Exam 1 Flashcards

1
Q

What are the 3 basic responsibilities of a Vet?

A
  1. Make Diagnoses
  2. Treat abnormalities using evidence based medicine (when possible)
  3. Keep up-to date on advances
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2
Q

What is the diagnostic reasoning process

A

Arrival at a diagnosis by obtaining complex, convoluted, and confusing information on a patients and comparing it to what is expected to be normal “art of veterinary science”

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3
Q

What is the Problem-oriented approach? and why do we use it? ** learning objective**

A

Idea that medicine should be practiced with a set of rules in order to cope with the complex information obtained about a patient. Ensures each animals problems are diagnosed and managed logically and thoroughly. Foundation rests on (1) Systematic collection of info and (2) assembly of a database that is the same for each patient

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4
Q

What does the problem-orientated approach database include? (9 main points/steps)

** Learning objective**

A
  1. Signalment
  2. Owners complaint
  3. History
  4. Physical Exam
  5. Working Problem List
  6. Differential Diagnosis (DD) list - use “DAMNIT” to jog your memories
  7. Plan to rule -in/-out each DD
  8. Treatment Plan and Prognosis
  9. Therapeutic plan and monitor its efficacy via SOAP
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5
Q

Signalment

A

age, breed and sex first thing you should know or tell another clinician about a patient

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6
Q

Owners Complaint

A

What you should always address. Ensure owners interpretation is correct.

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7
Q

6 General Rules of Taking a History

** Learning Objective**

A
  1. Avoid confusion. Use simple english and ask one question at a time
  2. Cross-check statements for accuracy
  3. DO NOT use leading questions
  4. Establish a chronological timeline
  5. OPEN_ENDED QUESTIONS!!!
  6. Summarize understanding to owner to avoid miscomm6unications
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8
Q

What is the most common cause of disputes b/w owners and vets?

a. miscommunication
b. money
c. diagnosis
d. sports

A

miscommunication

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9
Q

What is a: Working Problem List

A

Identification and prioritization of a patients problems. Some problems can be “lumped” together if thought to be due to a common cause. Make less urgent problems “inactive” , rather than discarding them Focus on distinguishing CS ( ex. dark feces, pale mucous membranes) and avoid general CS (ex. anorexia, lethargy)

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10
Q

What does DAMNIT stand for?

**Learning objective**

A

D- developmental, degenerative

A- anatomical, autoimmune, allergies

M- metabolic

N- neoplastic, nutritional

I- idopathic, iatrogenic, inflammatory, infectious

T- toxicities, trauma

Textbooks also outline DDx’s

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11
Q

What should you consider when you devise a diagnostic plan?

A

Choose diagnostic test that:

    • cause minimal pain/stress
  • -safe
  • -simple
  • -can rule-in/-out multiple DDx simultaneously
  • -can diagnose common diseases
  • -cheap
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12
Q

Master Problem List

A

Summary of the patients problems and medical history. Includes updated list of DDx, plans and important test results until definitive diagnoses is made

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13
Q

What should be discussed with the owner in your treatment plan?

A

– best treatment and prognosis for each disease – probability the animal will recover with and without treatment – how much each treatment will cost

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14
Q

What should you use to monitor the efficacy and side-effects of therapies/treatment plans?

** learning objective**

A

progress notes in problem-oriented record system

the progress notes are written using the SOAP format

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15
Q

What does SOAP stand for?

** learning objective**

A

S- subjective- what the owner tells you

O- Objective- what you observe

A- Assessment- what you think is going on and if the treatment is working

P- Plan- what you intend to do

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16
Q

Why do we keep medical records?

** learning objective**

A
  1. legal requirement and important evidence should any disputes arise with a client
  2. To identify recurring problems and their most appropriate therapy
  3. Continuity of care in multi-vet practice
  4. Accurate costing an d financial management
  5. Research
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17
Q

Summarize the steps involved in diagnosing and treating a disease

A

–Signalment –Owners complaint and history –PE –Make problem list –determine a DDx list for each problem –Devise plan to Rule- in/-out each DDx for each problem –Revise DDx list as new information is generated –Make final diagnosis of each problem –Treat each problem –Monitor therapy –Keep accurate and thorough records

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18
Q

What is the general outline of how a physical exam is preformed? ** learning objective**

A

See notes… pretty basic stuff

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19
Q

Describe intracellular and extracellular spaces?

A

Intracellular space contains 2/3 of total body water (about 40% of body weight)- Cells are dehydrated first

Extracellular space has 1/3 of total body water; contains fluid that is not in the cells. Divided into 3 compartments

– Interstitial: ¾ of extracellular fluid

Intravascular: mostly plasma; within blood vessels

Transcellular: specialized fluid/areas (CSF, bile, synovial fluid, GI fluid)

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20
Q

What are three main reasons to give fluids?

A

Maintenance: the required volume needed per day to keep the patient in balance, with no change in total body water.

Dehydration: Decreased fluid in intracellular or interstitial spaces (intravascular space too if shock ensues).

Shock: Decreased fluid in intravascular space

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21
Q

What routes can you give fluids?

A

IV and SQ

IV is most appropriate for dehydration and shock

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22
Q

What is the normal PCV for dogs? grey hounds?

A

Dogs: 35-60%

Greyhounds: 65-70%

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23
Q

What is the best choice fluid if you have a unknown diagnosis and/or no lab results?

A

Crystalloid replacement fluids

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24
Q

In an “ideal world” what should you base your fluid type on?

A

Results of RBC count & chemistry profile (electrolytes, glucose)

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25
Q

Difference between crystalloid & colloid fluids? Provide Examples of each.

** Learning Objective**

A

1. Crystalloids: Solutes (electrolytes & non-electrolytes) that can move freely around the fluid compartments. Divided into groups based on tonicity (ability to shift water across semipermeable membranes) =Hypotonic, hypertonic and isotonic.

2. Colloids: Larger molecular weight. Remain in intravascular space & keep fluid in intravascular space. Compare to crystalloids which end up in interstitial spaces.

Natural: plasma, whole blood

Synthetic: hetastarch, dextran, pentastarch, ‘oxyglobin’

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26
Q

What are the 3 categories of crystalloid fluids?

