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Ross LAM I > Ross - Exam 1 > Flashcards

Ross - Exam 1 Flashcards

1
Q

How should oral medication be administered?

A

Syringe - add mixer/binder to powder and directly inject into side of mouth

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2
Q

How should oral medication NOT be administered?

A

Mixed in feed

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3
Q

What size needle is appropriate for IV injections? Why?

A

18G, 1.5”

Minimizes likelihood of inadvertent intra-carotid injection

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4
Q

Which syringe type is generally avoided?

A

Luer LOCK

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5
Q

Where should the jugular be accessed? Why

A

Mid to upper neck

Omohyoideus muscle separates jugular form carotid

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6
Q

What are the three main complications associated with jugular injection?

A 
Clostridium infection (contaminated needle)
Inadvertent intra-carotid injection
Laryngeal hemiplasia (perivascular injection)
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7
Q

What size needles are appropriate for intramuscular injections?

A

18/19/20 G 1.5” (no less than 21G)

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8
Q

What is the maximum amount that can be injected per IM site?

A

15-20cc

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9
Q

What are the three acceptable sites for IM injections?

What are the landmarks / considerations associated with each?

A

Neck
-ventral to ligamentum nuchae
-dorsal to lateral processes of cervical vertebrae
-cranial to leading edge of shoulder
Semi-tendinosus/membranosus
-one hand’s width below tuber ischia
-one hand’s width above start of gastroc tendon
-outside thigh
Pectorals
-do not place too high d/t risk of septic mediastinitis if abscess developed cranially

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10
Q

What is endotoxin?

A

The heat-stable LPS component of gram negative bacterial cell walls

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11
Q

How is endotoxin generated?

A

Primarily during death of gram negative bacterial, as well as during the rapid multiplication phase

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12
Q

What is responsible for most of the deleterious effects of endotoxin?

A

The Lipid A structure

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13
Q

Describe the role of LPS-binding protein (LBP) in endotoxemia.

A

Endotoxin gains circulation and binds LBPs, which are acute phase proteins produced by hepatocytes. LBPs act as shuttle proteins bringing LPS from aggregates to responding cells, including intravascular macrophages (IVMs)

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14
Q

Which pro-inflammatory mediators are produced in endotoxemia’s MyD88 pathway activation?

A

TNF alpha, IL-1, IL-6

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15
Q

Describe the features associated with the hyperdynamic state of endotoxemia.

A 
Overall vasoconstrictive stage
Pulses - strong
Temp - fever
MM - injected, bright red
CRT - normal
Periphery - warm
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16
Q

Describe the features associated with the hypodynamic state of endotoxemia.

A

Overall vasodilatory stage
Pulses - weak, thready
Temp - normo to hypothermic
MM - congested (blue to purple), toxic line
CRT - prolonged
Periphery - cold (centrally localizing blood volume)

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17
Q

What is the theoretical expected leukogram in endotoxemic patients? What does the actual leukogram look like?

A

Theoretically: decreased tWBC, decreased neutrophils, lymphocytes WNL
Practically: tWBC and neutrophils WNL, lymphopenia
The difference is due to the cumulative effects of stress + endotoxemia.

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18
Q

Which component of the CBC is most telling in endotoxemic cases? What are the differentials for that parameter?

A

Lymphopenia

DDx: stress (not actually endotox!) or viral disease

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19
Q

What 2 tests can directly measure circulating endotoxin?

A
  1. Limulous amoebocyte lysate assay (research)

2. Etox Dx (horse-side test)

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20
Q

What are the 4 goals of treatment in endotoxemia cases?

A
  1. Removal of the cause
  2. Circulatory support
  3. Neutralization of circulating endotoxin
  4. Inhibition of synthesis and effects of endotoxin-induced mediators
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21
Q

What is involved in ‘removing the cause’ of endotoxemia?

A

Antimicrobials (TMS, gentamicin, amikacin)

Surgical removal of compromised and/or necrotic bowel

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22
Q

What is involved in ‘circulatory support’ for endotoxemia?

A 
Goal: expansion of intravascular volume
Hypertonic saline (7.2%)
Hetastarch for protein loss
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23
Q

What is involved in ‘neutralization of circulating endotoxin’?

A
  1. Endoserum IV (currently out of favor)

2. Polymixin B IV (best choice)

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24
Q

What is involved in ‘inhibiting synthesis and effects of endotoxin-induced mediators?

