Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Ross LAM I > Ross - Exam 1 > Flashcards

Ross - Exam 1 Flashcards

(102 cards)

Start Studying
1
Q

How should oral medication be administered?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How should oral medication NOT be administered?

A

Mixed in feed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What size needle is appropriate for IV injections? Why?

A

18G, 1.5”

Minimizes likelihood of inadvertent intra-carotid injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which syringe type is generally avoided?

A

Luer LOCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where should the jugular be accessed? Why

A

Mid to upper neck

Omohyoideus muscle separates jugular form carotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What size needles are appropriate for intramuscular injections?

A

18/19/20 G 1.5” (no less than 21G)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

15-20cc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is endotoxin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is endotoxin generated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

The Lipid A structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

TNF alpha, IL-1, IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What 2 tests can directly measure circulating endotoxin?

A
  1. Limulous amoebocyte lysate assay (research)

2. Etox Dx (horse-side test)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Antimicrobials (TMS, gentamicin, amikacin)

Surgical removal of compromised and/or necrotic bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is involved in ‘circulatory support’ for endotoxemia?

A 
Goal: expansion of intravascular volume
Hypertonic saline (7.2%)
Hetastarch for protein loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is involved in ‘neutralization of circulating endotoxin’?

A
  1. Endoserum IV (currently out of favor)