A
  • Hypotonic: Lower osmolality than intravascular fluid so draws fluid into cells.
    • Ex. 0.45 % NaCl, 5 % dextrose in water
  • Hypertonic: Higher osmolality than blood cells and plasma. Will draw fluids from interstitial & intracellular spaces into intravascular space.
    • Ex: 7.5 % NaCl solution, 5% dextrose in following: Normosol M, 0.45 % NaCl, 0.9% NaCl, LRS, Plasmalyte 56 .
  • Isotonic: Same osmolality as blood cells and plasma so fluids will neither exit or enter cells. Used for perfusion support & volume replacement.
    • Ex: 0.9 % NaCl, Ringer’s solution, LRS, Normosol R, Plasmalyte A, 0.45 % saline with 2.5 % dextrose
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27
Q

What is the most common synthetic colloid fluid?

A

Hetastarch

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28
Q

Which type of crystalloid fluid is most common?

A

Isotonic crystalloids

LRS

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29
Q

Why would you use crystalloid fluids?

A
  1. correct dehydration
  2. expand vascular space in shock
  3. correct electrolyte/acid-base imbalances
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30
Q

Give examples of synthetic colloids. Which is most commonly used one?

A

Synthetic Colloids: hetastarch, dextran, pentastarch, ‘oxyglobin’

Hetastarch is most commonly used!

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31
Q

What could happen if you give a large amount of crystalloid?

** Learning Objective**

A

Peripheral edema

Since crystalloids are freely permeable to enters cell membranes. 2/3 enters interstitial space.

Most common if too much, too rapidly and if the patient has low albumin or heart condition

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32
Q

Differences between replacement and maintenance fluids & when to use them.

* Learning Objective*

A
  • fluid replacement - Na concentration is close to normal plasma Na of about 140 mmol/l
    • Can give rapidly!
    • Designed to replace fluid loss
    • K is similar to that as plasma
    • Ex. Ringers, LRS, Normosol R, 0.9 % saline, PlasmaLyte
  • fluid maintenance - Na conc is close to normal total body conc of about 70 mmol/l
    • DONT give rapidly
    • Designed to replce daily Na losses without Na overload
    • Poor at explanding blood volume and thus often combined with colloids in patients with low albumin
    • Some lack K, so you should add it
    • Ex. Normosol M, 0.45 % NaCl with 2.5 % dextrose, PlasmaLyte 56
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33
Q

When and Why shoudl you switch to maitnance fluids when a patient is on replacement fluids?

A

Switch from replacement to maitenance after 24 hours

If used for longer periods, patient may become hypernatremic which can lead to swelling of the brain and then CNS signs.

If replacement fluids are used for maintenece , you should add K and should monitor serum Na.

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34
Q

Why would replacement fluid be used for maintenance? What problems could you encounter?

*Learning Objective*

A

To save money. You dont want to charge client for additional bags of fluids when they have not finished one. Also so the hospital does not have to stock as many types of fluids.

Problems: hypernatremic patient –> brain swelling –> CNS signs.

Should add K and monitor Na levels.

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35
Q

What are the two main groups of colloids? and why would you use them?

*learning objective*

A
  • (1) Natural: used when goal is to restore RBCs, clotting factors, AT III, or albumin
    • Plasma: if albumin, AT III, clotting factors needed
    • Whole blood: if RBCs needed – only if animal is ANEMIC
  • (2) Synthetic: used when goal is to rapidly improve perfusion in patient that does not have obvious blood loss or clotting problem. Often used in addition to regular fluid therapy.
    • Dextran -Polysaccharide
      • Adv: isotonic. Stored at room temp. Increases plasma vol 1.38 x the vol. infused.
      • Disadv: increase in BMBT, PTT but no clinical bleeding. Fibrinogen conc decreases. Blood glucose level may increase.
    • Hetastarch: most commonly used synthetic colloid in vet med
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36
Q

When would you use Hetastarch fluids?

A

Used in cases that need oncotic support but don’t need clotting factors

Increases plasma volume by 1.37% of volume infused

Most commonly used synthetic colloid- last longer than dextran in circulation.

Ex: Cases with low albumin (vasculitis, PLN, PLE, liver failure, sepsis, etc)

Contraditions: heart failure & cats get restless and/or salivate

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37
Q

What is acontraindication of using hetastarch fluids?

A

Heart failute

Some cats get restless and/or salivate

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38
Q

What are potential side effect of colloids?

A

Fluid overload and pulmonary edema

Coagulopathy

Renal failure

Human albumin: could cause life threatening allergic reaction in dogs

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39
Q

What should you first use to correct dehydration?

A

Isotonic Replacent fluids which can be given rapidly

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40
Q

Why is using replacement fluids for maitnance usually not a serious clinical problem? In what cases would it be a problem?

A

Because most patients with functioning kidneys will simply increase renal sodium loss to compensate when hypernatremic.

big problems occur when impaired kidney function and if Na >170 –> Salt toxicity–> swelling of brain –> CNS signs

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41
Q

Can I combine colloids and crystalloids in dehydration or shock cases?

* Learning objective*

A

YES! But remeber….

  • Colloids are not used to replace dehydration deficits because you need crystalloid to get into interstitial and intracellular spaces
  • Colloids are helpful to keep fluids in intravascular space so used in cases with low albumin or vasculitis or those with peripheral edema or ascites.
  • By combining both you decrease the amount of crystalloid you have to use and restore the fluid deficit of intravascular space more rapidly.
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42
Q

What would be your fluid therapy plan for a 6kg dog with 10% dehydration from diarrhea and a low serum ablbumin at 1.5 mg/dl?

A
  • Start replacement crystalloid to correct for dehydration
  • Piggy-back a colloid (plasma would be good choice, but could use hetastarch if you didn’t have plasma).
  • Once you calculate the mls of colloids you will be using, subtract that number from the calculated dehydration deficit. By using colloid, you decrease the amount of crystalloid you have to use.
  • If you gave only replacent fluids you run the risk of those fluids causing peripheral edema/ascities/pleural effusion because of the low oncotic pressure from low albumin
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43
Q

What would be your concerns when providing fluid therapy to a cardiac patient? Which fluid is best to use?

A
  • Beware of using high Na-containing fluids (replacement fluids) to patients with known or suspected cardiac disease.
    • The high sodium load can unmask pre-clinical congestive heart failure, as water follows sodium, and volume overload can result.
  • The ‘classic’ fluids for a cardiac patients are 0.45% NaCl (as opposed to 0.9%) and are made isotonic through the addition of dextrose.
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44
Q

What is the classic fluid to use in patients with cardiac issues?