A
  1. Flunixin meglumine - NSAID
  2. Pentoxyfylline (currently out of favor)
  3. DMSO - reduces edema
  4. Lidocaine - inhibits inflammatory mediators, improves GI motility
  5. Heparin - increases effect of ATIII (provided sufficient levels)
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25
Q

What complications are seen with endotoxemia? (4)

A
  1. Ileus and olic
  2. Laminitis
  3. Renal failure
  4. Thrombosis and DIC (associated with hypercoagulable state)
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26
Q

What are the 3 main pathologic components of DIC?

A
  1. Initiated by pathologic expression of intravascular tissue factor (TF)
  2. Induction of production of thrombin and consumption of coagulation inhibitors (AT III and protein C)
  3. Development of a hypercoagulable state
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27
Q

What 3 chemical parameters are indicative of DIC in the horse?
Which parameter is expected, but not seen in the horse?

A

Increased clotting times (PT)
Thrombocytopenia
Increased FDPs (3+)

*Hypofibrinogenemia expected, but not usually detected d/t methodology (‘normal’ low value is 0), and increased fibrinogen from inflammation associated with previous illness

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28
Q

How is DIC treated?

A

Heparin +/- ATIII as needed

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29
Q

What signalment is associated with laminitis?

A

> 1 year old

QH common - large frame, small feet

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30
Q

What primary conditions are associated with laminitis? (4)

A
  1. Sepsis
  2. Pars intermedia pituitary dysfunction
  3. Equine metabolic syndrome + insulin resistance
  4. Exogenous steroid administration
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31
Q

What are the two types of displacement seen in laminitis?

A

Rotational

Vertical (sinking)

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32
Q

What clinical findings are associated with laminitis?

A
  1. Palpation of digital pulses (symmetrical lateral/medial, with both front or all 4 feet affected)
  2. Elevated hoof temperature
  3. Swelling/edema of coronary band, depression may be palpated (indication of sinking)
  4. Pain at toe (detected by hoof testers)
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33
Q

How is laminitis staged?

A

No CS –> developmental
CS acute
CS >72 hours, no collapse –> subacute
CS + mechanical collapse –> chronic

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34
Q

How is laminitis managed?

A

Cryotherapy - ice baths up to 48 hours

Digital support - soft bedding, styrofoam insulation, rolled gauze over frog

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35
Q

What percentage of BW is normal blood volume?

A

8%

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36
Q

When would overhydration be utilized? (3)

A
  1. Liquefaction of respiratory secretions
  2. Intestinal impactions
  3. Renal dz
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37
Q

What parameters indicate MILD (5%) dehydration?

A

1-3 sec skin tent
mm moist to slightly tacky
CRT normal
HR normal (

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38
Q

What parameters indicate MODERATE (8%) dehydration?

A 
3-5 sec skin tent
mm tacky
CRT 2-3 sec
HR 40-60bpm
*decreased arterial BP
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39
Q

What parameters indicate SEVERE (10-12%) dehydration?

A 
>5 sec skin tent
mm dry
CRT >4 sec
HR >60bpm
*reduced jugular fill
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40
Q

What parameters indicate LIFE THREATENING (12-15%) dehydration?

A

HR >100bpm
Obvious sunken eyes and shock
*Death imminent at 15%

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41
Q

When is oral fluid administration contraindicated?

A

Reflux, gastric distension, ileus

42
Q

What is the maximum flow capacity of a STAT IV set?

A

28 L/hr

43
Q

What are the flow capacities of the following catheters?
14G
12G
10G

A

14G –> 13 L/hr
12G –> 25 L/hr
10G –> 35 L/hr

44
Q

What materials are used in long term / short term catheters?

How long can short term catheters be left in?

A

Long term: polyurethane (least thrombogenic) / silicone
Short term: teflon / polyethylene
-maximum 72 hours

45
Q

What fluid is given as an alkalinizing solution?

A

LRS

46
Q

What fluid is given as an acidifying solution?

A

Normal saline (0.9%)

47
Q

What fluid is akin to giving free water?

A

D5W (5% dextrose)

48
Q

What fluids are given in cases of hypoproteinemia?

A

Dextran 70, Hetastarch

49
Q

What fluid is given for immediate expansion of plasma volume?
How much is given?
What are the contraindications for its use?

