space loss
c. Head trauma, pulmonary edema
d. Capillaries leaky
e. SIRS
Examples of colloids
5. Examples:
a. Hetastarch
b. Dextran 70
c. Whole blood – if PCV drops below 20% and TP < 3.5 (1 mL of blood per pound will raise hematocrit 1%) then give 20 mL/kg
d.Oxyglobin – same as above at a rate of 15-30 ml/kg
e.Whole plasma
If there is evidence of ongoing blood loss into the abdominal cavity what should you do?
snug compressive bandage should be applied, being careful not to impair respirations
Hypertonic Saline uses
1. Pulls fluid out of interstitial space (7%)
2. Used w/ colloids
# of lips in toxocara canis
3
5 routes of transmission of T. canis
Direct
if under 3 months old is tracheal
If over 3 months old is somatic
Transuterine – Somatic in bitch, tracheal in pup
Lactogenic – Somatic in bitch, no migration in pup
ingestion of parantenic host – Somatic in parantenic host
CS of infection with T. canis
•Pot-bellied, dull coat, tucked-up abdomen, D+, anemia
Where can adults be recovered of T. canis
•Adults are ofen recovered from feces or V+
Type of zoonisis with T. canis
OLM, VLM
Possible the only sign of atopy will be what?
pruritis
Atopy responds well to what.
corticosteroids
Causes of atopy
pollen, fungus,food
Define flea allergy dermatitis
•Hypersensitivity to flea saliva w/ or without evidence of fleas or flea dirt
Anti bodeis in flea allergy dermatitis?
•Both IgE and IgG antiflea Abs have been noted
CS of flea allergy dermatitis
•Most common sign is compulsive biting and chewing
•Finding fleas or flea dirt is NOT essential for dx
• Lesions are concentrated in triangular area of caudal dorsal lumbosacral region
Etiology of pyoderma
•Most frequently caused by Straphylococcus intermedius or Pasteurella multocida
Causes of pyoderma
• Caused by:
a. Allergy
b. Parasites
c.Endocrine dz – hypothyroidism, hyperadrenocoriticis, sex hromone imbalance
d.Immune incompentency – steroids, young animals
e.Seborrhea – acne, Schnauzer Comedo syndrome
f.Conformaiton
g.Trauma – pressure points, grooming, scratcing , rooting behavior, irritants
h.Foreign body – foxtail, grass awn
What is Seborrhea
– Primary keratinization disorder
Define Seborrhea
•Excessive or abnormal shedding of ipidermal cells results in clinical presentation of cutaneous scaling
•Primary cellular defect causing accelerated epidermopoiesis and hyperporliferation of seborrheic ipidermis, follicular infundibulum and sebaceous gland
Seborrhea 2 types
• Dry (sicca) and greasy (oleosa)
Hoe do you differential seborrhea from others
non pruritic
Tx seborrhea
• Use a keratolytic shampoo (Sulfur, Salicylic acid, Benzoyl peroxide, Ethyl lactate, Tar)
Kennel cough etiology
Adeno 2, bordetella
Definition of KK
Cararrhal to mucopurulent tracheobronchitis
Sequela to KK
secondary bronchopneumonia
***Corneal Ulcers***
***Corneal Ulcers***
Blue
– corneal edema, light source in normal cornea should be crisp
White
minerals or lipids
Brown
melanin, pignmentary keratitis
Red
blood vessels
Gray
fibrosis/scar
Yellow
– WBC, hypopyon
Tan
deratic ppts, severe uveitis, inflammatory debris, aqueous flow
T of F- hip dysplasia is an inherited disease
F
Truths about hip dysplasia
• Not 100% inherited, only 25-85% genetics (but OFA claims it 100%)
• ***Body size and body type ARE involved
• Giant breeds w/ acromegally characteristics and 5-10% fat in soft tissues of hind quarters are most as risk
• Genetics are an alele one chromosome
• Large and giant breeds are more recognized
• Multi-factoral dz; things that predispose to hip dysplasia:
Multifactorial causes of hip dysplasia
- inc fat (5-10% in soft tissues)
-inc activity (double height, triple support)
-inc calories
-*** inc calcium
-ad lib feeding
-excessive CHO, proteins & Vit C
-more weight
-Heavy exercise as a puppy causing laxity between the femoral head and acetabulum
-Quick growth
Things that decrease chances of hip dysplasia
of hip dysplasia:
- inc muscle
- slower growth rate – remember that rate of growth does NOT effet final adult size
Are hips normal at birth?
yes
Pathogenesis of hip dysplasia
-Develops at birth and 8 months
-Femoral head can subluxate at 30 days & delayed craniodorsal acetabular rim
Signalment of hip dysplasia
•Any breed can get hip dysplasia
-Any sex
Susceptible breeds to hip dysplasia
• Susceptible breeds:
- St. Bernard
- GSD
- Lab
Young dogs cs of hip dysplasia
•Young dogs will have jt laxity and minimal DJD w/ acute episodes of lameness, pain and dec exercise
Older dogs cs of hip dysplasia
- dec exercise
- stffness
- difficulty standing
Older dogs have hip dysplasia secondary to?
Older dogs will have DJD secondary to CHD:
Pathogneumonic cs of hip dysplasia
bunny hop
CS of hip dysplasia
Clinical signs
•Bunny hopping lameness
•Narrow stance w/ hind legs
•Muscle atrophy
•Ortiloni sign
How do you test for ortiloni sign?
put dorsal pressure on femur w/ thumb and then pull knee away (abduct) from body; a positive test will pop back into acetabulum
Ortiloni sign will only occur in what?
The ortiloni sign will only occurs in young dogs w/ a deep acetabulum. Older dogs w/ CHD will have a shallow have a shallow acetabulum
Make sure you also check for this in hip dysplasia
•Ortho exam will often have other problems (need to do neuro exam in older animals and look for lumbosacral back problems)
•Should have FULL hind leg extension (more sensitive than x-rays)
Abnormalities seen on rads of hip dysplasia
Abnormalities include:
1.Less than 2/3 of the femoral head in the acetabulum
2.Non-parallel jt space from the craniodorsal fovea capitis
3.Sclerosisi of subchondral bone at cranial margin of ht acetabulum
4.Rounding or osteophyte formation the craniolateralmargin of the acetabulum
5.Thickening of the femoral neck
6.Periarticular osteophytes
Pain from hip dysplasia comes from
from microfx & collapse of subchondral bone, synovitis & tearing of capsule & ligaments
Hip dysplasia leads to what?