A

0.45% NaCl that is made isotonic through the addition of dextrose.

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45
Q

Why should you add K to fluids?

How do you determine how much K should be added?

How rapidly can you give fluids with K added?

A

Due to obligate renal K loss, patient who are not eating will become hypokalemic within dats.

The amount added is based on the patients existing K levels and the “sliding scale of scott”

**NEVER give more than 0.5 mEq/kg/hr (Kmax)**

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46
Q

Sliding Scale of Scott

A

Chart/Table that helps detemine how much K to add to a liter of fluids based on the patient’s current K levels.

If have only 1/2 a bag of fluids, just add half as much that is indicated!

Never give more than the Kmax = 1/2 of the animals body weight= 0.5 mEq/kg/hr

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47
Q

K max

** VERY IMPORTANT for class and OSCE**

A

0.5 mEq/kg/hr

half of the body weight (kg)

Never give more due to life threatening hyperkalmia can result in death

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48
Q

When should you use Hypertonic saline?

A

(1) large dogs that are in shock due to gastric dilatation-volvulus;
(2) patients that should not receive large volumes of fluid , e.g. those with head trauma or cerebral edema

Hypertonic saline pulls fluid into vascular spaces from interstitial and intracellular spaces (short lived).

Used to replace volume deficit with less fluid in hypervolemic shock and improves blood flow. It is useful in patient that need to recieve a large amount of fluid quickly.

Hypertonic saline is normally diluted with a colloid solution to 7% (Ex. To achieve a 7.5% dilution, add 17 ml of 23% hypertonic saline solution to 43 ml of a colloid solution in a 60 ml syringe.)

Never give to a dehydrated animal!

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49
Q

What are indication and contraindication to use hypertonic saline? What are side effects?

A
  • Indications of hypertonic saline:
    • Cases of hypovolemic shock that do not have dehydration or hypernatremia
    • Head trauma cases
  • Contraindications of hypertonic saline:
    • Dehydration
    • Hypernatremia
  • Side effects
    • Rapid administration may cause bronchoconstriction, bradycardia & hypotension
  • Dose: Over a 20-minute period, dogs should receive 4 to 7 ml/kg; cats ½ this dose.
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50
Q

Tell me about enteral administration of fluids

A

Used in mild dehydration

ONLY IF the GI function is normal (no vomit), airway is controlled and if mental status is ok.

Common in large animals

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51
Q

When would you use intraosseuous administration of fluids?

A

In pediatric and/or severly dehydrated patients.

Usually femur (trochanteric fossa) or humerus (greater tubercle)

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52
Q

When do you use IV?

A

For dehydration and shock

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53
Q

When would you use sub-q route for fluid therapy? What are things to consider?

A

Most commonly in chronic renal failure or parvo puppy that cannot pay to stay in hospital.

DONT swab with alcohol or use fluid with glucose

Will want to warm isotonic fluids in warm water before giving.

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54
Q

What is a cut down?

A

cutting the skin over a vein so you can see it…

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55
Q

What perfusion parameters should you monitor during fluid therapy?

*** KNOW THESE!!****

A

Perfusion parameters: HR, CRT, MM, Pulse
pressure, temperature, blood pressure

** KNOW THESE***

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56
Q

How much does 500 ml weigh?

A

1 pound = 500 ml

Weight is a good indication if you are correctly/keping up with fluid loss.

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57
Q

What is dehydration?

What are causes? clinical signs?

A

Fluid loss from intracellular &/or interstitial spaces; occasionally the vascular space (in that order). Loss of total body water

Causes: inadequate water intake, excessive fluid losses from vomiting, diarrhea, polyuria without compensatory polydipsia, peripheral edema

Signs: – Decreased skin turgor – Tacky or dry mucous membranes – Sunken eyes

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58
Q

What are the clinical signs of

A

Subclinica- undetectable

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59
Q

What are the clinical signs of 5-7%/Mild dehydration?

A

Mild dehydration = 5-7% (7%)

Subtle loss of skin elasticity

tacky mucous membranes

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60
Q

What are the signs of Moderate (8-11%) dehydration?

A

Moderate dehydration = 10%

Prolonged skin tent

Tacky MM

Signs of volume depletion

Proloned CRT (CRT >2 sec)

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61
Q

What are clincal signs of severe (12-15%) dehydration?

A

Severe dehydration = 13%

Skin tent stands in place

Tacky MM

Sunken eyes

>2 sec CRT

depressed

Maybe signs of shock (tachycardia, poor pulse)

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62
Q

What is the difference between shock and dehydration?

A

Dehydration: fluid loss from intracellular & /or interstitial space; sometimes vascular space if severe dehydration

Hypovolemic shock: fluid loss from vascular space. Results in inadequate oxygen delivery to tissues.

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63
Q

How do you calculate the dehydration deficit in liters ?

A

Fluid deficit in liters = % dehydrated x body weight in kg

– Ex: 10 % dehydrated x 10 kg = l liter needed

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64
Q

How do you calculate the daily maintenance fluid?

A

Some differences in formulas. 40-60 mL/kg/day (dog high end; cat low end).

During fever, the maintenance rate increases an extra 15-20 mL/kg/day (total 55-80 ml/kg/day)

Has to be given over 24 hours, even if the patient wont be there the whole time

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65
Q

How do you calculate the ongoing fluid losses?

A

Estimate of losses that occur from diarrhea, vomiting, polyuria, or ‘third space’ sequestration.

Some use the same number as daily maintenance and then just double it.

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66
Q

What do you do if you have to give IV fluids over a shorter period of time? (less than 24 hours)

A

Give 50% of the dehydration deficit over 4-6 hours.

Then give the remaining 80%-100% of the remainder of the dehyration deficit fluid over the next 6 ish hours.

Maintian daily maitnance and ongoing fluid loss rates on a 24 hour basis.

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67
Q

What should you do if your patient is staying over night for fluid therapy, but you are leaving in 4 hours?

A

Give 50% of the dehydration deficit fluid amount over 4 hours. Re-asses, then give the remainder of the dehydration deficit fluid amount over the remaining 20 hours (if no changes upon re-assesment)

Keep maitnance and on-going loss amounts on 24 hours basis.

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68
Q

How much should fluid should a 10kg dog that is 10% dehydrated get?

