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SA Medicine > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Specific periods of the pediatric period

A

Neonatal period: birth - 2 weeks
Transitional period: 2 - 4 weeks
Socialization period: 4 - 12 weeks
Juvenile period: 12 weeks - puberty

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2
Q

Three most common neonate issues

A
  1. Hypothermia
  2. Hypoglycemia
  3. Sepsis
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3
Q

At what age do neonates become more like “small adults”?

A

4 weeks

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4
Q

Normal neonate temperature, pulse, respiration rate

A

96 - 96 F, 100 F by 4 weeks
Pulse: >220 bpm
RR: 15-35 bpm

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5
Q

Normal weight gain in neonates

A

Weight should be doubled by 2 weeks of age

Puppies: gain 2-4 g/day/kg of adult weight

Kittens: ~100g at birth, gain 10-15 g/day

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6
Q

How are neonates grouped at 24 hours old?

A
  1. Majority group: weight gain at 12 and 24 hours
  2. Portion of group: weight loss of <10% of birth weight
  3. Critical group: weight loss of > 10% of birth weight
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7
Q

Why can’t skin turgor be used to assess hydration in neonates? What should you use instead?

A

Neonates are 75% water and have non-cornified skin

Use MM dryness

Use USG as they age (can’t concentrate urine yet)

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8
Q

When do neonates’ eyes open? Menace present? Vision normal?

A

Eyes open: 10-14 days

Menace: present by 21 days, fully developed by 2-3 mo

Vision normal: 3-4 weeks

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9
Q

When are neonates’ ear canals open? What is the best way to assess hearing?

A

Ear canals open by 14 days

BAER best way to assess hearing but should not be done before 6 weeks of age

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10
Q

Is sinus arrhythmia normal in neonates?

A

No, they should have a normal sinus rhythm

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11
Q

What murmur is commonly heard in neonates?

A

Functional, soft murmur at left cardiac base

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12
Q

Why will atropine during bradycardia not be effective in increasing the heart rate of a neonate?

A

Their autonomic nervous system is not well developed so they have minimal response to vagal stimulation

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13
Q

By what age should testicles be descended in puppies?

A

Normally by 4-8 weeks, 16 weeks at the latest

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14
Q

By what age are postural reactions developed in puppies/kittens?

A

6-8 weeks

Non-visual placing: 2-3 days
Visual placing: 2-3 weeks
Extensor postural thrust: 3 weeks
Walking: 3-6 weeks

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15
Q

By what age do puppies/kittens have a righting response? Air righting response?

A

Righting response - birth

Air righting response - kittens 21-30 days

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16
Q

How are puppies/kittens assess on the Neonatal Viability Scoring System?

A

Activity/muscle tone, pulse/HR, reflexes, MM color, and RR assessed

Can earn up to 2 points per parameters

0-2 = weak vitality
4-6 = moderate vitality
7-10 = normal vitality
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17
Q

How does PCV of neonate compare to adult? USG?

A

PCV is higher than puppy or adult (42%)

USG = 1.018 because they do not fully concentrate urine

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18
Q

Why does radiography technique need to be adjusted for neonates?

A

Needs to be adjusted because of

  1. Partially mineralized bones
  2. Thinness of soft tissues
  3. Amount of water

Use high detail intensifying screens

Decrease kvp to 1/2 adult at same thickness

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19
Q

The most common cause of problems for neonates?

A

Husbandry issues

poor nutrition, hypothermia

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20
Q

Ideal ambient temperature for orphan neonates?

A

86-90 F for first week

Gradually decrease over next 3 weeks to 75 F

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21
Q

Causes of sepsis in neonates?

A

Often gram negative bacteria that enter bloodstream via

GI and peritoneal infection
Respiratory infection
UTI
Skin/wound infection

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22
Q

Clinical signs of sepsis in neonates?

A 
Sudden death
Crying, restlessness, weakness
Hypothermia
Dehydration
Diarrhea
Altered respiratory rhythm
Cyanosis
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23
Q

What should you look for if you suspect a neonate is septic?

A

Check the umbilicus and look for puncture wounds

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24
Q

Treatment for sepsis in neonates?

A 
Keep warm
Fluids (IV or IO)
Antibiotics (B lactam)
O2
Glucose
Monitor weight 2-3 x day
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25
Q

What is fading puppy/kitten syndrome?

A

Death within first 1 - 12 weeks

Most vulnerable periods:
In utero
At time of birth
Immediately after birth - 2 weeks
Post-weaning
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26
Q

Causes of fading puppy/kitten syndrome?

A 
Congenital defects
Teratogenic effects
Malnutrition
Low birth weight
Trauma
Neonatal isoerythrolysis
Infectious disease
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27
Q

Diagnosis of fading puppy/kitten syndromes relies heavily on

A

Necropsy

Have the necropsy discussion prior to whelping

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28
Q

At what point should an owner of a neonate call the vet because the neonate is sick and will decline rapidly?

A
  1. Neonate crying for more than 20 minutes in presence of littermates and/or mother
  2. Neonate refuses to nurse or is not interested in nursing
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29
Q

Most common cause of chronic renal failure in pediatric patients?

A

Renal dysplasia

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30
Q

What primary lesions are suggestive of renal dysplasia in pediatric patients?

A
  1. Fetal or immature glomeruli/tubules
  2. Persistent mesenchyme
  3. Persistent metanephric ducts
  4. Atypical tubular epithelium
  5. Dysontogenic metaplasia
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31
Q

Most common liver disease seen in pediatric patients?

At what age do clinical signs manifest? What are the clinical signs?