•Leads to arthritis (but they are not the same
What is the grading system for hip dysplasia
OFA grades (only first three get grades):
1 Excellent
2 Fair
3 Good
4 Mild dysplasia
5 Moderate dysplasia
6 Severe dysplasia
What is the Norberg angle measurment used for hip dysplasia?
A line drawn from center of one femoral head to center of the other, to the tip of the craniolateral margin of the acetabulum. This theory has been proven not reliable
What is the distraction index or laxity test for hip dysplasia
Stress radiograph that promotes luxation (‘action shot’)
Dog in dorsal recumbency w/ femurs perpendicular to table
Bar placed between femoral dyaphyses and stifles are pressed together, levering the hips out
Dogs w/ a distraction index more that 0.5 develop hip dysplasia
What is the dorsal acetabular rim evaluation used for in hip dysplasia
Dorsal Acetabular Rim (DAR)
Craniodorsal projection centered on and parallel to the dorsal acetabular rim
This view of hip allows accurate evaluation of the amount of dorsal coverage provided for femoral head
Contrived for TPO evaluation
Pathogenesis of hip dysplasia
•Hip Dysplasia = Hip laxity = Positive Orlani sign = JUVENILE dog (prearthritis
tx djd
• Tx of DJD
a. Conservative
b. Femoral head & neck osteotomy (FHO)
c. Total hip
Treatment for young dogs with hip dysplasia
a. In young dog have two choices for treatment:
-TPO – triple pelivc osteotomy
-Develop DJD – how fast, how bad can’t predict – rads are NOT clinical
Conservative management of hip dysplasia
1. Must have exercise to build muscle mass. The less the muscle, the more the bone has to bear weight
2. Meds decrease PAIN due to inflammation (give every other day)
3. Try to do low impact exercise (Monday, Wednesday, Friday minimum)
4. On Tuesday & Thursday, rest w/ meds
5. Check Fee T4 for hypothyroid
6. Calculate kcal ((30 x kg) + 70; give specific number of cans to feed per day
7. MUST LOSE WEIGHT
8. Keep dog in warm environment
9. Give 6-8 week trial period, if fails, need surgery
Dont do surgery in hip dysplasia if?
a.Dog is NOT limping (can’t improve a non-limping dog!)
b.Don’t tx if < 50% is weight bearing
Do surgery for sure if?
Go to surgery if 50-80% lameness
Indications for a TPO and management
FHO (Gridlestone procedure)
1. Pain is from bone on bone
2. Indicated for dogs w/ significant pain due to DJD 2 to CHD
3. This procedure cuts the femoral head off
4. More successful in little dogs
5. Obesity & muscle quality plays more of a role and decrease results
6. Daily exercise shold be encouraged after suture removal
Do this in addition to FHO
Muscle ‘biceps’ Sling
1. In addition to FHO
2. Biceps femoris between femur and acetabulum
3. Causes a lot of pain
4. Slower recover, less wt, bearing
5. Less extension, shorter leg
Why would you do a TPO
Triple pelvic osteotomy (TPO)
1. Prevent hip subluxation by rotating the dorsal rim of the acetabulum laterally to provide more coverage of the femoral head
2. See drawing
3. Indicated fo dogs w/ minmal degenerative changes radiographically
4. Ideally should be 6-7 months old w/ deep acetabuli and no radiographic evidence of DJD
5. Contraindications are shallow acetabulum, loss of dorsal rim, femoral neck osteophytes and nerve damage
6. Excellent results w/ dogs w/ no DJD
What is a Total Hip arthroplasty (THA)
1. Replaces femoral head and acetabulum w/ artificial components
Indications for Total Hip arthroplasty (THA)
a. over 40 pounds w/ pain and lameness due to CHD
b. irreducible chronic hip luxations
c. failed femoral head and neck excision
d. irreparable femoral head/neck
e. acetabular fxs
f. failed THAs that need revised
Contraindication of Total Hip arthroplasty (THA)
a. lack of pain or lameness regardless of radiographic appearance
b. Infection anywhere in the body (cystitis, bacterial dermatitis, gingivitis)
c. Neurologic dz affecting rear legs
d. Concurrent orthopedic problems (cruciate rupture)
e. Open trochanteric physis
What is the Norberg angle measurment used for hip dysplasia?
A line drawn from center of one femoral head to center of the other, to the tip of the craniolateral margin of the acetabulum. This theory has been proven not reliable
What is the distraction index or laxity test for hip dysplasia
Stress radiograph that promotes luxation (‘action shot’)
Dog in dorsal recumbency w/ femurs perpendicular to table
Bar placed between femoral dyaphyses and stifles are pressed together, levering the hips out
Dogs w/ a distraction index more that 0.5 develop hip dysplasia
What is the dorsal acetabular rim evaluation used for in hip dysplasia
Dorsal Acetabular Rim (DAR)
Craniodorsal projection centered on and parallel to the dorsal acetabular rim
This view of hip allows accurate evaluation of the amount of dorsal coverage provided for femoral head
Contrived for TPO evaluation
Pathogenesis of hip dysplasia
•Hip Dysplasia = Hip laxity = Positive Orlani sign = JUVENILE dog (prearthritis
tx djd
• Tx of DJD
a. Conservative
b. Femoral head & neck osteotomy (FHO)
c. Total hip
Treatment for young dogs with hip dysplasia
a. In young dog have two choices for treatment:
-TPO – triple pelivc osteotomy
-Develop DJD – how fast, how bad can’t predict – rads are NOT clinical
Conservative management of hip dysplasia
1. Must have exercise to build muscle mass. The less the muscle, the more the bone has to bear weight
2. Meds decrease PAIN due to inflammation (give every other day)
3. Try to do low impact exercise (Monday, Wednesday, Friday minimum)
4. On Tuesday & Thursday, rest w/ meds
5. Check Fee T4 for hypothyroid
6. Calculate kcal ((30 x kg) + 70; give specific number of cans to feed per day
7. MUST LOSE WEIGHT
8. Keep dog in warm environment
9. Give 6-8 week trial period, if fails, need surgery
Dont do surgery in hip dysplasia if?
a.Dog is NOT limping (can’t improve a non-limping dog!)
b.Don’t tx if < 50% is weight bearing
Do surgery for sure if?