A 
Hypertonic saline (7.2%, 2400mOsm)
4-8L only, expansion of 10x the volume infused
Contraindicated in:
1. uncontrolled hemorrhage
2. hyperNa
3. hypoK
50
Q

What solution might be given to prolong the effects of hypertonic saline?

A

6% dextran 70

51
Q

What are the general guidelines for fluid therapy?

A

D: % dehydration x BW (kg) = L of fluid (give in first hour)
O: L vomiting/diarrhea/reflux
M: 60 mL/KG/day or 30 mL/LB/day
(give 2x maintenance for overhydration)

52
Q

What is the maximum shock dose of fluids that can be given?

A

60-90 ml/kg/hr

53
Q

What is the maximum K+ IV administration?

What is the general guideline for supplementation?

A

No more than 0.5 mEq/kg/hr

Guideline 10-20 mEq/L for maintenance fluids

54
Q

What are the guidelines for treating Na+ disturbances?

A

Acute disturbance (

55
Q

What is the most common acid/base disturbance in the horse?

How is it treated?

A

Metaoblic acidosis

  1. Alkalinizing solution (LRS)
  2. Bicarb ONLY if HCO3
56
Q

How is PCO2 related to pH?

A

For every 10 mmHg increase (from 40) in PCO2

there is a corresponding 0.05 decrease (from 7.4) in pH

57
Q

What are the three pathways of muscular energy generation?

A
  1. Phosphocreatinine
    - initial seconds of exercise only
  2. Anaerobic glycolysis
    - rapid production of small amounts of ATP
    - occurs in cytoplasm
  3. Aerobic
    - occurs in mitochondria
    - utilizes CHO and FFA
58
Q

What is the pattern of muscle fiber recruitment?

A

I –> IIA –> IIAX –> IIX

59
Q

What is the best assessment of performance in the horse?

A

VO2max (measure of O2 consumption)

=HR x SV x (a-v)O2

60
Q

What heart sounds are heard in the horse and what do they correspond with?

A

S1 (lub) - closure of AV valves (mitral/tricuspid)
S2 (dub) - closure of semilunar valves (aortic/pulmonic)
S3 (ahh) - end of rapid filling phase
S4 (ba) - atrial contraction

61
Q

Where is the PMI for each cardiac valve?

A

Mitral (left AV) - left 5th ICS, midway elbow to shoulder
Aortic (L semilunar) - left 4th ICS, below shoulder
Pulmonic (R semilunar) - left 3rd ICS, cranioventral to aortic PMI
Tricuspid (right AV) - right 3-4 ICS, midway elbow to shoulder

62
Q

What is the most frequent manifestation of high vagal tone (physiologic) in the horse?

A

Second-degree AV block (Mobitz I)

-gradual increase in PR interval before beat is dropped

63
Q

What is the most common pathologic arrhythmia?

What predisposes horses to this arrhythmia?

A

Atrial Fibrillation

  1. large atrial mass
  2. underlying vagal tone - asynchrony in atrial repolarization
64
Q

What signalment and presentation is typical with atrial fibrillation?

A 
Race horse
Exercise intolerance (quitting at 3/4 post)
65
Q

What are the two forms of atrial fibrillation?

A
  1. Paroxysmal: occurs during race and disappears with deceleration of HR
  2. Sustained
66
Q

How is atrial fibrillation diagnosed?

A
  1. Auscultation of irregularly irregular rhythm
  2. Variable pulse strength
  3. ECG: f waves
  4. NORMAL echo
67
Q

How is atrial fibrillation treated?

A

*Ensure normal K status

HR 60: digoxin –> quinidine

72 hrs: oral (preferred)

68
Q

What etiologies are associated with ventricular tachycardia?

A

*Shocky animals
Myocarditis
Lytes/metabolic disturbances
Sepsis, endotox

69
Q

How is ventricular tachycardia diagnosed?

A

ECG: QRS wide and bizzarre with >4 VPCs

70
Q

How is ventricular tachycardia treated?

When is treatment indicated?

A

Indicated when arrhythmia seen at rest, or rate >120bpm

Lidocaine administered in small boluses

71
Q

Which is the most common congenital cardiac defect in the foal?

A

Ventricular septal defect

72
Q

What presentation is associated with mitral insufficiency?

A

Exercise intolerance
Weight loss
Respiratory distress

73
Q

What are the etiologies associated with mitral insufficiency?

A

Degenerative /inflammatory changes of the valve

Bacterial endocarditis

74
Q

How is mitral insufficiency diagnosed?