A

1L or 1000 ml

(ideally over 24 hours)

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69
Q

Do you Understand the differences between fluid calculations for dehydration, maintenance, and on-going losses?

A

Dehydration deficit
Fluid deficit in liters = % dehydrated x body weight in kg

Can give over 6-24 hours. Re-asses as needed.

Daily maintenance:
40-60 mL/kg/day (dog high end; cat low end).
During fever, increase an extra 15-20 mL/kg/day.

Give over 24 hours

Ongoing fluid losses:
– Measure the losses (catheter, measure the vomit, weigh pee pad) –or– estimate by doubling maintenance.

Give over 24 hours. Re-asses as needed.

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70
Q

What is the shock dose for a dog and cat? How should you give it?

A

Shock fluid dose: 90 ml/kg/hr dog; 45-60 ml/kg/hr cat.

Give 1/4 of the dose within 15 minutes then reasses.

Can calculate 1/4 of dose simply by adding a zero to the animals weight in pounds to get the mls of fluid

(represent the total blood volume)

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71
Q

What fluids should you give in shock?

A

Replacement crystalloids

Sometimes hypertonic saline in GDV or head trauma HBC patient. (NOT when dehydrated or if cardiac issues)

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72
Q

CASE 3:Calculate amount of fluids needed to correct 13 % dehydration in a 5 kg cat.

– How rapidly would you administer those fluids?
– What type of fluids would you choose to give if the cat had a serum K of 3.0 mEq/L (normal 4.2-5.4 mEq/L)
– If you added K to your fluids, at what rate can you administer those fluids now?

A

See Answer Key

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73
Q

CASE 4: A 15 year old, 10 kg, dog with a history of heart failure was hit by car (HBC).
– If it is in shock, what parameters will you be looking for to confirm shock?
– What is the calculated shock dose for this dog?
– How rapidly would you administer the fluids?

A

See Answer Key

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74
Q

Case 5
• A 5 year old, 20 kg, dog has an albumin of 2.3 mg/dl because of a protein-losing enteropathy. It has been having diarrhea severe enough to result in 7 % dehydration.
– What type of fluid(s) would be best to use in this case?

A

See answer key

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75
Q

What are the 5 classifications of circulatory shock?

A

Hypovolemic (hemorrhagic, non-hemorrhagic, redistribution)

Cardiogenic

Vasodilatory or Distributive

Obstructive

Combination of above

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76
Q

Compare hemorrhagic, non-hemorrhagic and redistribution causes of hypovolemic shock

A

Hemorrhagic- blood loss (ususally >15% of blood volume)

Non-hemorrhagic - vomit, D, wounds, burns, polyuria

Redistribution- fluid shift to body cavitis, bowel, peripheral tissues.

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77
Q

Causes of Cardiogenic Shock

A

Due to:

(1) Acquired heart disease (myocardial trauma, myocarditis, pericardial tamponade, arrythmias)
(2) Congenital heart disease
(3) Anesthetic overdose

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78
Q

Causes of Obstructive Shock

A

Obstruction to flow: GDV, pericardial effusion, venous thrombosis, tension pneumothorax

USUALLY obstruction of venous return (as in GDV), but sometimes it is arterial obstruction (e.g. saddle thrombus)

Rx: relieve obstruction and use IV fluids

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79
Q

Cause of Vasodilatory or distrutive shock?

A
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80
Q

Sepsis and Septic Shock

A
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81
Q

What are the two phases of Sepsis, endotoxemia, septic shock?

A
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82
Q

What should you check before you give whole blood?

A

PCV

83
Q

What are the shock organs of dog, horses, cats ruminant?

A

Dog: GI and Liver

Horse: GI and Lungs

Cat & Ruminants, Pig: Lungs

84
Q

What happens in the compensated stage of shock?

A
85
Q

What happens during the decompensated stage?

A
86
Q

What are the clinical signs of hypovolemic and cardiogenic shock?

A
87
Q

What IV catheter size should you put in rapid fluid replacement (if no head or lung injury)?

A

THE BIGGEST AND SHORTEST ONE YOU CAN GET IN!!

18-20 g in CATS

14-18 in DOGS

use intraosseous if no acess (femur, humeral shaft, tibial crest)

88
Q

When would you use 0.9% NaCl crystalloid replacement fluids?

A

Patients with projectile vomiting or patients with a metabolic alkalosis

0.9% NaCl is more acidic than isotonic palanced pH fluids (ie normosol R, PlasmaLyte A, LRS)

89
Q

Do I give shock dose if dog has low albumin?

A

YES!

Piggy back colloids onto it.

90
Q

What should you do if your shock patient has trauma or lung injuries?

A

Hypertonic saline helps draw fluid into the intravascular space - resulting in a rapid, but transient, increase in circulating volume.

Concurrent colloid use allows hypertonic saline tostay in the vascular space for longer. Then follow with crystalloids at maintenance.

91
Q

How do you treat hemorrhagic hypovolemic shock?

A

Transfusion of whole blood and packed RBC.

Transfusion of oxyglobin

Dog universal donor (DEA 1.1 neg)

Recommend cross matching or typing in cats, if possible.

92
Q

Oxyglobin

A

Binds to pulmonary O2 and carries it to tissues

Able to pass through microcirculation

Indications: severe anemia, hypovolemic shock caused by blood loss or maldistribution of blood

Has vasoconstrictive effect (reduces needed volume)

(NOT in USA =/)

93
Q

Treatment of Septic Shock?

A
  • Fluid therapy as noted for hypovolemic shock
  • Broad-spectrum antibiotics based on suspected pathogen (do you remember the GI bugs?)
  • If peritonitis: surgical exploration/drainage
  • Cover for GI ulceration with what?
  • Heparin to improve efficacy to antithrombin III in neutralizing activated coagulation factors.
  • Oxygen via cage, nasal catherter, face mask, ventilator.
  • Vasopressor considered if:
    • Jugular vein distended
    • Crackles are heard on auscultation
    • CVP > 10 cm H20
  • All these parameters tells us that continued administration of IV fluids or blood/blood products is contraindicated (due to fluid overload)
  • Prognosis very guarded in these cases
  • Intestinve care needed
  • Vasodepressors: dopamine, dobutamine
94
Q

Treatment of Cardiogenic Shock

A
  • Oxygen
  • Minimal fluid therapy until caridiac function can be accurately determined
  • CHF = furosemide
  • Arrhythmias = manage appropriately
  • Vasodilators
  • Positive inotropes
95
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome = Imbalance of pro-inflammatory (excess) & anti-inflammatory mediators (not enough) on a systemic scale in response to an insult.

  • Pro-inflammatory cytokine: TNF, IL 1, IL 6
  • Anti-inflammatory cytokine: IL 4, IL 10, IL 13
  • Other molecules that up-regulate inflammation: leukotrienes, prostaglandins, thromboxanes, nitric acid, platelet activating factor, free radicals

Inflammation is a normal response to infectious and non-infectious insults, characterized by pain, heat, redness, swelling and loss of function.
Usually inflammation in contained. SIRS results when inflammation is NOT CONTAINED

96
Q

Non-infectious SIRS Etiology?

A

Non-infectious causes of SIRS

  • Hypotension
  • Trauma & hemorrhage
  • Hypoxia & ischemia
  • Pancreatitis
  • Burns
  • Neoplasia
97
Q

Infectious SIRS is also called…

A

Sepsis

98
Q

What is the second hit theory?

A
  • Initial event primes the immune system (Ex: HBC trauma)
  • Second event occurs (loss of blood leading to hemorrhagic shock)
  • Second event can result in excessive inflammatory response because immune system has been primed
99
Q

What is MODS?

A

Multiple Organ Dysfunction Syndrome (MODS)

  • Altered function of 1 or more organs in an acutely ill patients such that homeostasis cannot be maintained without intervention
  • Mortality 50 + %
  • Can be progression of SIRS or septic shock
  • Respiratory failure, hepatic failure, GI bleeding, renal failure, etc. leading to hypovolemic, vasodilatory or cardiogenic shock and death.
100
Q

Second hit theory occurs in what syndrome?

A

SIRS-Systemic Inflammatory Response Syndrome

101
Q

What are the three mechansisms of diarrhea?

A

Secretory
Malabsorptive/Maldigestive
Osmotic

They are clinically indistinguishable. In clinical practice, it is rare to have diarrhea as a result of only 1 mechanism.

102
Q

5 examples of Mucosal damage leads to an inability to absorb fluid and nutrients in diarrhea

A
  1. Villous atrophy
  2. Unabsorbed nutrients create osmoticcomponent to diarrhea
  3. Colonic fermentation ensues
  4. Production of D-Lactate(calves)
  5. Toxin stimulates increased H2O and electrolyte secretionby gut epithelium (crypt cells)
103
Q

What does samage to the villus tips cause?

A

Damage to the villus tips causes:

1) Proliferation of immature crypt cells
2) Relative increase in secretion

104
Q

What clinical signs do you see with osmotic diarrhea?

A

Voluminous, bulky stools with high osmolarity
Steatorrhea
With fasting, diarrhea usually abates

105
Q

What are the differences in net losses in Secretory/Maldigestive/Malabsoprtive -vs- Osmotic diarrhea

A

Secretory, Maldigestive/Malabsorptive Diarrhea = Net losses of:

  1. Water and sodium
  2. Potassium
  3. Bicarbonate (metabolic acidosis)

Osmotic Diarrhea = Net losses of:

  1. Water
  2. Potassium
  3. Bicarbonate
106
Q

True or False:

Dehydration = Low Body Water and/or High Plasma Osmolality

A

TRUE

107
Q

Osmolality

A

mOsm of solute/kg of solvent (mOsm/kg)
Determined by the number of particles in solution.

108
Q

Effective -vs- Ineffective osmoles

A
  • Ineffective osmoles–Diffuse across membranes
  • Effective osmoles–_DO NOT_diffuse across membranes
    • Effective osmoles create an osmotic gradient and pull water across the membrane.
    • Osmolality of ECF = 2(Na +K) + glucose/20 + BUN/3
    • Tonicity = Effective osmolality
109
Q

What are the 3 forms of hehydration?

A

1) Hypertonic Dehydration
2) Isotonic Dehydration
3) Hypotonic Dehydration

The name reflects the tonicity of the ECF after water is lost.

110
Q

Hypertonic Dehydration

Pathogenesis, Biochemical changes, 2 causes?

A

Pathogenesis
Increased solutes in the ECF –>creates osmotic gradient –> H2O moves from ICF to ECF to maintain volume

Biochemical changes
PCV and TP increase
Na+ and Cl-increase= hyperosmolality

Causes

  1. Osmotic diarrhea
    • Nonabsorbable solutes accumulate in the gut lumen –> H2O moves from plasma into the gut
    • Plasma becomes hypertonic
  2. Maldigestion/Malabsorption
    • Damage to intestinal epithelial barrier
    • Disrupts absorptive pathways
111
Q

What are the two causes of Hypertonic Dehydration?

A
  1. Osmotic diarrhea
    • Nonabsorbable solutes accumulate in the gut lumen –> H2O moves from plasma into the gut
    • Plasma becomes hypertonic
  2. Maldigestion/Malabsorption
    • Damage to intestinal epithelial barrier
    • Disrupts absorptive pathways
112
Q

Isotonic Dehydration

Pathogenesis? Biochem changes? Cause?

A

Pathogenesis= Water loss = electrolyte loss

  • Decrease in ECF volume
  • No change in osmolality, no osmotic pressure
  • No shift between the ICF and ECF

Biochemical changes

  • PCV and TP increase
  • Serum Na+and Cl-do not change

Causes

  • Some diarrheas
  • Some renal diseases
113
Q

Hypotonic Dehydration

pathogenesis? biochemical changes? 3 causes?

