Physiology Flashcards

1
Q

Substances responsible for the vasoconstriction as part of acute inflammatory response

A

“Vasoconstriction is stimulated by vasoactive agents such as catecholamines, serotonin, bradykinin, and prostaglandins that are released from surrounding tissues and by norepinephrine released by the sympathetic nervous system.15”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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2
Q

Substances associated with vasodilation as a result of acute inflammation include

A

“Vasodilation is induced by vascular smooth muscle changes mediated by nitric oxide, histamine, leukotrienes, prostaglandins, and complement factors.”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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3
Q

Name the four phases of acute vascular response to inflammation and briefly outline their mechanism and importance

A

Vasodilation - follows a brief period of vasoconstruction. Mediated by nitric oxide, histamine, leukotrienes and complement factors. Allows increased blood flow and delivery of soluble mediators and inflammatory cells.

Permeability - increase in the number of intercellular endothelial gabs mediated by serotonin and histamine. Allows the formation of transcytoplasmic channels for transcytosis of plasma products onto the site of inflammation.

Stasis - Secondary to fluid loss to hemoconcentration. Allows greater contact time in between erythrocytes /leukocytes and the endothelial membrane

Leukocyte extravasation - promoted by the interaction of endothelial adhesion glycoproteins called “selectins” and their corresponding ligands on leukocytes. Adhered Leukocytes migrate to the outside of vessels (particularly peripheral venules) through the process known as diapedesis.

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4
Q

Discuss the mechanism and anatomy of a left-to-right and a right-to-left (reverse shunt) in a patient with PDA

A

The ductus arteriosus is a fetal vessel communicating the descending aorta and the main pulmonary artery, allowing shunting of fetal oxygenated placental blood from the pulmonary artery to the systemic circulation and bypassing the non-functioning fetal lung. This structure quickly contacts due to increase oxygen tension and is meant to undergo fibrosis and necrosis within a few weeks after birth. If the ductus remains patent, blood continues to partially bypass the lungs in a left to right pattern (Aorta to pulmonic artery, due to higher pressure gradient) leading to a murmur, increased pulmonary blood flow and gradual left ventricular eccentric hypertrophy that may evolve into ventricular failure and pulmonary edema. Common clinical features include a bounding pulse and loud murmur. Reverse shunting (pulmonic artery to aorta, or right to left) occurs when there is an increase in the pulmonary vasculature. These dogs have diminished pulmonary flow, small left ventricle and marked hypertrophy of the right ventricle (due to increased pulmonary vascular resistance). Clinical features are very different from those of the most common left to right shunt, and include a soft or no murmur, differential cyanosis (cyanosis of caudal mucous membranes with pink cranial membranes) and secondary polycythemia/hyperviscosity due to renal hypoxemia.

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4
Q

Discuss the mechanism and anatomy of a left-to-right and a right-to-left (reverse shunt) in a patient with PDA

A

The ductus arteriosus is a fetal vessel communicating the descending aorta and the main pulmonary artery, allowing shunting of fetal oxygenated placental blood from the pulmonary artery to the systemic circulation and bypassing the non-functioning fetal lung. This structure quickly contacts due to increase oxygen tension and is meant to undergo fibrosis and necrosis within a few weeks after birth. If the ductus remains patent, blood continues to partially bypass the lungs in a left to right pattern (Aorta to pulmonic artery, due to higher pressure gradient) leading to a murmur, increased pulmonary blood flow and gradual left ventricular eccentric hypertrophy that may evolve into ventricular failure and pulmonary edema. Common clinical features include a bounding pulse and loud murmur. Reverse shunting (pulmonic artery to aorta, or right to left) occurs when there is an increase in the pulmonary vasculature. These dogs have diminished pulmonary flow, small left ventricle and marked hypertrophy of the right ventricle (due to increased pulmonary vascular resistance). Clinical features are very different from those of the most common left to right shunt, and include a soft or no murmur, differential cyanosis (cyanosis of caudal mucous membranes with pink cranial membranes) and secondary polycythemia/hyperviscosity due to renal hypoxemia.

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5
Q

Phases and sub phases of healing

A

Phase 1 - Inflammation
Sub-phase a) Hemostasis
b)cell migration
c) debridement

Phase 2 - Proliferation
Sub-phase a) fibroblast proliferation
b) capillary proliferation
c) epithelial proliferation

Phase 3 - Remodeling

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6
Q

The phase and sub phases of healing when granulation tissue is formed

A

Second phase (proliferation), sub-phases fibroblast and capillary proliferation.

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7
Q

How long it takes for epithelial cells to migrate across and completely cover a properly closed surgical wound?

A

48 hours

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8
Q

The percentage point by which soft tissue wounds remain weaker than the original tissue. Two exceptions to this rule.

A

Most wounds remain 15 to 20% weaker than the original tissue. The urinary bladder and the bone regain 100% strength

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9
Q

Expected electromyographic change seen with demyelinizing disease

A

“The duration, or the time between the initial baseline deflection of the M-wave and the time it takes to return to a flat baseline, can be prolonged. These changes are indicative of a demyelinating process.”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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10
Q

Conditions possibly responsible for a decrease in the amplitude of M-wave during electromyogram

A

“A decrease in M-wave amplitude is a nonspecific finding, in that it may be seen in neuropathies or myopathies (those involving the muscle used to record the M-wave). In addition, loss of as few as two consecutive internodes of myelin results in the conduction block of a neuron, so diminished amplitude may also be seen with demyelination. This phenomenon (conduction block) can be seen in other situations as well: (1) when metabolic insults occur in a nerve with preservation of axons (neurapraxia) or (2) before completion of Wallerian degeneration in a recently injured axon (axonotmesis).”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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11
Q

What are the two primary components of the innate immune system?

A

Phagocytes and natural killer cells

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12
Q

What are the primary components of the acquired immune system?

A

B & T lymphocytes

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13
Q

Cell line responsible for carrying out immune surveillance throughout the body

A

Lymphocytes

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14
Q

Eight classes of central nervous system pathology

A

1) Contusive
2)Compressive
3) inflammatory
4) vascular
5) metabolic
6) toxic
7) degenerative
8)neoplastic

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15
Q

List six possible causes of thrombocytopenia caused by decreased production of platelets.

A

“Drug-induced disorders
Immune-mediated megakaryocytic hypoplasia
Viral (feline leukemia virus [FeLV], feline immunodeficiency virus [FIV])
Chronic rickettsial disease (ehrlichiosis)
Estrogen-secreting neoplasm
Myelodysplasia
Megakaryocytic leukemia
Cyclic thrombocytopenia (Anaplasma platys)
Radiation
Idiopathic bone marrow aplasia
Postvaccination”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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16
Q

List five possible causes of thrombocytopenia caused by increased destruction of platelets

A

“Immune-mediated thrombocytopenia
Primary
Idiopathic
Evans syndrome (immune-mediated thrombocytopenia and immune-mediated hemolytic anemia)
Systemic lupus erythematosus (SLE)

“Secondary
Drugs
Live virus vaccination
Tick-borne disease
Neoplasia
Bacterial infection
Nonimmune disorders
Drug-induced
Ehrlichiosis
Rocky Mountain spotted fever
Dirofilariasis”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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17
Q

List six possible causes of thrombocytopenia caused by increased consumption or sequestration of platelets

A

“Disseminated intravascular coagulation
Microangiopathies
Splenic torsion, hypersplenism
Sepsis
Hepatic disease
Severe acute hemorrhage
Severe hypothermia
Hemolytic uremic syndrome”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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18
Q

List six possible causes of acquired thrombopathia.

A

Drugs (NSAIDS, Abx, heparin)
Uremia
Anemia
Hepatic disease
Hypothermia
Colloid hemodilution
Myeloproliferative disorders and paraproteinemias
Ehrlichiosis
Snake venom
Disseminated intravascular coagulation”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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19
Q

List 2 of the most common inherited Thrombopathias of dogs and cats

A

“von Willebrand disease (many dog breeds, rare in cats)
Signal transduction disorders (Basset Hound, Spitz)
Glanzmann’s thrombasthenia (Otterhound, Great Pyrenees)
Chédiak-Higashi syndrome (gray Persian cats)
Selective adenosine diphosphate (ADP) deficiency (Cocker Spaniel)
Cyclic hematopoiesis (gray Collie)
Procoagulant expression disorders (German Shepherd Dog)
Macrothrombocytopenia (Cavalier King Charles Spaniel)”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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20
Q

List five possible causes of acquired secondary coagulopathy (secondary hemostasis)

A

“Vitamin K deficiency
Hepatopathy
Disseminated intravascular coagulation
Pharmacologic anticoagulants
Hemodilution (dilutional coagulopathy)
Severe hypothermia
Acidemia
Shock
Massive trauma”

Excerpt From
Veterinary Surgery: Small Animal Expert Consult
Spencer A. Johnston VMD, DACVS & Karen M. Tobias DVM, MS, DACVS
https://books.apple.com/us/book/veterinary-surgery-small-animal-expert-consult/id1250368401
This material may be protected by copyright.