Go to surgery if 50-80% lameness
Indications for a TPO and management
FHO (Gridlestone procedure)
1. Pain is from bone on bone
2. Indicated for dogs w/ significant pain due to DJD 2 to CHD
3. This procedure cuts the femoral head off
4. More successful in little dogs
5. Obesity & muscle quality plays more of a role and decrease results
6. Daily exercise shold be encouraged after suture removal
Do this in addition to FHO
Muscle ‘biceps’ Sling
1. In addition to FHO
2. Biceps femoris between femur and acetabulum
3. Causes a lot of pain
4. Slower recover, less wt, bearing
5. Less extension, shorter leg
Why would you do a TPO
Triple pelvic osteotomy (TPO)
1. Prevent hip subluxation by rotating the dorsal rim of the acetabulum laterally to provide more coverage of the femoral head
2. See drawing
3. Indicated fo dogs w/ minmal degenerative changes radiographically
4. Ideally should be 6-7 months old w/ deep acetabuli and no radiographic evidence of DJD
5. Contraindications are shallow acetabulum, loss of dorsal rim, femoral neck osteophytes and nerve damage
6. Excellent results w/ dogs w/ no DJD
What is a Total Hip arthroplasty (THA)
1. Replaces femoral head and acetabulum w/ artificial components
Indications for Total Hip arthroplasty (THA)
a. over 40 pounds w/ pain and lameness due to CHD
b. irreducible chronic hip luxations
c. failed femoral head and neck excision
d. irreparable femoral head/neck
e. acetabular fxs
f. failed THAs that need revised
Contraindication of Total Hip arthroplasty (THA)
a. lack of pain or lameness regardless of radiographic appearance
b. Infection anywhere in the body (cystitis, bacterial dermatitis, gingivitis)
c. Neurologic dz affecting rear legs
d. Concurrent orthopedic problems (cruciate rupture)
e. Open trochanteric physis
Pro's of Total Hip arthroplasty (THA)
-Cementless implants – bone grows ONTO implant – helps decrease bone lysisi due to rxn w/ bone cement
- Don’t need to repair the ischial or pubic osteotomy sites b/c they’re not weight bearing bones and will heal on their own. Leave the blate on the ilium (no reason to remove)
Important post surgery care of THA?
- Avoid excessive activity for a month
- Bad complications – but are only 10%
# of teeth in hookworm
margin of 3 prs of teeth.
Define Urinary incontinence?
Loss of voluntary control of micturition, usuallyobserved as involutary urine leakage
Urinary incontinence most common in
Most common in middle aged to old neutered female dogs (medium to large breed dogs most often affected
What increases risk of Urinary incontinence
Neutering and obesity
If a neurologic disease is the cause of Urinary incontinence what will you see
Will see distended bladder and neuroogic defici
Neurologic causes of Urinary incontinence
A. disrupution of local neuroreceptors peripheral nerves, spinal pathways or higher center invovled in conrol of micutrition
b.Lesions of sacral spinal cord (congenital, cauda equina syndrome, LS disk dz, fx or dislocation
c.Lesions of cerebellum or cerebral micturition center affect
What are the signs of urinary storage dysfunction?
a.Intermittent urinations at night or while animal is sleeping
b.Small urinary bladder is palpated
c.Increased frequency of urinations
Causes of urinary storage dysfunction?
d. UTI
e. Chronic inflammatory disorder
f. Infiltrative neoplastic lesion
g. External compression
h. Chronic partial outlet obstruction
i. Congenital urinary bladder hypoplasia w/ ectopic ureters
j. Idiopathic detrusor instability in FeLV cats (unknown in dogs) – will see Anisocoria (unequal sized pupils)
What causes Intermittent urinations at night or while animal is sleeping, Small urinary bladder is palpated
Urethral disorders
Causes of Urethral disorders
c. Urethral closure via smooth & striated muscle and CT to prevent leakage
d. Congenital urethral hypoplasia or incompetence
e. Acquired urethral incompentence – reproductive hormone responsive urinary incontenency
f. RTI or inflammation
g. Prostatic dz or sx
h. Vestibulovaginal anomalies
Anatomic causes of urinary incontinence
a.Diversion of urine from normal storage
b.Ectopic reters can terminate in distal urethra, uterus or vagina
c.Patent urachal remnants divert urine outflow to the umbilicus
d.Vestibulovaginal anomalies, congenital urocystic hypoplasia
e.Urethral hypoplasia can also interfere w/ continence
Urine retention happens when what?
a. Intravesicular prssure exceeds outlet reisstance
Diagnosis of incontinence
– must differentiate volutary from involuntary; normal urethral discharge; normal cat spraying
1. Urinalysis to r/o UTI
2. Bloodwork to r/o PU/PD disorders
3. Contrast radiography, excretory urography, double contrast cystography to id lesions
4. U/S
5. Neuro exam
6. Urethral catheterization
Treatment of urinary incontinence?
• Medical therapy:
a. Reproductive hormones
- Stilbesterol
- Diethylstilbesterol
- Testosterone
b. Alpha adrenergic agonists
- Phenylporpanolamine
- Phenylephrine
- Pseudoephedrine
- Imipramine – tricyclic antidepressent w/ anticholinergic and alpha agonis actions that provides at alternative to tx
- Can be used in combo w/ reproductive hormones for synergistic effect
c. Detrusor instability
- Manage w/ anticholinergic or antispasmodic agenst such as oxybutynin, propantheline, imipramine, flavoxate, dicyclomine
******
How do you rule out the following diseases with bloodwork?
*******
******
How do you rule out the following diseases with bloodwork?