A

Most Common, especially in diarrhea

Pathogenesis : Electrolyte loss > Water loss

  • water shifts from vasculature to cells
  • volume depletion and cerebral edema

Biochemical Changes

  • PCV and TP increase
  • Na+ decreases = hypoosmolality

3 Causes

  • Secretory diarrhea (calf scours)
  • Vomiting
  • 3rd space loss (Displaced abomasum & GI atony)
114
Q
  • Volume* is regulated by adjusting __________
  • Osmolality* is regulated by adjusting ____________
A
  • Volume* is regulated by adjusting [Na]
  • Osmolality* is regulated by adjusting H20 balance
115
Q

Responses to Dehydration

A

Volumeis regulated by adjusting [Na+]= Influenced by changes in vascular pressure

  • Renin-Angiotensin-Aldosterone System (RAAS)
    • Aldosterone acts on the kidney to conserve Na and excrete K. Water will follow Na abck into the body.
  • ADH will also be released for hypovolemia
  • Osmolalityis regulated by adjusting H2O balance.* = Influenced by 1-2% change in osmolality
  • ADH release –> Thirst & ↑ H2O resorption from the kidney
116
Q

Sodium and Diarrhea

A

GI losses of Na, Cl, K, +/- HCO3 in secretory diarrhea

  • Loss of Na and H20–> hypotonic dehydration

BUT remeber, in Osmotic diarrhea

  • Nonabsorbable solutes accumulate in the gut lumen –> H2O moves from plasma into the gut
  • Plasma becomes hypertonic due to hypernatremia
117
Q

Why is GI fluid rich in Bicarbonate?

A

[HCO3-] in intestinal fluid > [HCO3-] in plasma because….

  1. Biliary and pancreatic secretions
  2. Secretion of HCO3-in exchange for Cl-in the ileum
118
Q

What does a loss in bicarbonate lead to? (2 things)

A
  1. Loss of buffering system –> acidosis –> H+/K+ shifts
  2. Loss of electroneutrality –> kidney retains Cl- –> ↑[Cl-]
119
Q

Potassium in Diarrhea

A

K is lost in diarrhea but this loss may be masked when there is a loss of bicarbonate and thus an acidosis. This is because the excess H will enter cells in exchange for K, thus masking the total body deficit

120
Q

Why would animals with diarrhea have hyperchloremia or normochloremia when Cl is lost in diarrhea?

A
  • Will be Hyperchloremic due to the kidneys retaining Cl to replace the last bicarbonate
  • BUT somtimes will be normochloremic if the necrease in colonic pH leads to an increase in Lactobacillus spp. growth in the GI. This is because Lactobacillus spp. produces large amounts of L & D Lactate that will act as anions and contribule to the electroneutrality (thus reducing the need to retain Cl)
121
Q

What happens in severe diarrhea? (5 things)

A

Metabolic acidosis (loss of HCO3-)

Hyperchloridemia ( to Maintains electroneutrality)

  • -or–
  • *Normochloridemia** (Increased lactate (unmeasured anion) = contributes to electroneutrality)
  • *Hyponatremia** (Secretory diarrhea)
  • -or–
  • *Hypernatremia** (Osmotic diarrhea)
122
Q

Calf Scours

A

ETEC E. coli causes a secretory diarrhea (due to enterotoxin) that may lead to sepsis

Diarrhea will be yellow and watery. Calf will be dull, weak, and have a loss of palpebral reflex

Affects calves/piglets 2-3 days old

Blood work: dehydration, hypoglycemia (due to sepsis = increase metabolisma and decrease production), low pH. hyper D/L lactatemia and maybe hyperkalemia.

Lose H2O, Na+, Cl-, K+, and HCO3-

Acidosis occurs due to (1) H production - hypovolemia and negative energy balance (2) H titration of depleted HCO3

123
Q

What tube should you use to measure lactate?

A

Grey top!

POC machines in office measure L-Lactate

ONLY Wisconsin Vet Lab measured D- Lactate

124
Q

D vs L Lactate

A

Lactobacillus spp. produce abundant L-and D-Lactate
L-lactate is cleared but D-lactate accumulates –> Metabolic acidosis

D- Lactate

  • D-lactate has direct neurotoxic effect
  • will cause the loss of palpebral reflex in ETEC calves
  • Mainly produced by microbial production
  • It is slowly metabolized by the mitochondria of mammals

L- Lactate

  • Produced by mammalian cells in cytosol when O2supply is low
  • Concentration rises with:
    • Exercise, Shock & Hypoxia/Anoxia
125
Q

Horses with ACUTE Diarrhea (

A

Combined increase in:

    1. High anion gap metabolic acidosis
    1. Metabolic alkalosis

Characterized by:

    1. Significant hyponatremia ↓↓Na+
    1. Hypochloridemia↓Cl-
    1. Hyperkalemia
  • Fluid Imbalances and shock
126
Q

Horses with intermediate Diarrhea

A

Severe acidemia
Hyperchloremic metabolic acidosis commonly found (43%)

127
Q
A
128
Q

Horses with Chronic Diarrhea ( >4 weeks)

A
  1. Greater compensatory ability
  2. Blood gas and electrolyte values usually WNL
  3. Persistent low normal K+ values
  • Likely reflect whole body K+ deficit
  • Need for K+ supplementation
129
Q

In small animals sever electrolyte and acid base disorders are ___________ ____________ if diarrhea is the sole problem

A

If diarrhea is the sole problem: Severe electrolyte and acid-base disorders are relatively uncommon in small animals

130
Q

In small animal diarrhea, Electrolyte imbalances and acid-base disorders become more likely with _______ & ___________

A

Severe and protracted diarrhea

&
Diarrhea that is accompanied by vomiting

131
Q
A
132
Q

_________________occurs primarily in enteric villi

_______________ occurs primarily within intestinal crypts.

A

Absorption occurs primarily in enteric villi

Secretion occurs primarily within intestinal crypts.

133
Q

If you have black undifested blood feces, where is the diarrhea coming from?

A

Small intestines

134
Q

If you have red blood and mucous in your diarrhea, where is your diarrhea coming from?

A

Large Intestines

135
Q

True or False:

In healthy animals, absorptive processes exceed the secretory processes

A

True

In diarrhea the secretory processes predominate
Different disease processes can convert some portion of the GI tract from an absorptive organ into a secretory organ.

136
Q

4 Pathophysiological Mechanisms of Diarrhea?

A
  1. Osmotic (Malabsorption/ Maldigestion)
  2. Secretory
  3. Increased permeability (exudative)
  4. Altered motility
137
Q

Osmotic Diarrhea

A

Develop when osmotically active molecules remain in the intestinal lumen (malabsorption). This promotes movement of water from the plasma to the intestinal lumen.

(1) As a result, the absorptive capability of the small and large intestine are overwhelmed.

Ex. GI overload

(2) also occur when there is interference with digestion and therefore the absorption of nutrients “what is not digested cannot be absorbed”

Ex. Exocrine pancreatic insufficiency in dogs and TGE in young pigs

138
Q

Steatorrhea

A

Feces that are pale and full of fat

Due to exocrine pancreatic insufficiency

139
Q

What type of diarrhea does the corona virus cause in pigs?

A

Osmotic diarrhea due to villous attenuation/atrophy in the small intestines

Aka TGE

140
Q

Secretory Diarrhea is a _________ process

A

Secretory diarrhea is a active process

It is usually caused by a infectious adjant that adheres to the mucosa and distripts the secretion of the enterocytes.

Certain bacterial toxins can also activate secretion of Na, Cl and other electrolytes

141
Q

Cause of Exudative diarrhea? Example?

A

Loss of normal epithelial lining/cytokines –> increased permeability –> passive loss of fluid

Ex. Rhodococcus equi

142
Q

In animals (non-human) diarrhea due to motility abnormalities is usually:

a. a primary disroder
b. secondary due to stimulation of peristalsis by increased intraluminal volumes

A

b. secondary due to stimulation of peristalsis by increased intraluminal volumes

143
Q

Examples of Primary vs. Secondary Disease

A

Primary: Rhodococcus equi enterocolitis in foals

Secondary: Excocrine pancreatic insufficiency, Renal disease (uremia induces vasculitis and mineralization of the mucosa)

144
Q

Acute vs. Chronic Diarrhea

A

Acute- usually self-limiting but in some it is due to systemic illness.

Ex. dietary indiscretion, dietary intolerance, parvo, panleukopenia, salmonella, pancreatitis

Chronic- diagnosis requires more extensive work-up, possibly a biopsy

Ex. IBD, neoplasia, chronic parasitism/fungal infection

145
Q

if you have a single older cow in a large herd presenting with weight loss, muscle atropy and intermittent diarrhea, what is your top diagnosis? What kind of diarrhea is it?

A

Johnes Disease!!!

Exudative diarrhea (increased permeability) *** & Osmotic diarrhea (secondary) due to the diffuse granulomatous enteritis and proliferation of macrophages that will result in mucosal damage and inflamamtion. Loss of the normal epithelial lining / tight junction causes an increase in permeability and passive loss of fluid. Protein losing enteropathy

Have diffuse granulomatous enteritis in the ileum/ ileocecal area as well as local lymph node involvement (enlarged ileocecal lymph node)

Cattle are infected when they are younger than 6 months, then only a few present with the chronic condition. If in herd, you should test and cull carriers.

In sheep/goats you will have a granulomatous lymohangitis with lymphangiectasia (prominant lymphatics vessels)

Other DDx would be neoplasm of the GI tract

146
Q

If you have an outbreak of profuse watery diarrhe in young dairy cattle. The calves are dehydrated and died in a few days, even with treatment. Several farm workers also got sick with GI issues. What is your top differential? What are some other DDx’s? What kind of diarrhea is present?

How will this disease present in snakes? bird?

A

Cryptosporidium! - due to the agem CS, and zoonosis

other DDx: E. coli, rotavirus, salmonellosis, corona virus

Osmotic /Malabsoption Diarrhea

(TGE is another good example of osmotic diarrhea in swine)

If preform histology of a very fresh intestinal mucosa you will see protozoa (2-3 um) on the apical surface of the enterocytes

  • In snakes*, this causes a chronic disease of hypertrophic gastritis with prominant rugal folds (enlarged abdomen), weight loss, and inappetence.
  • In birds,* cryptodporidium will be found in the lungs, bile ducts and GI tract.
147
Q

Turkey/Chicken- also with yellow diarrhea, inappetance, ruffled feather, eyes closed, dead down, blue/violet discoloration of head, combs and wattles. Animals died soon after first clinical signs.

Top DDx? What type of diarrhea is it? How do the birds contract it?

A

Black Head/ Histomoniasis

Increased permeability/Exudative diarrhea

Vectored by Heterakis (chicken ascarid)

More common in chickens, but the disease is less severe. You should not house chickens and turkeys together.

Lesion in the Liver and cecum. Yellow multifocal to coalescing eosinophilic, granulomatous, necrotising hepatitis. Cecum is enlarged, yellow, and contains a course, fibronecrotic material in the lumen of the cecum, typhlitis. Secondary infections will increase the lesion severity.

148
Q

One of the most important part of bone healing is___ _____

A

blood supply

149
Q

What are the 3 modes of blood supply to MATURE bones (in mature animals)

A
  1. Principle Nutrient Artery: supplies medullary supply of the bone.
  2. Metaphyseal Artery: Distal ends of the bone
  3. Periosteal Artery Proximal end of bone
150
Q

What is the blood supply to immature bones (with the resence of growth plates)?

A

Epiphyseal and Metaphyseal arteries

151
Q

In fractured bones, the chemical mediators secreted that develop an extraosseous blood supply are referred to as ____________

A

OSTEO-INDUCTIVE FACTORS

152
Q

______ healing is bone healing through the formation of an intermediate callus

A

Indirect

153
Q

______ healing of bone is primary via osteonal reconstruction

A

Direct

154
Q

Contact and Gap healing of bone are the two types of _____ healing

A

direct

155
Q

_________ bone healing occurs when there is an unstable mechanical environment and a gap >1 mm between fracture fragments

A

Indirect

156
Q

The _____ stage of indirect bone healing begins immediatly after the fracture forms, lasts 3-4 dayd and results in the development of a clot at the fracture site and the induction of extraosseous blood supply within hour.

A

Inflammatory

157
Q

Development of a ______ at the fracture site is very important due to the release of osteoinductive growth factors that stimulate angiogeneis and bone formation.

A

clot

158
Q

During the _______ stage of indirect bone healing, the clot changes into ________ tissue by the action of mononuclear cells and fibroblasts.

A

Repair , granulation

Results in the formation of a solf callus, which provides a slight increase in mechanical strength

159
Q

During the repair stage of indirect bone healing, Mesenchymal cells become osteoblasts which form a medullary and external callus (fibrocartilage). The
Resorption and mineralization of this fibrocartilage forms a ________

A

hard callus

160
Q

The formation of a hard callus during indirect bone healing creates a ____ union of the fracture

A

bony

161
Q

The repair stage on indirect bone healing last approx. ________

A

2 months

162
Q

What is the longest stage of indirect bone healing?

a. inflammatory stage
b. repair stage
c. remodeling stage

A

remodeling stage

it can last up to 6-9 year (in humans) and accounts for 70% of the healing time

163
Q

The concave are of the bone is the area of ___________

A

compression

it is weaker than the convex area

164
Q

The convex are of the bone is the side of ______

A

tension

It is stronger than the are of compression (concave).