A

Congenital PSS

As early as 6-8 weeks of age

CS (puppies):

Intolerance to anesthetic agents or tranquilzers that are metabolized by the liver

Intermittent neurologic abnormalities associated with eating high protein foods

Ammonium biurate crystals or uroliths

CS (kittens):

Hypersalivation
Seizures
Ataxia
Tremors 
Depression
Small body stature, think, unkempt
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32
Q

Most reliable and consistent way to diagnose PSS in pediatric animals

A

Fasted pre- and post-serum bile acids

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33
Q

Treatment of PSS in pediatric animals

A

Medical management:

Low protein diets in frequent, small meals

Antimicrobial agents

Lactulose

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34
Q

Causes of inflammatory pancreatic disease (affecting only the exocrine portion) in animals <6 mo old

A

Trauma

Infection (Parvo, FIP)

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35
Q

Effects of drop in body temperature on neonates

A

Heart rate drops

GI ileus more likely to occur

Less ability for lymphocyte transformation

Mother rejects neonate with cool skin

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36
Q

Single most important predictor of neonatal survival

A

Birth weight

Toy breeds: 100-200 grams
Large breeds: 400-500 grams
Giant breeds: 700 grams
Kittens: 100 grams

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37
Q

PSS seen in which cat breeds?

A

Himalayan
Persian
Mixed breeds

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38
Q

Localization of lesion with discolored urine AND stanguria? Without stranguira?

A

Stranguria -> lower urinary tract
(bladder, urethra, prostate)

No stranguria -> upper urinary tract
(kidneys, prostate, systemic disease)

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39
Q

How to differentiate between hemoglobinuria and myoglobinuria?

A

Look at plasma color

Pink -> hemoglobinuria
Clear -> myoglobinura

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40
Q

When is an antibiotic trial okay to do for a patient with suspected bacterial cystitis?

A

Dog with LUT signs (first occurrence)

Owner declines UA and culture

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41
Q

When is an antibiotic trial NOT okay to do for a patient with suspected bacterial cystitis?

A

Dog is acting systemically sick or seems obstructed

Cat -> more likely to have an inflammatory cystitis or may be obstructed

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42
Q

Difference between polyuria and pollakiuria?

A

Polyuria: daily urine output greater than 50 ml/kg/day

Pollakiuria: increased frequency of urination (but not necessarily increased volume)

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43
Q

What factors control thirst?

A

Osmotic factors:

Dehydration stimulated osmotic receptors in the hypothalamus

Non-osmotic factors:
Fever
Pain
Drugs
Hypovolemia
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44
Q

What factors control the secretion of ADH?

A 
Hyperosmolarity (dehydration)
Hypovolemia
Hypoglycemia
Stress
Pain
Fever
Exercise
Angiotensin
Drugs
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45
Q

Ddx for PU/PD in young patients

A 
Congenital renal abnormalities
PSS
HyperCa (malignancy, vit D intoxication)
Pyelonephritis
DI
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46
Q

Ddx for PU/PD in adult patients

A 
CKD
DM
Hepatic failure
HyperT4
Cushing's
Addison's
HyperCa (malignancy, 1 HPT, renal 2 HPT, Vit D, granulomatous dz)
Pyelonephritis
Neoplasia
DI
Pyometra

MOST CAUSE 2nd NDI

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47
Q

What type of diets may cause PU/PD?

A

High salt (treats -> pig ears)
Low protien
Vit supplementation

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48
Q

When should you perform water deprivation test?

A

ONLY when remaining ddx are CDI, primary NDI, and psychogenic polydipsia

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49
Q

Pathophysiology of secondary NDI

A

Osmotic diuresis or chronic PU/PD ->

Renal medullary solute washout ->

Impaired response to ADH

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50
Q

Normal bilirubin metabolism

A

Heme -> biliverdin -> unconjugated bilirubin (bound to albumin)

Unconjugated bilirubin goes to liver -> conjugated bilirubin

Conjugated bilirubin goes to bile -> SI -> LI -> converted to urobilinogen -> urobilin (yellow) and sterobilin (brown) -> excreted in feces

Small portion of urobilinogen reabsorbed by liver, some excreted by kidneys

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51
Q

What type of bilirubin is freely filtered by the kidneys?

A

Conjugated

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52
Q

Causes of pre-hepatic, hepatic, and post-hepatic icterus

A

Pre-hepatic:
‣ Hemolysis

Hepatic:
‣ Hepatitis, hepatic lipidosis, neoplasia, cirrhosis, toxins/drugs, sepsis

Post-hepatic:
‣Pancreatitis (most common cause in dogs)
‣Biliary neoplasia (most common cause in cats)
‣Cholangitis
‣Cholecystitis
‣Choleliths
‣ GB mucocele

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53
Q

Lab findings with pre-hepatic cause of ELE

A

Moderate to severe anemia, hemolyzed serum, spherocytes, heinz bodies

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54
Q

When can you detect icterus in serum and tissues?

A

Serum bilirubin > 1.5 mg/dl

Tissues - bilirubin > 2.0 mg/dl

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55
Q

What factors can artifactually cause elevated bilirubin?

A

Iatrogenic hemolysis

Lipemia

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56
Q

Elevated bilirubin with normal liver enzymes may be an indicator of

A

Sepsis

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57
Q

Acholic feces are seen with what type of disease

A

Chronic bile duct obstruction

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58
Q

Cellular origin of ALP, GGT, ALT, AST

A

ALP: membrane associated, inducible

GGT: membrane-associated, inducible

ALT: cytosolic, seen with necrosis/inflammation

AST: cytosol and mitochondria

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59
Q

What is important to know about ALP in cats?

A

Short-half life means this enzyme should go back to normal very quickly. Persistent elevations in the cat is always significant

No steroid-induced isoenzyme

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60
Q

ALP&raquo_space; ALT is indicative of

A

Cholestasis

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61
Q

ALT&raquo_space; ALP is indicative of

A

Hepatocellular disease

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62
Q

Pros and cons of liver sampling techniques

A

FNA:
Pros: good for specific masses or diffuse neoplasia, vacuolar changes

Cons: poor for inflammatory conditions

Biopsy
Pros: will provide better answers than cytology

Cons: more invasive, has a greater risk for hemorrhage, and usually requires heavy sedation or anesthesia

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63
Q

What is hepatocutaneous syndrome?

A

Crusting, ulcerative lesions on paws/footpads seen with liver disease

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64
Q

Common CBC finding with liver disease?

A

Microcytosis

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65
Q

What pattern of liver enzyme increase indicates hepatic lipidosis in cats?

A

Increased ALP with normal (or near normal) GGT

ALP significantly higher than ALT

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66
Q

What is Protein C used for?

A

Used to help differentiate PSS from portal vein hypoplasia

If normal, probably not a shunt

Low protein C activity common in shunts, but not present with portal vein hypoplasia

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67
Q

Does a normal appearance of the liver on ultrasound exclude hepatobiliary disease?

A

No

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68
Q

How to distinguish between small vs large bowel diarrhea

A

Small bowel
‣ Normal- increased volume
‣ Mucus rare
‣ Melena

Large bowel
     ‣ Normal-decreased volume
     ‣ Mucus common
     ‣ Hematochezia
     ‣ Urgency and tenesmus common
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69
Q

Causes of small bowel diarrhea

A 
Malabsorptive
     ‣ Dietary responsive
     ‣ Parasites (Giardia)
     ‣ Antibiotic responsive
     ‣ IBD
     ‣ Neoplasia
     ‣ Fungal
PLE
     ‣ Lmphangiectasia
     ‣ Lymphoma
     ‣ Severe IBD
     ‣ Fungal
     ‣ GI hemorrhage
     ‣ Massive hookworm/whipworm infection
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70
Q

Causes of large bowel diarrhea

A 
Dietary responsive
Fiber responsive
IBS
Parasites (tritrichomonas)
Bacterial disease
Fungal
IBD
Neoplasia
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71
Q

How does a patient’s clinical status affect diagnostic evaluation of chronic diarrhea?

A

Patients that are anorexic, cachexic, or hypoproteinemic are not good candidates for therapeutic trials as this may result in significant morbidity and mortality from delayed treatment if the therapy is incorrect

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72
Q

What is the cytological difference between Giardia and Tritrichomonas?

A

Giardia
‣ Small number trophozoites
‣ “Falling leaf” movement

Tritrichomonas
‣ Undulating membrane
‣ Larger numbers

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73
Q

Utility of diagnostic imaging in patients with chronic diarrhea

A

Ultrasound most helpful
‣ Rarely gives definitive diagnosis
‣ Allows for lesion location prior to endoscopy
‣ Focal lesions for aspiration

Contrast study and radiographs
‣ Rarely helpful

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74
Q

What are the pros/cons of endoscopic versus surgical liver biopsy?

A

Endoscopic
‣ Advantages
• Less invasive
• Requires little recovery time (outpatient procedure)
• Allows visualization of mucosal surfaces
• Less expensive than surgery
‣ Disadvantages
• Limited evaluation of the GI tract (essentially the whole jejunum is off limits)
• Only being able to biopsy the mucosa (not full thickness biopsy)
• Not being able to evaluate other organs/structures

Surgical
‣ Advantages
• Allows evaluation and full-thickness biopsy of the entire GI tract as well as other intraabdominal organs.
‣ Disadvantages
• Invasive procedure
• Usually requires 2-3 days of hospitalization post-operatively for recovery

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75
Q

What is the treatment approach to antibiotic responsive diarrhea?

A

Broad-spectrum antibiotics effective against aerobes and anaerobes for minumum of 2-3 weeks

     ‣ Tylosin  (20-40 mg/kg PO q12h)
     ‣ Amoxicillin (22 mg/kg PO q12h)
    ‣ Metronidazole (15 mg/kg PO q24h) + enrofloxacin (7 mg/kg orally every 24 hours)

Severe cases:
‣ Tetracycline (22 mg/kg PO q12h)

Can also try:
‣ Probiotics
‣ Fecal transplantation

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76
Q

Use of immunosuppressives for treatment of IBD

A 
Corticosteroids
Prednisone/prednisolone
Methylprednisone
Dexamethasone
Busesonide
Cyclosporine
Azathioprine
Chlorambucil

Treat 2-4 weeks beyond resolution of clinical signs, then start to taper 25% every 2-4 weeks

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77
Q

Treatment of EPI

A

Supplement pancreatic enzymes (Pancreazyme, Viokase)
Supplement cobalamine
Treat dysbiosis (antibiotics)
+/- low fat diet

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78
Q

What is the role of diet in treatment of lymphangiectasia?

A

Because low fat diets lack long-chain fatty acids, they prevent intestinal lacteal engorgement and protein loss

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79
Q

What fraction of seropositive cats shed coronavirus?

A

1/3

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80
Q

Do seronegative cats shed coronavirus?

A

No

except for in non-domestic felids

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81
Q

What kind of cat is most at risk for developing FIP?

A

Young (<2 years old)
Purebred (Persian and Birman)
Male
Live in multi-cat environment

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82
Q

Clinical signs of FIP

A 
Antibiotic unresponsive fever
Rapid weight loss
Icterus
Anorexia
Depression
Body cavity effusions
Abdominal masses
Neurologic signs
Uveitis
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83
Q

How is FIP associated with intestinal obstruction?

A

Focal granulomatous lesion of colon or ileocolic junction

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84
Q

Lab findings for patient with FIP

A 
Neutrophilia +/- mild L shift
Nonregenerative anemia
Lymphopenia
Hyperproteinemia
Hyperglobulinemeia
Hyperbilirubinemia
ELE

MAY ALL BE NORMAL

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85
Q

What is the rivalta test?

A

8 ml distilled water + 1 drop acetic acid + 1 drop effusion

Mix thoroughly

If effusion congeals -> positive for FIP

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86
Q

FIP effusion analysis

A

Modified transudate with pyogranulomatous inflammation

Color: clear, straw, yellow

Consistency: viscous, frothy when shaken, may clot in cold

Protein: >3.5 g/dl, low A:G ratio <0.45

Cellularity: <5000/uL, non-toxic neuts, macrophages, lymphs

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87
Q

FIP CSF analysis

A

Extremely high protein (>200 mg/dl)

Extremely high nucleated cells (>100/ul)

Risk of herniation during CSF collection

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88
Q

Necropsy findings FIP

A

White plaques on serosal surfaces

Adhesions of omentum, mesentery

Lymphadenopathy

Pyogranulomas

Vasculitis

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89
Q

Are adult cats more at risk for developing FIP if they live/lived with a cat that was diagnosed with FIP?

A

Adult cats not at risk

Seronegative kittens - yes

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90
Q

Treatment of FIP

A

Prednisolone

Maybe antiviral and immunomodulating drugs (UC Davis study)

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91
Q

How can healthy cats be screened for FIP?