*******
Anemia
PCV, TP
Dehydration
PCV, TP
Renal failure
BUN
Diabetic keotacidosis
Hyperglycemia, glucosuria, ketonuria and metabolic acidosis
Hypoadrenocortism
Renal azotemia, dec Na, inc K, inc Ca, hypoglycemia (need ACTH stim test to make definitive dx)
Electrolyte imbalance
important for V+ and D+ and for obstructed cats
Definition of COPD
• Chronic coughing occurring for 2 consecutive months that is not attributable to another cause (neoplais, CHF)
hallmark of tracheobronchial irritation
coughing
dry, gagging, owner may misinterpret as
V+
Diagnostic tool of COPD
tracheal palpation causes coughing
Primary rule out for COPD
CHF
COPD biggest factor of getting this
obesity
What will you see on bloodwork with COPD
eosinophillia
Lung pattern on rads with COPD
– bronchial pattern
DX of COPD
•TTW or BAL will show infalmmatory cells w/ segs, eosinophils or Mac
TX COPD
a. Moderate exercise (not forced) is useful in facilitating secretion clearance and assisting wt loss in overweight animals
b. Antitussives when cough is non productive, continuous or debilitating
- Butorphanol
- Hydrocodone
- Codeine
c. Steroids will decrease airway inflammaiton and coughing regardless of underlying etiology – use short term when case is not infectious in nature
d. Bronchodilators
e. Beta agonists
- Terbutaline
- Albuterol
- Theophylline
- Aminophylline
Parvo mode of infection
Oronasal infection
Trophic=
– prefers gut epithelium
Primary viremia of parvo replicates in
thymus and meseneric ln
Secondary viremia of parvo replicates in
crypt cells of small intestine
Viral secretion in feces for how long?
-first 2 weeks of infection (some shed intermittently over a year!)
Parvo prognosis
1. If only D+ - good prognosis w/ Abs & fluids
2. If D+ w/ parasites – poor prognosis b/c synergistic rxn
CS of parvo
Clinical signs –
D+ via malabsorption
Leukopenia via extravascular WBC or WBC missing b/c virus is I/S
Secondary Gram – bacteria overgrowth
Myocardial dz
Environment persistance of parvo
up to 5 mos
Intervertebral disk dz
IVDD 2 types
1. Hansen Type I
2. Hansen Type II
Describe hansen type I
Chondrodystrophic dogs
Nucleus propulsus calcifies, pushes dorsally b/c annulus fibrosis in thinnr here. Goes into spinal cord
Most common sites are C2-C3 & T12-T13
Describe Hansen Type II
All breeds, but older dogs
Fibroid (not calcification) changes bulges, stretches and pushes against spinal cord
Harder to fix than type I
CS IVDD
Clinical signs
Pain
Ataxia
Paresis/paralysis
Analgesia – tiny fibers deep in spinal cord lack deep pain
DDX IVDD
Rads will r/o other dzs (trauma, disco, tumor)
But since you can’t r/o meningitis or IVDD w/ rads, r/o meningitis
TX IVDD
Medical tx
1. Steroid tx and cage rest is ‘usual’ or rDVM therapy. Steroids make the dog feel better, so owner will let out of cage. Back to square one or even worse.
2. Low dose steroids can be used for pain management (1/4 to ½ mg/kg Pred)
3. In bruising, steroids ARE indicated. High dose steroids given in bruising of spinal cord itself where sx won’t help
4. Solu Medrol is first choice & needs to be started 8 hours after injury to do any good
5. Cage rest, cage rest, cage rest
Congestive Heart Failure AKA
Mitral Insufficiency Emergency
Define CHF
Degeneration of mitral valve (endocardiosis) with a thickened, knobby valve
CHF causes what?
Causes large left atrium and pulmonary edema. May take years to progress
How does CHF present
as an emergency
Causes of CHF
a.Undetected mitral regurgication
b.Ruptured cordae tendinae due to increased blood turbulence causing fulminant pulmonary edema
c.Fluids during routine surgery
d.Sudden increase in salt in diet causing increased water retention
e.Heat
f. Digitalis toxicity
Signs in general of CHF?
Signs of Left heart failure (pulmonary edema)
Cardiac radiographs of CHF
a.pulmonary veins are larger than arteries indicating pulmonary venous congestion
b.Round, enlarged heart
c.Enlarged left atrium
d.Tracheal elevation
e.Perihilar edema first
What do you see on ECG with CHF?
a.Left atrial enlargement
b.Wide P wave
c.Tachycardia
Echo of CHF looks like what?
a.Mitral valve thickening
b.Left atrium and left ventricle lumen is enlarged
c.M mod – contractility is ok or even increased
d.Left atrium to aortic ratio should be 1:1, in mitral regurg will be 3:1
*** Describe the 4 stages of CHF and their therapies****
*** Describe the 4 stages of CHF and their therapies****
Class I
a.Murmur only, no therapy needed
b.Get CXR, and recheck in 6 months
Class II
a.Exercise intolerance
b.Enalapril – ACE inhibitor, vasodilator to decrease afterload
c.H/D diet or restrictive salt diet
d.Decrease exercise
Class III
a.Respiratory diestress, cough especially at night, pulmonary edema, tahcycardia, enlarged heart
b.Diuretics to decrease fluid (see below)
c.Enalapril – ACE inhibitor, vasodilator to decrease afterload
d.Digoxin – slows heart, increases contractility
e.Monitor kidney for axotemia
f.Low salt diet (H/D) – low palatability
g.Watch for food aversion if introduced at the hospital
Class IV
a.Emergency, cyanosis, pulmonary edema (severe)
b.Nitroglycerine topically – venodilator, decrease preload (thorax, ear)
c.Na nitroprusside – very potent vasodilator for severe pulmonary edema, slow drip
d.Dobutamine – contractility has gone
What is the MOA of Digoxin
-slows HR and increases contractility
-positive ionotrope and negative chronotrope
-increases Ca absoprtion
-increases vagal tone and slows AV conduction
Side effects of digoxin?
include small therapeutic window and long t ½ so need careful loading
Never use loding dose in digoxin except when?
dose except in supraventricular tachycardia and CHF in life threatening situation
Very sensitive to digoxin?
dobie
What monitoring parameters should you be aware of with digoxin?