165
Q

You typically put bone plates on the ______ side of the bone

A

tension/convex

166
Q

According to ______ Law:

Osteoclast work on the tension/convex side

Osteoblast work on the compression/concave side

A

Wolfe’s

167
Q

Balance of osteoclast resorption and osteoblast depostion to provide optimal function and strength to a bone fracture occurs in the _____ stage of indirect bone healing

A

remodeling

168
Q

Direct bone healing can take ______ for appropriate mechanical strength

A

6-12 months

169
Q

Contact Healing occurs when the defect between the fracture is _____ mm and the interfragmentary strain is ___%

A
170
Q

Contact Healing result in lammellar bone oriented in the _______ axial direction

A

normal

171
Q

_______ is Initiated by cutting cones of osteoclasts directly followed by osteoblasts

A

Contact Healing

Cones travel at 50-100 micrometers/day

172
Q

In Direct Gap Healing of bones, the fracture gap is ____ mm

A
173
Q

Bony union and remodeling occur _______ in contact healing, and _____ in gap healing

A

Simultaneously in contact

Seprately in gap

174
Q

Initially in gap healing, Osteoblasts deposit laminar bone in fracture gap _________to long axis

A

perpendicular

175
Q

Which of the following is false about healing of Cancellous Bone:

  1. More stable than cortical bone(fractures)
  2. heals by callus formation
  3. Woven bone deposited on trabeculae
  4. Bridging of fracture site occurs before union of cortical shell
A
  1. heals by callus formation = FALSE

Cancellous bone does NOT heal by callus formation

176
Q

Physeal Fracture of Zone of Hypertrophy will heal by ________

A

continued growth of physeal cartilage

177
Q

Physeal fracture of Zone of Proliferation will heal by _______

A

endochondral ossification

178
Q

Physeal fracture of which zone (hypertrophy/proliferation) will resule in premature ossification and closure of the growth plate?

A

proliferation

Zone of hypertrophy is where condocytes differentiate, thus fracture WONT alter normal growth

179
Q

Location of fracture, Stability , Method of fixation, Biological environment, Blood supply and Biomechanical vs. biological osteosynthesis are all ….?

A

factors that affect fracture healing

180
Q

The biomechanical approach to fracture healing will result in what 3 things?

A
  1. Anatomical reduction
  2. Rigid fixation
  3. Will compromise soft tissue to achieve
181
Q

Why is the biological osteosynthesis approach to fracture healing better?

A
  1. Restore overall length
  2. Restore overall alignment
  3. Limit surgical approach
  4. Limit soft tissue disruption

“look but do not touch” - it emphasizes the role of soft tissue integrity and th use of bone grafts

182
Q

Plates may result in ___ healing of bones

A

direct

183
Q

ESF, IM pins w/ wires, casts, splints, and no fixation are more likely to result in _______ healing

A

indirect

184
Q

Intramedullar pins and interlocking nails distrupt _______ & _______ blood supply

A

endosteal & medullary

185
Q

Which bone implant causes no significant distruption of blood supply?

A

Cerclage wires and external fixators

External captations will also Not distrupt blood suuply

186
Q

__ ____ distrupt periosteal blood supply

A

bone plates

187
Q

The use of a cast or splints to help stabilize a limb or fracture (instead of surgery) is termed what?

**NEED TO KNOW***

A

External coaptation

It distrupts no blood supply, but it not very stable and thus some fractures cannot heal this way

188
Q

What enhances healing but will not compensate for unstable mechanical environment in bone healing?

A

bone grafts

189
Q

Comminuted fractures, fractures with bone loss, delayed/nonunion fractures and arthrodeses are all indications to use ___ ___

A

bone grafts

190
Q

What are the three origins of bone grafts?

A

Autograft

Allograft

Xenograft

191
Q

What are the three types of bone grafts?

A

Cancellous
Cortical
Cortical-cancellous

192
Q

_________ is the laying down of new bone by osteoblasts

A

Osteogenesis

cancellous autogenous and cortical-cancellous bone grafts promote osteogenesis

193
Q

________ is the recruitment of host mesenchymal cells to form new bone or osteogenesis

A

Osteoinduction

Cancellous and cancellous-cortical bone graphs promote osteoinduction

194
Q

_____ is the providing of a scaffold for the growth of new bone

A

osteoconduction

cortical* and cancellous bone graphs are osteoconductive

195
Q

What is the most commonly used/gold standard bone graft?

A

Autogenous Cancellous

196
Q

Autogenous cancellous bone grafts:

  1. promote osteogenesis
  2. are osteoinductive
  3. are osteoconductive
  4. are readily available
  5. avoid immune reactions
  6. all of the above
A

All of the above

it is the only bone graft that is osteogenic

197
Q

What are 5 problems of Autogenous Cancellous Bone Grafts?

A
  1. Mechanically weak
  2. Increased surgical time
  3. Limited storage time
  4. Pain at donor site
  5. Intraoperative blood loss
198
Q

What are both good/bad things about cancellous bone grft allographs?

A
  1. Available as frozen chips or powder
  2. Decreased surgical time
  3. Readily available
  4. No donor site problems
  5. Can mix with autograft to increase volume
  6. Expensive
  7. Lack osteogenic properties (only osteoinductive and osteoconductive)
199
Q

What are the 4 phases of Cancellous bone graft effect?

A
  • *Phase I – inflammation**(within hours)
  • *Phase II – revascularization and osteoinduction**(2 weeks)
  • *Phase III – osteoconduction**(3-4 weeks)
  • *Phase IV – mechanical support**(up to 12 weeks)
200
Q

Cortical bone graphs have _______ properties

A

osteoconductive

(they have no osteogenic activity and very little osteoinductive activity)

201
Q

Where hare autopharph cortical bone grafts taken from?

A

ribs, ulna, fibula, & ilial wing

202
Q

What are the phases of cortical bone graft effect?

A

Osteoclasts move into graft and resorb bone
Osteoblasts follow and lay down new bone

Mechanical strength of graft maintained.

AKA “Creeping substitution”

203
Q

What are 4 properties of a cortical-cancellous bone graft?

A

Provides immediate mechanical support
Promotes osteogenesis
Osteoinductive
Osteoconductive