A

Can’t, no screening tests

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92
Q

What are the most reliable confirmatory tests for FIP?

A

Rivalta test
Effusion analysis
Biopsy

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93
Q

How is FIP spread from cat to cat?

A

Coronavirus spread fecal-oral route

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94
Q

How can FIP be prevented?

A 
Decrease stress
Pedigree analysis (don't breed cats that have had or produced kittens with FIP)

Vaccination is NOT recommended

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95
Q

Cardiac arrhythmias seen with hyperkalemia

A

No p waves
Spiked T waves
Bradycardia

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96
Q

When should you consider supplementing calcitriol in patients with CKD?

A

Used to reverse secondary hyperparathyroidism

Only if serum phosphorous < 7 mg/dl

Cannot use in conjunction with Epakitin (phosphate binder)

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97
Q

IRIS staging for AKI

A

Grade 1: Cr <1.6 mg/dL, non-azotemic, oliguric or anuric

Grade 2: Cr 1.7 - 2.5 mg/dL, documented AKI and azotemic, oliguric or anuric

Grade 3: Cr 2.6 - 5.0 mg/dL, increasing severity of azotemia

Grade 4: Cr 5.1 - 10.0 mg/dL

Grade 5: > 10.0 mg/dL

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98
Q

IRIS staging for CKD

A

At risk: history of toxin exposure, breed, infectious dz, old age

Stage 1: Cr <1.4 (dogs), <1.6 (cats), nonazotemic, inadequant concentrating abilty, abnormal renal palpation or imaging, proteinuria, increasing Cr

Stage 2: Cr 1.4 - 2.0 (dogs), 1.6 - 2.8 (cats), mild azotemia, absent or mild CS

Stage 3: Cr 2.1 - 5.0 (dogs), 2.9 - 5.0 (cats), moderate renal azotemia

Stage 4: Cr > 5.0 increasing risk of systemic clinical signs and uremic crisis

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99
Q

Clinical signs acute vs chronic kidney disease

A

Acute: oral necrosis, bradycardia, hypersalivation, large kidneys, normal BCS, severely depressed, seizures, coma, oliguric (except AG)

Chronic: retinal detachment, pale MM, oral ulcers, murmurs, hypersalivation , small kidneys, decreased BCS, renal osteodystrophy, polyuric

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100
Q

Treatment of metabolic acidosis and electrolyte imbalances in AKI

A

Ca gluconate
Dextrose
Bicarb

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101
Q

Treatment for persistent oliguria/anuria

A

Furosemide
Mannitol
Dopamine
Fenoldopam

(Controversial, none shown to improve outcome but some vets still use)

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102
Q

Goals of AKI treatment

A

Reverse anuria/oliguria
Keep up with fluid losses
Enteral nutrition if possible
Wean off fluids slowly

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103
Q

IRIS staging - UPC

A

Proteinuric =

> 0.5 dogs
0.4 cats

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104
Q

When is SDMA relevant?

A

A persistent increase in SDMA about 14 ug/dL suggests reduced renal function

May be a reason to consider a dog with Cr <1.4/1.6 mg/dl as IRIS stage 1

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105
Q

What is azodyl?

A

Probiotic/prebiotic used for it’s propensity to metabolize urea, creatinine, uric acid, various carcinogenic amines, guanidine and indole metabolites and phosphate

“Intestinal dialysis”

Little clinical evidence

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106
Q

When should you consider dialysis for renal failure?

A

Acute, anuric renal failure due to toxin or infection

For CKD, to improve condition prior to transplant

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107
Q

What is pre-renal proteinuria?

A

Proteinuria due to abnormal plasma content of proteins (hemoglobin, myoglobin, bence-jones proteins, globulins)

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108
Q

What is renal proteinuria?

A

Proteinuria due abnormal renal loss/handling of normal plasma proteins

Functional - due to altered renal physiology secondary to a transient extra-renal cause (strenuous exercise, fever)

Pathological - due to structural or functional renal lesion (glomerular, tubular, or interstitial)

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109
Q

What are the three types of pathological renal proteinuria?

A

Glomerular - due to lesions that alter the permselectivity properties of glomerular capillary walls

Tubular - due to lesions that impair tubular resorption of proteins that would be expected to cross the normal glomerular capillary wall

Interstitial - results from inflammation that causes exudation of proteins into urine (proteins come from peritubular capillaries)

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110
Q

What is post-renal proteinuria?

A

Due to protein that enters urine after the renal pelvis

Urinary - hemorrhage or exudation from urinary tract

Extra-urinary - hemorrhage or exudation from genital tract or external genetalia

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111
Q

How can you differentiate if proteinuria is urinary post-renal or renal?

A

Clinical signs of patient

If patient does not have fever -> more likely urinary post-renal

If fever present -> renal

112
Q

What magnitude of different in day-to-day proteinuria is considered clinically significant?

A

Dogs: difference of at least 40%

Cats: double

113
Q

Localization of lesion if UPC is > 2?

A

Most likely glomerular (pathologic)

114
Q

UPC levels of animals for which an underlying disease should be identified and should be treated for PLN

A

Azotemic dogs with UPC > 0.5

Azotemic cats with UPC > 0.4

Non-azotemic dogs/cats with UPC > 2.0

115
Q

Etiologies for glomerular disease

A

Membraneoproliferative glomerulonephritis (MPGN)

Membraneous nephropathy (MN)

Immunoglobulin A nephropathy

Amyloidosis

Hereditary nephritis

Minimal change disease

116
Q

Treatment for glomerulonephritis

A

ACE inhibitors (enalapril, benazepril)

Angiotensin receptor blockers (losartan, telmisartan)

Renal diet

Control hypertension

Thromboprophylaxis (asprin, clopidogrel)

Control hyperkalemia

117
Q

Breeds of dogs with familial glomerulopathies

A

Amyloidosis - beagle, sharpei, english foxhound

Hereditary nephritis - bull terrier, cocker, dalmatian, samoyed

Mesangiocapillary GN - bernese mt dog

Glomerulosclerosis, cystic glomerular atrophy - dobies, corgi, newfoundland

Glomerular vasculopathy and necrosis - greyhound

Atrophic glomerulopathy - rottweiler

118
Q

Infectious agents associated with membraneoproliferative glomerulonephritis (MPGN)

A

Borrelia
Babesia
Leishmania
HW

119
Q

Is it normal for protein to be found in the glomerular filtrate in Bowman’s space?