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21
Q

Name the end products of primary and secondary haemostasis and briefly describe how they are formed. (8 marks)

A

Primary hemostasis – end product: platelet clot; Endothelial disruption exposes subendothelial collagen to which platelets adhere via platelet glycoprotein VI receptor and to collagen-bound Von Willebrand’s factor via glycoprotein Ib receptor. Adherence stimulates the release of platelet cytosolic granular contents (ADP) which stimulate arachidonic acid metabolism and production of prostanoids like Thromboxin A2, recruiting and activate further platelets.

Secondary Hemostasis – end product: fibrin mesh; Simultaneously with platelet aggregation, blood cells are exposed to Tissue Factor (TF) immediately after tissue injury. TF is a cofactor to Factor VII, which then activated factors IX and X leading to the activation of prothrombin to generate thrombin. Thrombin is the central protein in the coagulation cascade, cleaving fibrinogen into fibrin and activating further platelets.

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22
Q

Describe the clinical signs expected in animals with significant defects in primary and secondary haemostasis. (8 marks)

A

Primary Hemostasis: Petechia, mucosal damage, prolonged bleeding at injury sites.
Secondary Hemostasis: hematomas, hemarthrosis, intramuscular hemorrhage, effusions.

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23
Q

State the beneficial properties of transfusions of fresh frozen plasma, fresh whole blood and packed red blood cells and give an example of a surgical clinical situation in which each of these products could be used

A

Fresh Frozen Plasma (FFP): contains all constituents of plasma, including coagulation proteins, vWF, natural anticoagulants, albumin and globulins. Indicated for inherited or acquired coagulation disorder, vWD and hypoproteinemia. Example: Doberman Pincher with vWD, presented with GDV.

Fresh Whole Blood: Same as FFP but including RBC’s. Low platelet concentration, requiring large volume to affect platelet levels. Example: Hemoabdomen (replaces volume, RBC’s and “some” platelets and clotting factors. Supplementation with FFP or Cryoprecipitate likely necessary depending on the level of platelet/clotting factor consumption).

Packed Red Blood Cells (pRBC’s): Does not contain clotting factors, vWF, natural anticoagulants, albumin or globulins. Exposes recipient to large amounts of RBC antigens. Example: Anemic but normovolemic patient who requires a surgical procedure (avoids fluid-overload); anemic patient with cardiac disease who needs surgery (volume -sensitive).

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24
Q

Describe how the integrity and strength of the sutured anastomosis changes over the timeline from incision to wound maturity. (7 marks)

A

Immediately following surgical incision, the strength of the wound is reliant upon the holding power of the sutures upon the collagen-rich layer (submucosa), as well as on a relatively fragile fibrin seal. Significant collagen breakdown occurs in the first 4 days due to upregulation of MMP’s, leading to relevant decrease in the strength of anastomosis (up to 70% for small intestines and colon). This is when dehiscence is most likely to occur. Risk factors include hypotension, poor O2 saturation, infection, excessive tissue trauma and tissue tension. Around 1 week post-surgery the intestines will have regained nearly 100% of the original bursting strength, but the strength of the scar will continue to increase for several months.

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25
Q

What is the basic formula to calculate basal energy requirement (BER) in patients greater than 2 kg?

A

“BER = (30 × (BW in kg) + 70.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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26
Q

What are the four primary types of plasma proteins produced by the liver?

A

“albumin, α- and β-globulins, prothrombin and fibrinogen.

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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27
Q

What are the normal H2O systemic venous pressure and normal portal pressure for dogs?

A

“The normal portal pressure in dogs is 8 to 13 cm H2O, which is 7 to 8 cm H2O higher than the systemic venous pressure ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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28
Q

What are the Four major metabolic abnormalities frequently observed in the biochemistry profile of a patient with mineralocorticoid deficiency?

A

“If mineralocorticoid secretion is suppressed, hyponatremia, hyperkalemia, acidosis, and/or azotemia may occur.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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29
Q

What precautions should be taken prior to anesthetizing patients with hypoadrenocorticism for minor versus major surgical procedures?