2. Polymixin B IV (best choice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What complications are seen with endotoxemia? (4)
1. Ileus and olic 2. Laminitis 3. Renal failure 4. Thrombosis and DIC (associated with hypercoagulable state)
26
What are the 3 main pathologic components of DIC?
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
27
What 3 chemical parameters are indicative of DIC in the horse? Which parameter is expected, but not seen in the horse?
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
28
How is DIC treated?
Heparin +/- ATIII as needed
29
What signalment is associated with laminitis?
>1 year old | QH common - large frame, small feet
30
What primary conditions are associated with laminitis? (4)
1. Sepsis 2. Pars intermedia pituitary dysfunction 3. Equine metabolic syndrome + insulin resistance 4. Exogenous steroid administration
31
What are the two types of displacement seen in laminitis?
Rotational | Vertical (sinking)
32
What clinical findings are associated with laminitis?
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)
33
How is laminitis staged?
No CS --> developmental CS acute CS >72 hours, no collapse --> subacute CS + mechanical collapse --> chronic
34
How is laminitis managed?
Cryotherapy - ice baths up to 48 hours | Digital support - soft bedding, styrofoam insulation, rolled gauze over frog
35
What percentage of BW is normal blood volume?
8%
36
When would overhydration be utilized? (3)
1. Liquefaction of respiratory secretions 2. Intestinal impactions 3. Renal dz
37
What parameters indicate MILD (5%) dehydration?
1-3 sec skin tent mm moist to slightly tacky CRT normal HR normal (
38
What parameters indicate MODERATE (8%) dehydration?
``` 3-5 sec skin tent mm tacky CRT 2-3 sec HR 40-60bpm *decreased arterial BP ```
39
What parameters indicate SEVERE (10-12%) dehydration?
``` >5 sec skin tent mm dry CRT >4 sec HR >60bpm *reduced jugular fill ```
40
What parameters indicate LIFE THREATENING (12-15%) dehydration?
HR >100bpm Obvious sunken eyes and shock *Death imminent at 15%
41
When is oral fluid administration contraindicated?
Reflux, gastric distension, ileus
42
What is the maximum flow capacity of a STAT IV set?
28 L/hr
43
What are the flow capacities of the following catheters? 14G 12G 10G
14G --> 13 L/hr 12G --> 25 L/hr 10G --> 35 L/hr
44
What materials are used in long term / short term catheters? | How long can short term catheters be left in?
Long term: polyurethane (least thrombogenic) / silicone Short term: teflon / polyethylene -maximum 72 hours
45
What fluid is given as an alkalinizing solution?
LRS
46
What fluid is given as an acidifying solution?
Normal saline (0.9%)
47
What fluid is akin to giving free water?
D5W (5% dextrose)
48
What fluids are given in cases of hypoproteinemia?
Dextran 70, Hetastarch
49
What fluid is given for immediate expansion of plasma volume? How much is given? What are the contraindications for its use?
``` Hypertonic saline (7.2%, 2400mOsm) 4-8L only, expansion of 10x the volume infused Contraindicated in: 1. uncontrolled hemorrhage 2. hyperNa 3. hypoK ```
50
What solution might be given to prolong the effects of hypertonic saline?
6% dextran 70
51
What are the general guidelines for fluid therapy?
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
What is the maximum shock dose of fluids that can be given?
60-90 ml/kg/hr
53
What is the maximum K+ IV administration? | What is the general guideline for supplementation?
No more than 0.5 mEq/kg/hr | Guideline 10-20 mEq/L for maintenance fluids
54
What are the guidelines for treating Na+ disturbances?
Acute disturbance (
55
What is the most common acid/base disturbance in the horse? | How is it treated?
Metaoblic acidosis 1. Alkalinizing solution (LRS) 2. Bicarb ONLY if HCO3
56
How is PCO2 related to pH?
For every 10 mmHg increase (from 40) in PCO2 | there is a corresponding 0.05 decrease (from 7.4) in pH
57
What are the three pathways of muscular energy generation?
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
What is the pattern of muscle fiber recruitment?
I --> IIA --> IIAX --> IIX
59
What is the best assessment of performance in the horse?
VO2max (measure of O2 consumption) | =HR x SV x (a-v)O2
60
What heart sounds are heard in the horse and what do they correspond with?
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
Where is the PMI for each cardiac valve?
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
What is the most frequent manifestation of high vagal tone (physiologic) in the horse?
Second-degree AV block (Mobitz I) | -gradual increase in PR interval before beat is dropped
63
What is the most common pathologic arrhythmia? | What predisposes horses to this arrhythmia?
Atrial Fibrillation 1. large atrial mass 2. underlying vagal tone - asynchrony in atrial repolarization
64
What signalment and presentation is typical with atrial fibrillation?
``` Race horse Exercise intolerance (quitting at 3/4 post) ```
65
What are the two forms of atrial fibrillation?
1. Paroxysmal: occurs during race and disappears with deceleration of HR 2. Sustained
66
How is atrial fibrillation diagnosed?
1. Auscultation of irregularly irregular rhythm 2. Variable pulse strength 3. ECG: f waves 4. NORMAL echo
67
How is atrial fibrillation treated?
*Ensure normal K status HR 60: digoxin --> quinidine 72 hrs: oral (preferred)
68
What etiologies are associated with ventricular tachycardia?
*Shocky animals Myocarditis Lytes/metabolic disturbances Sepsis, endotox
69
How is ventricular tachycardia diagnosed?
ECG: QRS wide and bizzarre with >4 VPCs
70
How is ventricular tachycardia treated? | When is treatment indicated?
Indicated when arrhythmia seen at rest, or rate >120bpm Lidocaine administered in small boluses
71
Which is the most common congenital cardiac defect in the foal?
Ventricular septal defect
72
What presentation is associated with mitral insufficiency?
Exercise intolerance Weight loss Respiratory distress
73
What are the etiologies associated with mitral insufficiency?
Degenerative /inflammatory changes of the valve | Bacterial endocarditis
74
How is mitral insufficiency diagnosed?
Auscultation of systolic murmur (left 5th ICS)
75
What presentation and signalment is associated with aortic insufficiency?
Generally asymptomatic | Older horses
76
How is aortic insufficiency diagnosed?
Auscultation of diastolic murmur (left 4th ICS)
77
What factors are pronostic for aortic insufficiency?
Size of aortic root (>8cm) | Presence of concurrent left AV valve insufficiency
78
What signalment is associated with vegetative endocarditis?
79
Describe the pathophysiology of valvular endocarditis.
High blood flow Structural endothelial damage Subclinical infection (pulmonary abscess) Bacteria adhere to endothelial surface Local release of thromboplastin activates coagulation
80
How is vegetative endocarditis diagnosed?
1. CBC: hyperprotein, neutrophilia, anemia 2. Blood culture 3. ECG: arrhythmias secondary 4. Echo: direct visualization of lesion
81
How is vegetative endocarditis treated?
Abx (K-pen IV, gentamicin) -4-6 weeks minimum Antiinflammatories (flunixin meglumine) Asparin to decrease PLT aggregation
82
What follow-up procedures should be performed when treating vegetative endocarditis?
Serial ECG Blood culture 60d after abx cessation (if patient was initially +)
83
What etiologies are associated with CHF?
Myocarditis Ionophore toxicity Endocarditis Pericarditis
84
What clinical signs are associated with CHF?
Ventral edema Poor pulses Weakness/listlessness Syncope
85
How is CHF treated?
Digoxin (+ inotrope) Furosemide (diuretic) Enalapril (ACEi)
86
What are the two classifications of pericarditis?
Effusive (idiopathic) | Constrictive (fibrinous)
87
How is pericarditis diagnosed?
ECG
88
How is pericarditis treated?
Effusive: pericardiocentesis / drainage Constrictive: pericardiocentesis with lavage / pericardectomy
89
How is RBC regeneration assessed in the horse?
1. BM aspirate | 2. RDW (>19)
90
Which parameters are elevated in anemia of chronic disease (functional iron deficiency)? What about true iron deficiency?
Functional Serum ferritin + Marrow iron stores increased True TIBC increased
91
How is iron deficiency anemia treated?
``` True: iron cacodylate (parenteral) ``` Functional: Treat inciting cause / underlying chronic dz
92
How is anemia associated with EPO treated?
Corticosteroids +/- transfusions
93
What are the two types of equine piroplasmosis/babesiosis?
Babesia caballi - less severe - extravascular hemolysis Theleria/Babesia equi - more severe - intravascular hemolysis - hemoglobinemia - hemoglobinuria
94
How is babesiosis diagnosed?
Giemsa-stained blood smears
95
How is babesiosis treated?
Imidocarb diproprionate - eliminates carrier state - do not use in donkeys
96
What is the pathophysiology of equine infectious anemia?
Biting fly vectors Lentivirus Infects macrophages Anemia is immune-mediated (no RBC infection)
97
What is the presentation of EIA?
Episodic disease -recurrent fever, depression, icterus, weight loss Extravascular hemolysis Thrombocytopenia
98
How is EIA diagnosed?
``` Coggins test (>45 days of infection) ELISA (false positives) ```
99
What are the isolation requirements for EIA?
Minimum 200 yards from closest horse
100
What etiologies are associated with IMHA?
Idiopathic Lymphosarcoma Infectious: EIA, Clostridia, etc. Drugs: penicillin, sulfas, phenylbutazones
101
What is the effect of blood loss on clin path parameters?
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
How is blood loss treated?
Volume replacement with crystalloids | 10 L blood --> 40L crystalloids

Ross LAM I (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions