Glossary of eninac

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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?
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?
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?
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:
2. Extracapsular
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
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?
Taut band in extension?
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 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?
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
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?
Tap should be _______ as compared to screw?
same size
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
Osteoinduction – major fxn
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?
Inguinal hernia
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?
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?
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 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?
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?
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?
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
What will reduce circulating estradiol to helpp treat mammary cancer?
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
-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
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
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?
Digitoxin toxicity
Hyperkalemia in AS usually secondary to what?
Urinary obstruction
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***
-Middle aged, fat, female dogs
-‘garbage eaters’
-‘sick’; depressed
- V+/D+
- Painful abdomen, tucked up abdomen
- 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 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
-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?
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
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?
-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
-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?
What species has amyloid depositions in islets throughout pancreas?
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?
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

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