A

“A protective steroid release normally occurs during surgery that prevents circulatory collapse; however, animals with hypoadrenocorticism may be unable to respond appropriately and often require glucocorticoid supplementation before and during surgery. When minor elective surgery is performed in animals with adrenocortical insufficiency, glucocorticoid therapy may be given intravenously before induction of anesthesia (Box 22.1). The same dose can be given intravenously or intramuscularly after recovery from anesthesia, and the animal is returned to its oral maintenance glucocorticoid therapy the day after surgery. A similar protocol is used for major surgery, except that glucocorticoid therapy is continued at approximately five times the maintenance dose for 2 to 3 days (Box 22.2). Normal maintenance doses are then reinstituted. Once the animal is eating, medications can be given orally (Box 22.3).”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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30
Q

Patients affected by Addison’s disease should receive corticosteroids prior to surgical procedures. What is the recommended corticosteroid form and what concerns can be associated with the use of dexamethasone?

A

“1. Prior to surgery give double the maintenance dose of oral glucocorticoids.
2. If oral supplementation is not reliable or feasible, then give:
• Prednisolone sodium succinate 1 mg/kg IV or
• Hydrocortisone sodium succinate 2 mg/kg IV
3. As soon as the patient can reliably take oral medications, repeat oral prednisolone.

“Dexamathasone is more ulcerogenic than other steroids and should be used with caution.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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31
Q

“Patients with HAC are catabolic and often protein depleted; this may adversely affect wound healing. Discuss the typical musculoskeletal changes associated with his condition and their metabolic impact.

A

“They may have connective tissue abnormalities and muscle wasting, resulting in a pot-bellied appearance, redistribution of fat, and thin, fragile skin. Pyodermas are common in affected dogs, which may cause postoperative suture line healing to be compromised. Affected dogs may pant because of their catabolic state, but intraabdominal fat deposition plus abdominal muscular weakness sometimes causes ventilatory abnormalities. Hypernatremia, hypokalemia, and alkalosis may be present; substantial abnormalities should be corrected before surgery. Concurrent abnormalities (e.g., congestive heart failure, diabetes mellitus [DM]) increase the patient’s anesthetic risk. Cardiovascular abnormalities may occur secondary to hypervolemia and hypertension; a thorough preoperative cardiac examination including blood pressure measurement is appropriate.
Animals with HAC are at increased risk for postoperative pulmonary thromboembolism (PTE). If hypercoagulability is suspected, preventive measures may be indicated before surgery. For prevention of PTE, animals may be started on heparin during surgery and continued on it postoperatively (see Box 29.1) or they may be administered clopidogrel (2–3 mg/kg per day in dogs); however, prospective studies are needed to determine the relative benefit of these therapies. Many animals with HAC have clinically silent urinary tract infection; therefore urine culture is indicated in all patients, regardless of urinalysis findings.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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32
Q

What is the Whipples triad and what does it indicate?

A

“• Clinical signs associated with hypoglycemia (usually neurologic abnormalities)
• Fasting blood glucose concentrations of ≤40 mg/dL
• Relief of neurologic signs with feeding or glucose administration”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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33
Q

What is the mechanism by which glucocorticoids help prevent hypoglycemia in patients with insulinoma?

A

“Glucocorticoid therapy (Box 22.12) may help prevent hypoglycemia caused by islet cell tumors by increasing hepatic glucose production and decreasing cellular glucose uptake”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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34
Q

List three drugs which may adversely affect the results of thyroid function tests in dogs?

A

“glucocorticoids, phenobarbital, and carprofen”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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35
Q

How can hypothyroidism affect a patient’s anesthetic in surgical status?

A

“Hypothyroidism may be manifested as lethargy, exercise intolerance, weight gain, constipation, nonpruritic symmetric alopecia, peripheral neuropathies (e.g., laryngeal paralysis, vestibular deficits), reproductive problems, cardiovascular changes (i.e., bradycardia and weak apex beat), and/or coagulopathies. Hypothyroidism may also result in diminished activity of factor VIII or of factor VIII–related antigen, which may predispose animals with von Willebrand disease (vWD) to spontaneous bleeding or serious hemorrhage during surgery. The mean von Willebrand factor/antigen (vWF) concentration in hypothyroid dogs has been found to be significantly reduced compared with that in euthyroid dogs. It appears that reduced concentrations of plasma vWF can be found in dogs in association with congenital vWD or with vWD acquired through hypothyroidism. Animals with untreated severe hypothyroidism and bleeding tendencies undergoing emergency procedures should be given oral L-triiodothyronine (Box 22.16) three or four times a day, or a single IV dose of L-thyroxine. Elective procedures should be postponed until replacement therapy has been maintained for a minimum of 2 weeks. If excessive bleeding is noted despite thyroid supplementation, whole blood, plasma, or cryoprecipitate should be given (see Box 4.1 and Table 4.5).”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

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36
Q

What are the three hormones produced by the thyroid gland?

A

“Thyroid secretions (T4, T3, and calcitonin)”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

37
Q

What are the main effects of thyroid hormone in adults versus juvenile patients? What is the overall effect/function of calcitonin?

A

“In adults, it causes an increase in the overall metabolic rate; in juveniles, it stimulates growth. Calcitonin (formed by parafollicular C cells) lowers blood calcium by stimulating calcium uptake.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

38
Q

What are the physiologic and pathologic consequences of hyperthyroidism? Roughly what percentage of cats will develop thyrotoxic heart disease versus congestive heart failure?

A

“Excessive circulating T4 causes multisystemic organ dysfunction. Thyrotoxicosis increases the metabolic rate and sensitivity to catecholamines and causes significant cardiovascular and metabolic abnormalities. Up to 80% of affected cats may have thyrotoxic heart disease; approximately 20% of these may have congestive heart failure. Hypertension is sometimes identified but does not appear to be as common as cardiac disease. Multifactorial mechanisms may cause neuromuscular and CNS dysfunction in some hyperthyroid cats. Neurologic signs associated with feline hyperthyroidism are listed in Box 22.17. T4 and T3 bind to receptor sites in the sarcoplasm that increase skeletal muscle heat production and mitochondrial oxygen consumption. The hyperthyroid state may reduce muscle contraction by uncoupling oxidative phosphorylation. Thyroid hormones may lower the threshold for cerebral tissue activation, may alter the activity of some brain enzymes, and may interact with catecholamines to alter the mental state of some affected animals. Abnormalities of the CNS may include hyperexcitability, irritability, aggression, seizures, confusion, and stupor.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

39
Q

List 6 neurologic abnormalities associated with hypokalemic hyper thyroid cats

A

“• Generalized weakness
• Neck ventroflexion
• Fatigue
• Muscle tremors
• Ataxia
• Incoordination
• Inability to jump
• Muscle atrophy
• Breathlessness (due to weakness of intercostal muscles)
• Collapse”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

40
Q

What is the typical radiographic/echocardiographic abnormality observed in the heart of cats with hyperthyroidism?

A

Hypertrophic cardiomyopathy leading to cardiomegaly

41
Q

What is the optimal test to diagnose hyperthyroidism and locate functional ectopic thyroid tissue?

A

“Thyroid scintigraphy is the optimal diagnostic test because it can both definitively identify hyperthyroidism and locate functional ectopic thyroid tissue.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

42
Q

What is the percentage of cats with hyper functional intrathoracic thyroid tissue besides the more obvious enlarged thyroid gland?

A

20%

43
Q

How can chronic kidney disease affect the diagnosis of hyperthyroidism?

A

“Hyperthyroidism increases glomerular filtration rate (GFR), which may lessen azotemia and thereby mask clinical signs of chronic kidney disease (CKD). This is important because successful therapy of hyperthyroidism may result in clinical manifestation of CKD. At the same time, CKD may lower serum TT4 concentrations (i.e., euthyroid sick syndrome) into the reference range, making diagnosis more difficult. The combined measurement of fT4 and TT4 may be necessary when trying to determine if cats with moderate to severe CKD have hyperthyroidism.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

44
Q

You are considering thyroidectomy for the therapy of a hyperthyroid cat, but wondering whether or not this patient’s renal function is normal. What can you do prior to surgery to verify if the procedure is safe for this patient?

A

“If in doubt as to the safety of thyroidectomy or 131I therapy, one may first administer a course of methimazole and monitor serum creatinine and blood urea nitrogen concentrations to see how the patient will tolerate euthyroidism. For cats that develop overt renal failure after establishment of euthyroidism, withdrawal of methimazole should result in improved renal function. Hypokalemia and concurrent muscle weakness may occur in cats with hyperthyroidism.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

45
Q

Possible (but rare) adverse effects of methimazole (3)

A

“hepatopathy, thrombocytopenia, and agranulocytosis occur with long-term therapy.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

46
Q

What blood test can be utilized to diagnose hyperparathyroidism?