A

Auscultation of systolic murmur (left 5th ICS)

75
Q

What presentation and signalment is associated with aortic insufficiency?

A

Generally asymptomatic

Older horses

76
Q

How is aortic insufficiency diagnosed?

A

Auscultation of diastolic murmur (left 4th ICS)

77
Q

What factors are pronostic for aortic insufficiency?

A

Size of aortic root (>8cm)

Presence of concurrent left AV valve insufficiency

78
Q

What signalment is associated with vegetative endocarditis?

A
79
Q

Describe the pathophysiology of valvular endocarditis.

A

High blood flow
Structural endothelial damage
Subclinical infection (pulmonary abscess)
Bacteria adhere to endothelial surface
Local release of thromboplastin activates coagulation

80
Q

How is vegetative endocarditis diagnosed?

A
  1. CBC: hyperprotein, neutrophilia, anemia
  2. Blood culture
  3. ECG: arrhythmias secondary
  4. Echo: direct visualization of lesion
81
Q

How is vegetative endocarditis treated?

A

Abx (K-pen IV, gentamicin)
-4-6 weeks minimum

Antiinflammatories (flunixin meglumine)

Asparin to decrease PLT aggregation

82
Q

What follow-up procedures should be performed when treating vegetative endocarditis?

A

Serial ECG

Blood culture 60d after abx cessation (if patient was initially +)

83
Q

What etiologies are associated with CHF?

A

Myocarditis
Ionophore toxicity
Endocarditis
Pericarditis

84
Q

What clinical signs are associated with CHF?

A

Ventral edema
Poor pulses
Weakness/listlessness
Syncope

85
Q

How is CHF treated?

A

Digoxin (+ inotrope)
Furosemide (diuretic)
Enalapril (ACEi)

86
Q

What are the two classifications of pericarditis?

A

Effusive (idiopathic)

Constrictive (fibrinous)

87
Q

How is pericarditis diagnosed?

A

ECG

88
Q

How is pericarditis treated?

A

Effusive: pericardiocentesis / drainage
Constrictive: pericardiocentesis with lavage / pericardectomy

89
Q

How is RBC regeneration assessed in the horse?

A
  1. BM aspirate

2. RDW (>19)

90
Q

Which parameters are elevated in anemia of chronic disease (functional iron deficiency)?
What about true iron deficiency?

A

Functional
Serum ferritin + Marrow iron stores increased

True
TIBC increased

91
Q

How is iron deficiency anemia treated?

A 
True:
iron cacodylate (parenteral)

Functional:
Treat inciting cause / underlying chronic dz

92
Q

How is anemia associated with EPO treated?

A

Corticosteroids +/- transfusions

93
Q

What are the two types of equine piroplasmosis/babesiosis?

A

Babesia caballi

  • less severe
  • extravascular hemolysis

Theleria/Babesia equi

  • more severe
  • intravascular hemolysis
  • hemoglobinemia
  • hemoglobinuria
94
Q

How is babesiosis diagnosed?

A

Giemsa-stained blood smears

95
Q

How is babesiosis treated?

A

Imidocarb diproprionate

  • eliminates carrier state
  • do not use in donkeys
96
Q

What is the pathophysiology of equine infectious anemia?

A

Biting fly vectors
Lentivirus
Infects macrophages
Anemia is immune-mediated (no RBC infection)

97
Q

What is the presentation of EIA?

A

Episodic disease
-recurrent fever, depression, icterus, weight loss
Extravascular hemolysis
Thrombocytopenia

98
Q

How is EIA diagnosed?

A 
Coggins test (>45 days of infection)
ELISA (false positives)
99
Q

What are the isolation requirements for EIA?

A

Minimum 200 yards from closest horse

100
Q

What etiologies are associated with IMHA?

A

Idiopathic
Lymphosarcoma
Infectious: EIA, Clostridia, etc.
Drugs: penicillin, sulfas, phenylbutazones

101
Q

What is the effect of blood loss on clin path parameters?

A
  1. Bleeding in first 4-6 hours: decreased TP
  2. PCV decrease not appreciated until 12-24 hours (48 hours to bottom out)
  3. 3-4 days post-hemorrhage: increased PCV
102
Q

How is blood loss treated?

A

Volume replacement with crystalloids

10 L blood –> 40L crystalloids

Ross LAM I (4 decks)

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