A

Yes

120
Q

What components of glomerulus aid in permselectivity of proteins?

A

Fenestrations in glomerular capillaries

BM (negative charge)

Podocytes

121
Q

What is the screening test for proteinuria? Confirmatory tests?

A

Screening: dipstick

Confirmatory: SSA, microalbuminuria

122
Q

Signs of anaphylaxiz post-vaccination

A

Vomiting, swelling, collapse, fever

123
Q

Types of non-immunologic reactions post-vaccination

A 
Cutaneous granuloma/vasculitis
Systemic fever/malaise
Febrile limping syndrome in cats
Neoplasia
Fetal resorption
Vaccine associate disease of akitas and HOD and juvenile cellulitis in weimeraners
124
Q

Types of immunologic reactions post-vaccination

A

Type 1: anaphylaxis
Type 2: IMHA
Type 3: blue eye or immune complex disease

125
Q

Age of critical period of susceptibility to disease where there are not enough Ab to protect from disease yet still too many maternal Ab to allow for active immunization

A

6-16 weeks

126
Q

Core vaccines for dogs and cats

A

Dogs - rabies, distemper, adenovirus, parvo

Cats - panleuk, herpes, calici, rabies, FeLV

127
Q

Priniciples that should be used in assessing an animal’s risk and selecting proper vaccinations

A

Vaccinate the largest possible number of animals in the population at risk

Vaccinate each animal no more frequently than necessary

Vaccinate only against infectious agents to which individuals have realistic risk of exposure, infection, and subsequent development of disease

vaccinate only when the potential benefits of the procedure outweigh the potential risks

128
Q

Do all adverse vaccine reactions need to be reported to the USDA Center for Veterinary Biologics and to the vaccine manufacturer?

A

YES

129
Q

Where should vaccinations NOT be given?

A

Intrascapular space

130
Q

What factors are triggers for disease outbreak recognition of and call to action?

A

Higher than expected number of cases

More severe or prolonged disease than expected

Failure of usual containment procedures to stop transmission

131
Q

When should you pursue further diagnostic testing in a disease outbreak?

A

Many affected animals

Severe or complicated disease

Deaths

Unusual disease patterns

132
Q

Quarantine time is directly related to what pathogen factor?

A

Pathogen incubation period

133
Q

Isolation time is directly related to pathogen factor?

A

Pathogen shedding period

134
Q

Largest amounts of pathogen shedding occur during

A

Preclinical incubation period

135
Q

Most favored diagnostic test for respiratory pathogens?

A

PCR

136
Q

What is the single most important step in managing disease outbreak?

A

Isolation of sick animals

137
Q

How long should a sick animal be isolated during the management of a disease outbreak?

A

Isolate for the length of the contagious period/pathogen shedding

138
Q

Why might an exposed animal not have clinical disease?

A

Infected but pre-clinical incubation period

Subclinical infection

Not infected due to immunity

ALL EXPOSED ANIMALS SHOULD BE QUARANTINED

139
Q

How long should an animal be quarantined for?

A

Pathogen incubation period

140
Q

How often should quarantined animals be monitored for clinical signs?

A

Twice daily

141
Q

Treatment for Amanita poisoning

A

Silimarin (milk thistle extract)

142
Q

Treatment for acetaminophen poisoning

A

Acetylcysteine

143
Q

Treatment for copper or riron accumuationg in liver

A

Chelation therapy with penicillamine or trientene

Zinc (inhibits copper absorption)

Limit copper in diet

144
Q

Treatment of hepatic lipidosis

A

E-tube
Feed high protein, high fat diet

Give slowly to avoid re-feeding syndrome

145
Q

Treatment for vacuolar hepatopathy

A

Good diet including increased protein +/- melatonin, lysodren

146
Q

Treatment of leptospirosis

A

Penicillin or ampicillin IV followed by doxycycline PO

147
Q

Treatment of bartonella

A

Enrofloxacin, doxycycline, azithromycin

148
Q

Treatment of Platynosonum concinum liver flukes

A

High dose praziquantel (20 mg/kg SC for 3 days or 20 mg/kg PO q 12 week)

149
Q

What is ursodiol?

A

Hydrophilic bile acid that replaces hydrophobic bile acids such as chenodeoxycholic acid that are extremely toxic

Used as anti-inflammatory and to increase bile flow in the treatment of cholangiohepatitis/cholangitis

CONTRAINDICATED in full bile duct obstruction

150
Q

Consequence of untreated bile duct obstruction

A

Cirrhosis

151
Q

Treatment of emphasematous cystitis or GB mucocele?

A

Sx

152
Q

Why is surgery the treatment of choice for liver tumors?

A

Chemo usually ineffective due to multiple drug resistance (MDR) gene that is constitutively expressed by liver tumor cells

153
Q

Treatment for chronic hepatitis

A

Immunosuppressive therapy (widely used but controversial)
Colchicine (anti-fibrotic therapy)
Sylimain (extract of mil thistle)

154
Q

What is choline?

A

Used in treatment of liver disease

Important in phospholipids so essential for exporting lipid from liver

155
Q

What is included in supportive therapy for patients with liver disease?

A 
Fluids
Plasma 
Nutrition (increased demand for protein and calories)
Folate
Choline
Vitamin C
156
Q

What is SAMe?

A

S-adenyl methionine

Synthesized in liver from methionine

Liver damage reduces SAMe synthetase activity in the liver which is important in methylation reactions that synthesize nucleic acids, amino acids, phosphatidylcholine, polyamines, and glutathione

Need to give 1 hour before meal

157
Q

Treatment for hepatic encephalopathy

A 
Glucose
Potassium
Sarmazenil
Protein-restriction
Lactulose
Neomycin, metronidazole
Albumin (binds tryptophan, an aromatic AA precursor for false neurotransmitters)
158
Q

How does lactulose work in the treatment of hepatic encephalopathy?