-Give med in a.m. then check in p.m. (therapeutic level should be 1 – 2.5 ng/ml 8 hours after last dose)
-Check dig levels 5-6 days after therapeutic maintenance or showing signs
These are the signs to tell an owner to stop giving the drug.
-V+/D+ and anorexia are first signs so tell owner to stop giving if not eating
What will you see on ECG with dig?
- On EKG, will see increase in PR interval and may drop some beats or be in V tach
- Animals w/ the following are more prone to dig tox
a. Renal dz
b. Hypokalemia
c. Thyroid
d. Quinidine, Verapamil, Chloramphenicol
Diuretic of choice
Lasix
Lasix affects what part of kidney
Affects ascending Loop of Henle
Lung effect of Digoxin?
Venodilation is mild in lungs
Side effects of lasix
May cause dehydration, hypokalemia and alkalosis
Monitor effect of lasx via?
Monitor via kidney azotemia:
a.Hypokalemia if > 2-3 mg/kg
b.Spirolactone – K+ sparing diurectic
c.Monitor CREA, if increases, then decrease diurectic dose
Adjunnctive therapy with CHF?
Adjunctive Therapy
1. Hycodan – cough suppresent b/c of left atrium putting pressure on main stem bronchus
2. Torbutrol – pain control
3. Morphine – to decrease anxiety, slow HR and reduce preload
***Acute Renal Failure***
***Acute Renal Failure***
What are the steps to manage acute renal failure
1.Rehydrate within 4 to 6 hours
2.Use colloids if low oncotic pressure
3.Monitor for overhydration via:
4.Induce diuresis:
5.Furosemide
6.Mannitol – not first choice
7.10-20% Dextrose
8.Dopamine
9.Correct Hyperkalemia
10.May need to correct Metabolic acidosis
Best fluids to use
a. Crystalloid fluids – Saline, ½ saline + 2.5% dextrose, LRS
Calculation for amount of fluids
BW (kg) x % dehydration
Use what if low oncotic pressure?
2.Use colloids if low oncotic pressure
a.dose colloids then decrease crystalloid volume by 1/3
How do you monitor for overhydration?
a. Central venous pressure (CVP)
- 0-5 normovolemia or volume contraction
- 5-8 ideal
- > 8 approaching overhydration
b. urinary collection system – see below in ‘ins and outs’
c. accurate body weight
d. Anxiety
e. Clear nasal discharge
f. Tachycardia
g. Increased skin turgor
Chemosis – swelling
Induce diuresis via?
a. 2x-4x maintenance rate to > 2 mL/kg/hour (maintenance is 66 mL/kg/24 hours)
b. Jugular catheter placement allows delivery of high fluid rates and measurment of CVP
c. ‘Ins and Outs’
- maintain central venous pressure < 10 cm H20
- Quantitate urine every 2-4 hour period
- Add volume of collected urine to insensible fluid loss (20 mL/kg/day) and ongoing losses (V+/D+) over the same 4 hour period and deliver this volume for the next 4 hours
- LRS, normosol most commonly used
- Potassium supplementation may be required in this phase
Use mannitol why and how?
a.2x-4x maintenance rate to > 2 mL/kg/hour (maintenance is 66 mL/kg/24 hours)
b.Jugular catheter placement allows delivery of high fluid rates and measurment of CVP
c.‘Ins and Outs’
-maintain central venous pressure < 10 cm H20
-Quantitate urine every 2-4 hour period
-Add volume of collected urine to insensible fluid loss (20 mL/kg/day) and ongoing losses (V+/D+) over the same 4 hour period and deliver this volume for the next 4 hours
-LRS, normosol most commonly used
-Potassium supplementation may be required in this phase
What supplementation may be required using mannitol
K+
10-20% Dextrose MOA
a. Osmotic diursesis through dextrose is metabolized and resorbed by the renal tubules
Pros vs cons of Dextrose
b.Safer, but less likely effective
c.Discontinue infusion if glucosuria does not occur
Dopamine uses?
a. Increases renal blood flow and Na excretion at low doses
b. In dogs only is this low dose effective
c. Higher doses will cause cardiotonic and pressor effect
d. Dopamine and Lasix (Furosomide) tx is effective to increase urine output but may not increase GFR
EKG abnormalities with hyperkalemia
- Bradycardia
-Peaked T wave, prolonged PR interval, wide QRS, absent P wave
Tx hyperkalemia
-Sodium bicarbonate
-Regular (short acting) insulin/Dextrose
-10% Ca gluconate
What about metabolic acidosis?
a. Mild – usually resolves w/ fluid therapy
b. Marked acidosis tx w/ sodium bicarb
Complications of bicarb therapy include:
- Ionized Ca deficits
- Paradoxic CSF acidosis
- Cerebral edem
Other things to do with ARF?
11. Antacid therapy
a. H2 blockers (cemididine, ranitindine) and omeperazole
b. Decrease hypergastinemia & ulcers

12. Sucralfate – gastrin protectant
13. Misoprostel – prostaglandin analogue, vasodilate microcirculation
14. Antimemetics
a. Metochlopromide – antidopanergic properties,  V+ center

15. Nutrition – tube feeding if not V+, TPN, but more PPN, parital parenteral nutrition
Needed for severe uremia signs, but signs that dz is still reversible (acute dz)?
Peritoneal Dialysis
DX of ARF
Surgical renal biopsy is required for dx
Prognosis if need dialysis
Generally the case decision is to euthanize or dialyze
MOA of dialysis
Infuses high osmolar fluid (dialysate) into abdomen and pulls extravascular fluid out
***Chronic Renal Failure**
***Chronic Renal Failure**
Chronic Renal Failure aka
polyuric
Management outline
1. Fluid therapy is less important
2.
3.Tx underlying dz
4.Management of uremic complications
What are the uremic complications?
a.Nutritional
b.Hyperphosphatemia
c. Hypocalcemia
d. Hypokalemia
e. Anemia
f. Metabolic Acidosis
g. V+/Uremic gastritis
Nutritional diet
-protein restricted diet – k/d
MOA of protein restricted diet?