A

“Measurement of PTH in animals with normal renal function is a sensitive test. High-normal or increased serum concentrations of PTH in hypercalcemic animals with normal renal function are strongly suggestive of hyperparathyroidism. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

47
Q

List six potential lymphatic system abnormalities which may cause lymphedema

A

(1) overload of the lymphatic system
(2) inadequate collection by the lymphatic terminal buds
(3) abnormal lymphatic contractility
(4) insufficient lymphatic
(5) lymph node obstruction
(6) central vessel (i.e., thoracic duct) defects.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

48
Q

Explain the pathophysiology of edema due to impaired venous or lymphatic drainage. What domestic species is most commonly affected?

A

“Regardless of the cause, edema results when capillary filtration exceeds the combined resorptive capabilities of the venous and lymphatic systems. This edema is relatively protein rich (2–5 g/dL). Because of the resultant high osmotic pressure, additional fluid is pulled into the interstitial space, worsening the edema. If the lymphatic system cannot adequately drain this interstitial fluid, collagen deposition and fibrosis may result. Hence, although the early stages are reversible, chronic edema is associated with thickening and fibrosis of tissue, making treatment difficult. The domestic species most commonly reported to have lymphedema is the dog.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

49
Q

Explain the difference between primary and secondary lymphedema

A

Primary lymphedema - caused by an abnormality or disease of lymphatic vessels or lymph nodes. Possibly due to congenital or hereditary diseases.

Secondary lymphedema - Occurs as a result of lymphatic obstruction of nodes or vessels by neoplasia, infection ( filariasis), Lymphoproliferative disorder‘s or surgical trauma.

50
Q

Can the age of onset be used to distinguish between primary and secondary lymphedema in dogs?

A

“Age of onset of clinical signs does not help distinguish between primary and secondary lymphedema because middle-aged animals may have acute signs of lymphedema that occur secondary to congenital lymphatic abnormalities. Although primary lymphedema is usually noted at birth or shortly thereafter, older animals may develop lymphedema associated with congenital abnormalities. In these animals, the lymphatic system functions normally until a precipitating cause (e.g., infection, trauma, or surgery) overwhelms the marginal lymphatic system. Congenital, hereditary lymphedema has been reported in bulldogs and poodles. A gender predisposition is not evident.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

51
Q

What is the typical clinical presentation for lymphedema?

A

“Lymphedema typically manifests as a spontaneous, painless swelling of the extremities with pitting edema. The onset may be insidious. The rear limbs are more commonly affected, and the swelling may be unilateral. Lymphedema usually begins in the distal extremity and progresses proximally. In severely affected animals, all four limbs and the trunk may be edematous. Although the patient may be less active than normal because of the weight of the limb or may carry the limb when ambulating, lameness and pain are uncommon without massive enlargement or cellulitis.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

52
Q

What are the primary differential diagnosis for a dog presented with lymphedema?

A

“The key differential diagnosis is abnormality of the venous system, such as venous stasis or arteriovenous fistula. The physical examination should eliminate systemic causes of bilateral edema, including heart failure, renal failure, cirrhosis, and hypoproteinemia. Other differential diagnoses include trauma, neoplasia, and foreign bodies.”

“Arteriovenous fistulae are vascular abnormalities in which a direct communication exists between an adjacent artery and vein. They may be congenital or acquired (e.g., after trauma, neoplasia, infection, or iatrogenic ligation of an artery and vein together). Clinical signs with arteriovenous fistulae vary depending on the location; however, palpation of strong pulsatile vessels, often of a fremitus or thrill, and auscultation of a machinery murmur (i.e., bruit) are classic findings. Angiography is necessary to confirm the diagnosis and determine the size, extent, and location of the fistula. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

53
Q

What is the currently utilized diagnostic modality to evaluate cases of lymphedema?