A

Increases incorporation of ammonia in microbial protein

Lowers pH of colon and converts ammonia to ammonium.

Ammonium is less lipophilic, is not absorbed as readily, and is instead excreted into feces

159
Q

Treatment for ascites associated with liver disease

A

Plasma (for hypoalbuminemia)
Salt restriction
Spironolactone
Therapeutic paracentesis

160
Q

Causes of hepatic lipidosis in cats

A

Idiopathic - MOST COMMON
DM
HypoT4
Pancreatitis/tiaditis

161
Q

Common causes of protozoal hepatitis and treatments

A

Leishmania: allopurinol
Toxoplasma: TMS, pyrimethamine
Hepatozoon: imidocarb

162
Q

Fungal hepatitis most commonly caused by

A

Histoplasmosis

Tx with itra

163
Q

Most common pathogen in bacterial cholecystitis?

A

E. Coli

164
Q

What is idiopathic chronic hepatitis?

A

Unknown etiology, possible immune-mediated

Doberman, Cocker Spaniel, Westies

Biopsy will show bridging necrosis, lymphocytic-plasmacytic infiltration, progressing to cirrhosis

Treat with immunosuppressive therapy, colchicine, sylimarin

Prognosis very guarded

165
Q

What is colchicine?

A

Microtubule inhibitor that inhibits collagen deposition, stimulated collagenase

Used as anti-fibrotic therapy and may decrease inflammation in patients with liver disease

No data on efficacy

166
Q

What is sylimarin?

A

Milk thistle

Antioxidant, leukotriene, and TNF inhibitor

Inhibits P glycoprotein, affects P450 enzymes

Uncertain efficacy

167
Q

Which supplements for liver disease act on methyl transfer?

A

Folate
B12
SAMe

168
Q

Which antioxidant vitamins may be helpful in liver disease?

A

Vitamin E

Vitamin C

169
Q

Causes of neurological signs with hepatic encephalopathy

A
  1. Ammonia from colon and kidney
  2. Inhibitory GABA receptor stimulation
  3. False neurotransmitters from aromatic amino acids
  4. Methionine/mercaptans
  5. Hypoglycemia
  6. Cerebral edema
  7. Hypokalemic alkalosis
  8. Dehydration
170
Q

What is often the only way to monitor liver disease?

A

Repeat biopsy

171
Q

What is the “triple therapy” for helicobacter infection?

A
  1. PPI
  2. Amoxicillin
  3. Bismuth
172
Q

Almost all underlying causes of changes in gut motility that cause vomiting are due to

A

Low protein

173
Q

When do you need to re-culture after treatment for UTI?

A

Complicated UTI

Culture 7 days after treatment started and 1 week after treatment has stopped

174
Q

How are colony numbers estimated in urine cultures where colonies are TNTC?

A

Estimating percentage of total area of the plate that is covered with a confluent lawn of bacteria and then x 10,000

175
Q

Most common pathogens in UTIs

A

More common: E.coli, proteus, staph, enterococcus

Less common: klebsiella, psuedomonas

176
Q

Which antibiotics are first line for uncomplicated UTI?

A

Clavamox

TMS

177
Q

What antibiotic is first line when suspecting pyelonephritis (and while awaiting culture results)?

A

Fluroquinolone

178
Q

Duration of treatment for UTI (uncomplicated and complicated)

A

Uncomplicated: 7-14 days
Complicated: 4 weeks

179
Q

Clinical signs of distemper infection?

A 
Cough
small intestinal diarrhea
Hyperkeratosis
“Chewing gum” seizures
Dentine damage and cardiomyopathy (neonates)
HOD?
Uveitits
180
Q

When can you get a weak false positive on parvo fecal antigen ELISA?

A

4-8 days after live vaccine

181
Q

How long will a parvo fecal antigen ELISA be postivie after infection?

A

10-12 days

182
Q

When is PCR for parvovirus most sensitive, how long will it detect virus post-infection, and does it detect vaccine?

A

Most sensitive at 10 days
Measurable as long as 54 days
Detects vaccine up to 14 days

183
Q

Diagnosis of distemper is based on what?

A 
Pattern of clinical signs
Cytoplasmic inclusions
CSF IgG vs serum IgG
Immunocytology of antigen 
PCR
Neutralizing Ab
ELISA for IgM or IgG
184
Q

What is a positive prognostic factor for parvo?

A

Higher C-reactive protein

Maintenance of WBC count during hospitalization

(Cholesterol lower in non-survivors)

185
Q

Main negative prognostic factor for distemper

A

Neurological signs

186
Q

Water requirements for animals being treated for parvo/distemper?

A

1 mL/lb/hr

Puppies need 2x

187
Q

Major risk of modified live distemper vaccine

A

Vaccine-induced encephalitis
HOD

(Especially in weimeraner)

188
Q

Which distemper vaccines give immunity >3 years?

A

Modified live

Recombinant canary pox vector vaccine

189
Q

Environmental risk factors for lepto

A 
High rainfall
Flooding
Standing water
Working dogs
Urban dogs exposed to rats
Overcrowded kennels
Contaminated water sources in dry areas
Warm, moist alkaline soil
190
Q

Serologic diagnosis of lepto requires:

A

Single titer > 800

4-fold increase or decrease in paired titers 1-3 weeks apart gold standard

191
Q

Lyme borreliosis is transmitted by

A

Ixodes ticks

192
Q

What percent of dogs are seropositive for lyme borreliosis? What percent show clinical signs?

A

75% are seropositive

5-10% have clinical signs

193
Q

Pathogenesis of lyme borreliosis

A

OpsA aids in attacghment to tick midgut

When tick feeds on host, OpsC upregulated and causes migration of borrelia to salivary gland

Increase in VlsE as tick engorges, allows borrelia to evade host immunity

Dermal inoculation causes inc in OpsC and Salp15 -> dissemination

194
Q

Clinical signs of lyme disease

A

Clinical signs occur 2-6 months after exposure

Polyarthritis, shifting leg lameness
Fever, anorexia, lethargy
Lymphadenopathy
Lyme nephritis (PLN caused by immune-complex deposition)

195
Q

Can cats get lyme borreliosis?