- protein causes higher blood pressure and  Crea and BUN
-Sodium restriction
- dec blood pressure; should be done gradually so kidneys can adjust
Homemade diets
- Homemade diets can provide high quality protein when needed (eggs, liver, cottage cheese and lean meats)
MOA of hyperphosphatemia
- Occurs w/ chronic renal failure as a result of decreased renal excretion. Concurrently, a decrease in the concentration of the active form of Vit D decreases the intestinal absorption of Ca, which, inconjunction w/ the impaired tubular resorption of Ca, decreases the plasma concentrations of ionized Ca. PTH increases in response to both decreased Ca and Vit D. This causes renal excretion of Ph and increased absorption of Ca as well as increased absorption of Ca from bones and the GI tract
The consequences of hyperphosphatemia are the following:
a. Osteodystrophy
b. Neuropathy
c. Bone marrow suppression
d. Soft tissue mineralization – if the product of Ca + Ph > 70, the animal is at risk for so
Oral phosphate binders
a. Amphogel
b. Patients often resist and is messy to administer
- Feed phosphorus restricted diet
Hypocalcemia should ideally base on
- Limiting phosphate will improve Ca absorption and retention
- TUMS is a good supplement
- Oral Calcitrol
a. will further decrease serum PTH (many believe this to be the major uremic toxin)
b. Early stages of CRF
c. Animal should be well hydrated and eating a Ph-restricted diet
d. Avoid Ca-containing enteric Ph binders
e. Also used for hypocalcemia tx
ionized Ca
will improve Ca absorption and retention
Limiting phosphate
Good supplement for hypocalcemia
TUMS is a good supplement
- Oral Calcitrol
a. will further decrease serum PTH (many believe this to be the major uremic toxin)
Be careful with this in hypocalcemia tx
c.Animal should be well hydrated and eating a Ph-restricted diet
d.Avoid Ca-containing enteric Ph binders
e.Also used for hypocalcemia tx
Hypokalemia is mostly a problem in ?
more common problem in cats
Damage caused by hypokalemia
-Can accelerate tubular damage
Tx hypokalemia
-Tx is oral Potassium Gluconate powder or tablets (Tumil-K)
Treatment for anemia needed only if?
Not needed for dogs w/ PCV > 30% and cats > 25%
TX for anemia
- Anabolic steroids not reliably effective
- Blood transfusions give only short term benefit
- Recombinant human erythropoietin – may develop Abs causing severe fall in PCV
Metabolic Acidosis can be monitored via?
Monitor via TCO2
Metabolic Acidosis tx
Can give sodium bicarb, but watch Na load & hypertension
V+/Uremic gastritis is stimulated by?
- Uremic toxins stimulate CTZ
TX V+/Uremic gastritis
- Use H2 blockers (Cimetidine, Ranitindin - Zantac, caragate, misoprostel
- Metochlopromide
- Oral phosphate binders may benefit
Hypertension parameters
Want to maintain systolic blood pressure at 120-160 mmHg and diastolic at 60-90 mmHg
Therapy for high blood pressure
. Low sodium diet
b. ACE inhibitors (Enalpril)
c. Beta blockers (atenolol, propanolol)
d. Vasodilators
e. Diuretics (Diltiezam)
Efficacy of SQ fluids in CRF?
-Only practical in cats and small dogs and owners willing to do it
-Can be effective
Monitoring for CRF?
1.No azotemia but impaired concentrating ability – measure PCV, BUN, SG & blood pressure at 6 month intervals
2.With azotemia – every 3 months plus Ca, Ph, Na and K, blood gases, UA
3.One or more abnormalities – every 4-8 weeks
4.Uremic animals – daily monitorin
•Follicle mite of dogs
Demodex canis
Demodex canis found where?
•Hair follicle adjacent to sebaceous glands in skin of dogs
Gross appearance
•Alligator/cigar shape, adults have 4 pairs of stumpy legs, larva only have 3 prs.
Life cycle D. Canis
Egg, larva, nymph & adult spent entirely on host.
D. Canis spread by
Mite is spread by direct contact from dam to offspring. Puppies acquire this mite from dam when nursing. NOT FROM DOG TO DOG! Has been associated with immunodefieciency
3 types of infection with D. Canis
1. Heavy infection is called demodecosis
2. Local demodectic acariasis – mild, clincial disease of patch of red skin.
3. Generalized demodectic acariasis – most severe, and pathetic canine skin diseases. Can have secondary infections
Dx D. Canis
Skin scrape
***Sarcoptis scabei***
***Sarcoptis scabei***
Role of female
Females form tunnels
Where are the tunnels formed
in epidermis of ears, albows, of humans, & animals, many varieties (i.e. variety porcine)
Identification
Females are twice as big as males. Suckers are on tips of long, unjointed pedicels (stalks
Life cycle
• Egg, larva, nymph & adult. Adults breed on surface, Females burrowns into epidermis & deposits eggs. Have 6 legged larva, larva tunnel at right angle.
Transmission
Highly transmittible and is spread by direct contact.
CS
Complete alopecia and PRURITIC. Skin may appear leathery & scabby.
DX
deep skin scrape
Transmission to human
Mites will invade human, but won’t tunnel
***Canine Hypothyroidism***
***Canine Hypothyroidism***
Two Causes
Autoimmune dz (lymphocytic thyroiditis)
Idiopathic atrophy (disappears w/o inflammation and replaced w// fat)
Main Pathogenesis
Primary dz in dogs
Gradual loss of thyroid tissue w/ a  T4 and and  TSH which stimulates remaining functional tissue
Thyroid tissue loss continues as T4 drops and clinical signs appear (threshold and clinical signs vary between individuals)
Don’t recover, but have compensation
Other pathogenesis’ (rare)
2 hypothyroidism – lack of TSH from pituitary
3 hypothyroidism – lack of TRH from hypothalamus (has never been shown)
Congenital hypothyroidism – very rare
Hypothyroidism in cats – remember that T4 normally drops in old or sick cats; a low T4 in cats simply rules out hyperthyroidism
Signalment
Middle aged
Medium to large sized breeds (but don’t r/o small breeds)
Goldens, Schnauzers, Boxers, Cockers, Dobies, Labs, Setters, Great Danes, Poodles
Genetic basis still questionable
Top three clinical signs in hypothyroidism
Hair coat, dermatological problems
Obesity
Lethargy
Less common clinical signs
Neurologic
Female fertility
Myxedema (face swelling)
Ocular disorders
Cretinism
DDx for wt gain, lethargy and symmetrical alopecia
Cushings
a. look for PU/PD, alk phos, pot belly
b. Go after Cushings FIRST – T4 may become normal after Lysogen tx
c. Remember it could be both Cushings and Hypothyroid
Growth hormone
Too much food
Dexamethasone and other drugs will lower thyroid
DDx for hyperlipidemia
Diabetes mellitus
Cushings
Nephrotic syndrom
Acute pancreatitis
Biliary obstruction
Primary lipid metabolism
Physical exam
Bilateral symmetric alopecia – not on head or legs
Non pruritic unless 2 infection
Hair epilates easily
Dry, flaky skin
Seborrhea
Lethargy
Wt. Gain
Exercise intolerance
‘Heat seekers’
Hyperpigmentation
Rat tail
Myexedema
Lab findings
Few abnormalities
-inc Cholesterol – due to dec receptor mediated clearance)
-Mild non-reg, normocytic, no
-inc Triglycerides
Hypothyroid Dx tests
Lesson
Rules out the dz if normal or high value
No real reason to measure total T3
Best single dx test presently
Best in combinations w/ total or free T4 – never use alone
Another useful test if included in a ‘package’
Reserve only for patients w/ unusual test results (especially total T4 or T3
Tx for hypothyroid
• L-thyroxine 20-40 g/kg SID
Start at 20 ug/kg BID, then after 12 wks go to 20 ug/kg SID (but may need to go back to BID)
• Only 10-50% of oral dose is absorbed
• Dog T ½ - 8 hours
Human T ½ - 7 days (pharmacist will think you’re crazy when asking for this high a dose)
Post pill testing
Good idea to evaluate levels every 8-10 weeks after starting therapy or after changing dosages.
Then, evaluate every 6-12 months
Draw blood sample 4-12 hours post pill, then run a total T4 test
Ideal levels are 30-60 nmol/L
DDx for abnormal recheck tests
High T4 – overdose
Low T4 – not giving pill or too low dose
Normal T4 but still showing signs – not hypothyroid
Overdosing?
• Overdosing is not common, but can occur if dose is not monitored especially in Giant breed dogs
• Signs of overdose:
PU/PD
Nervous
Panting
Wt. Loss
Hardpad disease aka
Distemper
Distemper etiology?
Morbillivirus, large RNA that is closely related to measles and rinderpest
Distemper shed via
Shed via all body excretions – expecially respiratory exudates
-Aerosol
MC signalment of Distemper
Young puppies (3-6 months old) are most susceptible
A susceptible puppy can be safely introduced into a household with previous distemper
1 month after removal of a puppy that died of CDV infection
Distemper replication
repilcates in Macrophages of lower respiratory tract and lymphoid tissue
Distemper spreads to?
Spreads rapidly to most epithelial tissue and CNS (especially immunodeficient puppies
CS of distemper
a. Ocular and nasal discharges
b. Pneumonia - Dry cough – rapdly becomes moist and productive
c. ADR, V+/D+, dehydrations
d. Neurologic signs 1-3 weeks after recovery from systemic dz – seizures, hyperesthesia, pacing, circling, paresis, rhythmic motor movements (“myoclonus’)
e. Multifocal chorioretintis – peripheral nontapetal fundus
f. Optic neuritis
g. Keratoconjunctiviits
h. Nasal and digital hyperkeratosis – hardpad dz
i. Abortion, stillbirths or birth of weak puppies
Cliin path of distemper
a. Lymphopenia – inclusions are rare
b. May see inclusions on impressions of conjunctiva or vagina during viremia
c. CSF -  protein,  cells (lymphocytes)
d. Specific CDV neurtralizing AB found w/ encephalitis
e. Intersitial/alveolar patter w/ severee bronchopneumonia
DX distemper
f. Virus neutralization of paired serum samples w/ fourfold rise confirms active infection
g. ELISA can also be used and is more sensitive, but less widely used
Tx distemper
• Supportive care only
• Even if tx is not effective, dogs should not be euthanized unless the neurologic distrubances are progressive or incompatible w/ good quality life
The Big Five Titers for CNS dz
Distemper, Toxoplasmosis, Neospora, Ehrlishia, Herpes virus
Infectious Canine Hepatitis
affects who?
• • Dogs and foxes serve as reservoirs and can be
Liver of dogs and foxes
Infectious Canine Hepatitis
etiology?
Canine adenovirus Type I – CAV-1
• Closely related to CAV-2
Serve as reservoirs of Infectious Canine Hepatitis
Dogs and foxes serve as reservoirs
Infectious Canine Hepatitis shed how?
-shed in urine from reservoirs for 6-9 months
•Highly contagious and transmitted by contact w/ infected animals, fomites and ectoparasites
•Oronasal exposure and localized in tonsils
CS of Infectious Canine Hepatitis
a. Signs of naturally occurring ICH are seen exclusively in unvaccinated dogs < 1 year old
b. Ocular lesions are seen in 20% of naturally occurring cases and in < 1% of dogs after attenuated vaccination
c. Peracute dz – fever, petechia, CNS, moriburn or dead
d. ADR, V+, fever, icterus, lymphadenopathy
e. ‘Blue eye” – anterior uveitis occurs days to weeks later
f. Tonsilitis
g. Chronic dz – cirrhosis, ascities, encephalopathy and wt loss
h. Glaucoma
i. Immune-complex glomerulonephritis
j. DIC
Clin path of Infectious Canine Hepatitis
a. Leukopenia, lymphopenia
b. inc ALT, AST, Alk phos
c. Bruria, Proteinuria
d. Increased bile acids
e. Hypoglycemia
f. DIC – coag abnormalities
g. Viral isolation – intranuclear inclusion bodies on tissue cultures
Prevention of Infectious Canine Hepatitis
• Vaccinate dam before breeding to increase level of maternal ab
• Recovery from ICH results in long lasting immunity
Infectious Canine Hepatitis
affects who?
• • Dogs and foxes serve as reservoirs and can be
Liver of dogs and foxes
Infectious Canine Hepatitis
etiology?
Canine adenovirus Type I – CAV-1
• Closely related to CAV-2
Serve as reservoirs of Infectious Canine Hepatitis
Dogs and foxes serve as reservoirs
Infectious Canine Hepatitis shed how?
-shed in urine from reservoirs for 6-9 months
•Highly contagious and transmitted by contact w/ infected animals, fomites and ectoparasites
•Oronasal exposure and localized in tonsils
CS of Infectious Canine Hepatitis
a. Signs of naturally occurring ICH are seen exclusively in unvaccinated dogs < 1 year old
b. Ocular lesions are seen in 20% of naturally occurring cases and in < 1% of dogs after attenuated vaccination
c. Peracute dz – fever, petechia, CNS, moriburn or dead
d. ADR, V+, fever, icterus, lymphadenopathy
e. ‘Blue eye” – anterior uveitis occurs days to weeks later
f. Tonsilitis
g. Chronic dz – cirrhosis, ascities, encephalopathy and wt loss
h. Glaucoma
i. Immune-complex glomerulonephritis
j. DIC
Clin path of Infectious Canine Hepatitis
a. Leukopenia, lymphopenia
b. inc ALT, AST, Alk phos
c. Bruria, Proteinuria
d. Increased bile acids
e. Hypoglycemia
f. DIC – coag abnormalities
g. Viral isolation – intranuclear inclusion bodies on tissue cultures
Prevention of Infectious Canine Hepatitis
• Vaccinate dam before breeding to increase level of maternal ab
• Recovery from ICH results in long lasting immunity
Canine Herpes virus signalment
Affects puppies < 3 weeks old
Etiology CHV
Enveloped DNA
CHV transmission
Transmitted transplacental, systemic via oronasal, or genital infection
CS CHV?
• Signs:
a. Abortion during last 1/3 pregnancy
b. Bright yellow, fluid stools in puppies
c. Persistent crying of puppies
d. Serous, mucopurulent or hemorrhagic nasal discharge
e. Petechial hemorrhaging
f. Erythematous rash
g. SQ edema on vetral abdomen and inguinal region
h. Persistent neurologic defcits in recovered puppies
i. Older puppies show mild resp
j. Adults can have nasal discharge, or genital secretions
Clin path CHV
a. Leukopenia and lymphopenia
b. inc ALT, AST, & Alk phos
c. Bruria and proteinuria
d. Increased bile acids
e. Coag abnormalities
f. Hypoglycemia
g. Signs look like hepatitis
h. Fourfold rising tier on serology
TX CHV
• Tx – supportive tx and fluides
• Maintain body temp
Prevention CHV
• One infection of hyperimmune serum may reduce mortialtiy
• Vaccine is not curretnly available
Parvovirus etiology?
CPV2
Parvovirus causes
severe gastroenteritis
Parvovirus Affinity for
***rapidly dividing cells***
a. intestinal crypt epithelium
b. Myocardium in puppies < 2 weeks old
c. Bone marrow
d. Lymphopoietic tissue
Parvovirus Persist in environment for
long periods and is most important for perpetuating the dz but can be inactivated by bleach
Parvovirus Sources:
a. Feces, slaiva and vomitus
b. Fomites and mechanical vectors are primary sources
Parvo signalment
Affects puppies 6 weeks to 6 months
Parvovirus cs
a. Fever
b. Gray, yellow blood streaked D+
c. Dehydration and wt loss
d. Death
e. Myocardial dz – 3 weeks to 27 months old; die of congestive heart failure
Parvovirus clin path
lymphopenia
Parvovirus dx
b. Virus detection is ost specific means of iconfirmation – Fecal hemagglutination, ELISA, or virus isolation
Parvovirus tx
• Tx
a. NPA
b. IV polyioin fluides w/ KCL
c. BS Abs
d. Hyperimmune serume or plasma tranfusion – esp w/ hypoalbumineim
e. Antiemetics if V+ is persistent and uncontrolable – chlorpromazine, metoclopramide, prochlorperazine
f. Recombinant human granulocyte cology stimulating factor (G-CSF) and antiendotoxin hyperimmune plasma
g. Tx parasites
h. Slowly introduce to small highly digestivel , low fiber low fat diet (cooked rice, low fat cottage cheese, boiled lean ground beef, chicken or commerical baby food)
Parvovirus prevention
• Vaccinate w/ a HIHG titer attenuated CPV2 vaccine up to 15 weeks old – especially the Rottweiller
• Disinfect contaminated areas and utensils and properly dispose of infected feces
Canine corona virus
causes what
Gastroenteritis in most Canidea
Canine corona virus shed
Host specific and is shed in feces
Canine corona virus most signalment
neonates
Canine corona virus affects which part of intestine
Affects villi of small intestine
Canine corona virus shed for how long
Shed in feces for 3-14 days after initial infection
Canine corona virus cs
Yellow green to oragne malodorous D+ begins simultaneously w/ V+
Canine corona virus recovery
Recovery is noted w/in 8-10 days
Canine corona virus dx
A fourfold rising IgG titer confirms infection
Canine corona virus prevention
It is difficult to assess the role of vaccines b/c infection are usually inapparent
Canine corona virus
causes what
Gastroenteritis in most Canidea
Canine corona virus shed
Host specific and is shed in feces
Canine corona virus most signalment
neonates
Canine corona virus affects which part of intestine
Affects villi of small intestine
Canine corona virus shed for how long
Shed in feces for 3-14 days after initial infection
Canine corona virus cs
Yellow green to oragne malodorous D+ begins simultaneously w/ V+
Canine corona virus recovery
Recovery is noted w/in 8-10 days
Canine corona virus dx
A fourfold rising IgG titer confirms infection
Canine corona virus prevention
It is difficult to assess the role of vaccines b/c infection are usually inapparent
Acute viral encpehalitis of all warm blooded animals

• s
• Stages:
• Negri bodies in CNS
Rabies
Rabies etiology
Rhabdovirus, bullet shaped