A

In lab setting, yes

Not naturally

196
Q

Criteria for lyme borreliosis

A
  1. History of exposure to ticks in an endemic area
  2. Typical clinical signs
  3. Specific Ab against B. Burgdorferi
  4. Prompt response to antibiotics
197
Q

Drawback of ELISA for diagnosis of lyme borreliosis?

A

Cannot distinguish between disease and vaccination

198
Q

What does the SNAP 4Dx specifically test for lyme borreliosis?

A

C6 antibody

VlsE (IR6) gene only expressed during infection and replication within mammalian host

Codes for C6 peptide

Vaccines do not induce false positives!

199
Q

What is the lyme multiplex assay?

A

Test by Cornell that quantifies amounts of OspA, OspC, and Osp F

200
Q

Should all dogs that test positive for lyme on SNAP test be treated?

A

No, only treat clinical dogs

201
Q

Treatment for lyme borreliosis?

A

Clavamox

Doxycycline

202
Q

Prevention of lyme borreliosis

A

Tick prevention

Vaccination (Osp A antibodies)

203
Q

Wy is there controversy over vaccination for lyme borreliosis?

A

Most infections are subclinical

Disease responds to antibiotics

Questionable vaccine efficacy

Post-vaccinal Lyme-like syndrome

OspA can be inflammatory and cause lyme nephropathy

204
Q

Can lyme for a dog be transmitted to a human?

A

No

Only serve as a sentinel for human disease

205
Q

Vector and infected cell type:

E. Canis, E. Ewingii, A. Phagocytophilium, A. Platys

A

E. Canis: Riphicephalus, monocytes/macrophages

E. Ewingii: Amblyomma, granuloctes

A. Phagocytophilium: Ixodes, granuloctes

A. Platys: Riphicephalus, platelets

206
Q

Cytologic finding with E. Canis

A

Morulae within macrophages

207
Q

What causes the most common labwork abnormality found with E. Canis infection?

A

Thrombocytopenia

Due to:

Platelet consumption

Decreased platelet half-life (splenic sequestration, immune-mediated destruction)

Increased PMIF inversely proportional to platelet count

208
Q

In which phase of disease is E. Canis most commonly diagnosed?

A

Chronic

209
Q

What labwork abnormality found with E. Canis warrants distinction from lymphoma?

A

Granular lymphocytosis

210
Q

Lab abnormalities found with E. Canis infection

A

Moderate - severe thrombocytopenia

Mild - moderate non-regenerative anemia

Granular lymphocytosis

Pancytopenia

Hyperproteinemia

Increased ALT and ALP

Protienuria

CSF - lymphocytic pleocytosis

Morulae on blood smear

211
Q

Diagnosis of E. Canis

A

Serology:

Fluorescent Ab test gold standard

Point-of-care ELISA (IDEXX 4Dx SNAP)

212
Q

Treatment for E. Canis

A

Doxycycline 21-28 days

Chloramphenicol for puppies <5 mo

Enro is NOT effective

213
Q

How do you assess response to therapy in treatment of E. Canis?

A

Resolution of signs

Increased platelet count

(Should normalize within 2 weeks)

214
Q

Clinical signs of E. Ewingii

A 
Polyarthropathy
Fever
Splenomegaly
Hepatomegaly
Thrombocytopenia
215
Q

Is erlichia zoonotic?

A

No reported cases

Needs vector for transmission

E. Canis DNA has been detected in humans with erlichiosis

(Use caution when handling ticks on dogs)

216
Q

Cytology/lab findings found with Analplasma phagocytophiliuum?

A

Morulae within neutrophils

Mild to severe thrombocytopenia

Moderate non-regenerative anemia

217
Q

Vector and target cells for rickettsia rickettsia

A

Dermacentor ticks

Vascular endothelial cells

218
Q

How does rickettsia rickettsia cause thrombocytopenia

A

VASCULITIS

219
Q

First and most consistent clinical sign of RMSF (rickettsia rickettsia)?

A

Fever

220
Q

What percent of patients with RMSF (rickettsia rickettsia) have neurologic signs?

A

80%

221
Q

Retinal hemorrhage is a clinical sign of which tick-borne disease?

A

RMSF (rickettsia rickettsia)

222
Q

How can RMSF cause death?

A

Hemorrhagic diathesis

Thrombosis of vital organs

DIC

Meningioencephalitits

Cardiovascular collapse

223
Q

Diagnosis of RMSF (rickettsia rickettsia)

A

Serology: > 4x increase in IgG titer, single titer < 1:1024

Direct FA of tissue (some false negatives)

PCR (whole blood or tissue)

224
Q

Treatment of RMSF (rickettsia rickettsia)

A

Doxycycline
Enrofloxacin
Chloramphenicol

225
Q

Zoonotic potential of RMSF?

A

No reported cases

226
Q

Which species of babesia may have direct transmission between dogs?

A

B. Gibsoni

227
Q

How does babesia cause a hemolytic anemia?

A

Direct RBC damage
Intravascular hemolysis
Extravascular hemolysis

228
Q

Which species of babesia is endemic in SE greyhound kennels?

A

Babesia canis vogeli

229
Q

Which species of babesia is known to cause a thrombocytopenia?

A

B. Canis

230
Q

How can you diagnose babesiosis on serology?

A

Increasing titers over 2-3 weeks

231
Q

What is the most sensitive and specific way to diagnose babesiosis?

A

PCR

232
Q

Teatment of babesiosis?

A

Imidocarb

or

Azithromycin + atovaquone

233
Q

Prevention of babesiosis includes:

A

Tick control

Blood donor screening

Don’t reuse needles

Sterile instruments

Control dog fighting

Treatment of symptomatic carriers

234
Q

How is bartonella transmitted?

A

Cat flea, possibly ticks

Transmission via infected cat blood (cat scratch, animal bite)

235
Q

What percent of healthy dogs are seropositive for bartonella?

A

10%

236
Q

Clinical signs of bartonella in the dog

A

Fever

Endocarditis (B. Visonii)

Pyogranulomatous lymphadenopathy

Peliosis hepatis (focal blood filled spaces in liver)

Cavitary effusions

237
Q

Clinical signs of bartonella in the cat?

A

Lethargy
Fever
Mild neurologic signs
Gingivitis/stomatitis

238
Q

Why is serology problematic in the diagnosis of bartonellosis?

A

5-12% of cats infected with B. Henselae seronegative

IgG persists for prolonged period following clearance

239
Q

How do you diagnose Bartonellosis?

A

Blood culture (Bartonella alpha-proteobacteria growth medium)

PCR

240
Q

Treatment of bartonella

A

Enrofloxacin + doxycycline

241
Q

What is cat scratch disease?

A

Zoonotic Bartonellosis, affects immunosuppressed people

242
Q

Clinical signs of hemotropic mycoplasma?

A 
Depression, inappetence, dehydration
Weight loss
Hemolytic anemia
Splenomegaly
Icterus
Febrile or hypothermic
243
Q

Lab abnormalities seen with hemotropic mycoplasma

A 
Autoagglutination
Regenerative anemia
Erythrophagocytosis
Elevated ALT
Hyoerbilirubinemia
244
Q

Main clinical sign of carrier phase of hemotropic mycoplasma

A

Relapsing anemia

245
Q

Diagnosis of hemotropic mycoplasma

A

PCR good for detecting acute phase, but not carrier

246
Q

Treatment of hemotropic mycoplasma

A

Doxycycline
Enrofloxacin
Pred (if IMHA)

Azithromycin is not effective

NO TREATMENT THAT COMPLETELY ELIMINATES ORGANISM

247
Q

How is canine hemotropic mycoplasma transmitted

A

Brown dog tick

248
Q

When do clinical signs of mycoplasma canis pop up?

A

If a dog has been splenectomized or immunsuppressed

249
Q

How is hepatozoon transmitted?

A

Tick ingestion

250
Q

Where does hepatozoon canis live in host?

A

Encysts in striated muscle

251
Q

Lab abnormalities with hepatozoon

A 
Severe leukocytosis 
Hypoglycemia
Hypoalbuminmia
Inc ALP
Inc BUN

CPK is usually normal

252
Q

Radiographic findings with hepatozoon

A

Periosteal proliferation along long bones

Similar to hypertrophic osteopathy

253
Q

Which muscles would you biopsy to diagnose hepatozoon

A

Biceps femoris or semitendinosis

254
Q

Treatment of hepatozoon

A

Triple therapy: TMS, Clindamycin, Pyrimethamine

Ponazuril
Decoquinate

No drugs eliminate all tissue stages of organism

Usually have shirt-lived remission 2-6 months before relapse

255
Q

Reservoir host for cytaux

A

Bobcat

256
Q

What are the main reasons cytaux causes clinical disease?

A

Blood flow obstruction and hemolytic anemia

257
Q

Prognosis of cytaux

A

BAD

Rapid course of illness and frequently death in less than 5-7 days

258
Q

How can you diagnose cytaux

A

Piroplasms on blood smear

PCR

259
Q

Treatment for cytaux

A

Azithromycin

Atovaquone

260
Q

How are FIV and FeLV spread?

A

FIV - fighting

FeLV - spread of bodily fluids

261
Q

Best test for FIV/FeLV testing?

A

IDEXX SNAP

Confirm with PCR [or IFA (FelV) or DIVA (FIV)]

262
Q

What type of dogs are candidates for being blood donors?

A 
Dogs:
> 50 lbs
PCV > 40%
Never been pregnant 
Never have had a previous blood transfusion
DEA 1.1 and 1.2 negative
Cats:
> 10 lbs
PCV > 35%
Never been pregnant
Never had previous blood transfusion
Indoor only
263
Q

What is the anticoagulant of choice when collecting blood for blood transfusion?

A

CPDA

264
Q

Advantage of plastic bag over glass bottle for collection of blood for blood transfusion

A

Bags have slightly les negative pressure so less likely to cause RBC damage

Bottles need to be vented so higher risk of bacterial contamination

265
Q

Volume of blood transfused should not exceed

A

22 ml/kg/day

266
Q

Calculations for blood volume to transfuse to achieve a given PCV

A

Donor blood (ml) = K x BW (kg) x [(Desired PCV - Recipient PCV)/PCV of donor blood]

2 ml of transfused whole blood per kg of BW rasies PCV by 1%

1 ml of transfused pRBC per kg of BW raises PCV by 1%

267
Q

What factors does frozen (stored) plasma lack and what is it mainly used for?

A

Lacks 5 and 8

Used in anticoagulant rodenticides, hemophilia B, colloid support

268
Q

What coagulation factors does cryoprecipitate have and what is it mainly used for?

A

VWF
Fibrinogen
Factor 8

Used in VWBD and Hemophilia A

269
Q

Why would you ever need to give albumin to a patient?

A

Life-threatening hypoalbuminemia

270
Q

Types of transfusion reactions

A

Hemolysis (immune-mediated and non immune-mediated)

Febrile, non-hemolytic reaction

Allergic reaction

Transfusion-related Acute Long Injury (TRALI)

Sepsis

271
Q

What is that cause of febrile, non hemolytic transfusion reaction?

A

Cytokines produced by WBCs during storage of the blood

272
Q

What is Transfusion Related Lung Injury?

A

Rare syndrome caused by WBC antibodies from donor plasma

Causes pulmonary edema, fever, hypotension, dyspnea, and hypoxia

273
Q

What causes non-immune-mediated hemoticis transfusion reactions?

A

Problems in storage or administration of blood

Temperature fluctuations, using pressure bags, pumps, or small needles

274
Q

What complications are associated with massive transfusion reactions?

A 
Citrate toxicity (hypoCa)
HyperK+
HypoK+
Hypothermia
Coagulopathies
275
Q

Primary indication for transfusing fresh frozen plasma?

A

Hypoprotienemia and coagulopathy

Will not maintain higher protein levels, still need to address underlying issue

276
Q

Main indications for transfusing cryo-poor plasma?

A

Vit K rodenticide

Hemophilia B

277
Q

The delay in resolution of icterus in patients which are clinically improving may be attributed to

A

Long half-life of delta bilirubin

SA Medicine (3 decks)

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