A

“Lymphoscintigraphy involves intradermal injection of high-molecular-weight, radiolabeled colloids. A gamma camera is used to obtain images of the affected limb over time to observe the progression of radioactivity through the lymphatics. Primary lymphedema typically shows slow absorption of the radiopharmaceutical, reduced visualization of lymphatic vessels and lymph nodes, and no interstitial activity. Secondary lymphedema typically shows poorly visualized primary lymph vessels and dilated secondary lymph vessels. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

54
Q

Benzopyrones are used to supplement the therapy for lymphedema. What is the mechanism of action of this drug class?

A

“Benzopyrones (Box 23.1) are a group of drugs that have been used to successfully treat experimental lymphedema in dogs and spontaneous lymphedema in human beings. All the drugs in this group appear to reduce high-protein edema. Their main action appears to be stimulation of macrophages, which promotes proteolysis. Protein fragments can then be reabsorbed into the blood. These drugs are active orally and topically, are inexpensive, and are relatively free of side effects. Included in this category of drugs are coumarin (5,6 benzo-[a]-pyrone), O-(β-hydroxy-ethyl)-rutosides, diosmin, and rutin.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

55
Q

What are the most important goals during the therapy of DIC?

A

Replacement of clotting factors and
ATIII

56
Q

Define renal failure

A

“Renal failure is when the kidneys are not able to maintain excretory, regulatory, and/or endocrine function, with subsequent retention of waste products and abnormalities in fluid, electrolyte, and/or acid-base homeostasis. This generally happens when 75% or more of the nephrons become nonfunctional. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

57
Q

Define azotemia and uremia

A

“Azotemia is defined as an increased concentration of nitrogenous waste products in the blood. Uremia is the clinical syndrome associated with sufficient loss of functional nephrons.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

58
Q

Define chronic kidney disease Vs Chronic renal failure

A

“Chronic kidney disease (CKD), the most common renal disease of dogs and cats, refers to patients with a permanent loss of functioning nephrons that have had renal damage, with or without a decreased glomerular filtration rate (GFR) for at least 3 months, or that have had a 50% reduction of GFR for at least 3 months. ”

“Chronic renal failure (CRF) is a progressive disease that occurs in patients with CKD with significant clinical signs (polyuria, polydipsia, weight loss, decreased appetite) and laboratory findings (azotemia, anemia, proteinuria).”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

59
Q

What kind of EKG abnormality can you expect to see in a patient with severe hypokalemia?

A

“Very severe hypokalemia may cause ECG changes (e.g., flattened T waves, U waves) and skeletal muscle weakness.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

60
Q

What should the normal urine output be for a normotensive patient under anesthesia?

A

“urine output should be monitored during surgery, with a urine output goal of at least 0.5 mL/kg per hour. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

61
Q

Hyperkalemia, such as caused by urethral obstruction or uroperitoneum, frequently leads to cardiac arrhythmias. What EKG abnormalities are typically observed at different levels of hyperkalemia?

A

“Hyperkalemia can cause “tented” or spiked T waves, absent or flattened P waves, prolongation of the P-R interval, widened QRS complexes, and/or bradycardia, in addition to predisposing to cardiac arrhythmias. Potassium concentrations greater than 7 mEq/L may cause irregular idioventricular rhythm, and potassium concentrations exceeding 9 mEq/L commonly cause atrial standstill.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

62
Q

Describe the acute treatment of hyperkalemia, such as caused by urethra obstruction, in cats. 

A

“1. Dilute by giving physiologic 0.9% saline solution IV or, once the obstruction is relieved, LRS IV.
2. If necessary to lower potassium immediately, give sodium bicarbonate (see Box 4.1) or regular insulin 0.2–0.4 U/kg IV plus dextrose (2 g/U of insulin).
3. If hyperkalemia is immediately life threatening, may give 10% calcium gluconate (0.2–1.5 mL/kg) for transient cardiac protection. Give slowly (over 5–10 min) while monitoring the patient’s ECG.
4. Provide intubation and controlled hyperventilation to rapidly reduce respiratory acidosis.”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

63
Q

Sodium bicarbonate can be administered IV for the treatment of severe hyperkalemia. Explain the pathophysiological rational for this therapy

A

“Although seldom required, life-threatening hyperkalemia may be treated with IV sodium bicarbonate. Bicarbonate therapy drives potassium into cells in exchange for hydrogen ions. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

64
Q

Anti-cholinergics are usually not recommended for trauma patients. Why?

A

The increase my cardio oxygen consumption and may predispose to arrhythmias

65
Q

Ketamine should be avoided or used at reduced dose in cats with urinary obstruction or renal dysfunction. Why?

A

“Because cats excrete the active form of ketamine in their urine, it should be avoided or used in lower doses if urinary obstruction or renal dysfunction is present. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

66
Q

List the five major differential diagnosis for hyperkalemia

A

“The major rule-outs for hyperkalemia are obstructive uropathy, acute renal failure, uroabdomen, adrenocortical insufficiency, and iatrogenic potassium intoxication. ”

Excerpt From
Small Animal Surgery E-Book
Theresa Welch Fossum DVM, MS, PhD, Dipl ACVS
https://books.apple.com/us/book/small-animal-surgery-e-book/id1367916984
This material may be protected by copyright.

67
Q

Effect of B1-receptor agonists. Examples

A

“β1-Receptor agonists primarily augment heart rate and contractility and ectopic pacemaker activity. ”

Isoproterenol, Dopamine, Dobutamine, Epinephrine

Excerpt From
Small Animal Critical Care Medicine
Deborah Silverstein & Kate Hopper
https://books.apple.com/us/book/small-animal-critical-care-medicine/id903782830
This material may be protected by copyright.

68
Q

Effect of B2-receptor agonist activity

A

“β2-Receptor agonist activity primarily causes vasodilation. ”

Isoproterenol
Epinephrine

Excerpt From
Small Animal Critical Care Medicine
Deborah Silverstein & Kate Hopper
https://books.apple.com/us/book/small-animal-critical-care-medicine/id903782830
This material may be protected by copyright.

69
Q

What are the two main methods by which animals that do not possess sweat glands lose heat?

A

Convection (direct contact with cooler surfaces)

Evaporative cooling (air passage through airways)

70
Q

List 5 risk factors for the development of hyperthermia in dogs

A

High ambient humidity
Upper airway obstruction
Laryngeal paralysis
Brachiocephalic airway syndrome
Collapsing trachea
Obesity
Previous history of hyperthermia

71
Q

You presented with a dog in respiratory distress, hyperemic mucous membranes any rectal temperature of 104.5°F. This dog has been working very hot, humid day for over two hours prior to collapsing. You suspect exercise induced hyperthermia. Are nonsteroidal anti-inflammatories indicated as antipyretics in this case? Why?

A

Nonpyrogenic hyperthermia results from the body’s inability to dissipate heat adequately. Therefore, antipyretic agents are often ineffective in reducing body temperature and are actually contraindicated due to potentially adverse side effects of decreasing renal perfusion and increased chance of gastrointestinal ulceration.

72
Q

Discuss the structure and function of the RAAS system, including the effects of its most important end products

A

The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure, fluid and electrolyte balance, and systemic vascular resistance.[2]

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to a decapeptide called angiotensin I.[3] Angiotensin I is subsequently converted to angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.[4] Angiotensin II has a short life of about 1 to 2 minutes. Then, it is rapidly degraded into a heptapeptide called angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues.

Angiotensin III increases blood pressure and stimulates aldosterone secretion from the adrenal cortex; it has 100% adrenocortical stimulating activity and 40% vasopressor activity of angiotensin II.

Angiotensin IV also has adrenocortical and vasopressor activities

Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure.[5] Angiotensin II also stimulates the secretion of the hormone aldosterone[5] from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium which in consequence causes the reabsorption of water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.

73
Q

Define acid Vs base

A

An ACiD is a molecule that donates a hydrogen ion (h+) when a base molecule accepts one.

74
Q

Define “buffer” and name the primary extracellular and intrcellular examples

A

a BUffeR is a weak acid or base, which helps protect against large changes in ph.
» The primary extracellular buffer is bicarbonate.
» The intracellular buffers are phosphate, pro-
teins, and hemoglobin.
» Bone also acts as a buffer.

75
Q

Prametrs for acidemia and alkalemia

A

Acidemia is a blood ph < 7.35;
Alkalemia is a blood ph > 7.45.

76
Q

What are the four types of acid-base disturbances ccording to henderson–hasselbach? Define each type

A

Henderson–hasselbach approach:

1.Metabolic acidosis: a primary gain in acid or loss of base
2.Metabolic alkalosis: a primary gain in base or loss of acid
3.Respiratory acidosis: retention of co2 due to co2 production outpacing alveolar ventilation
4.Respiratory alkalosis: removal of co2 (by ventilation) outpacing co2 production

77
Q

PaO2 Vs PaCO2 (or PvCO2) - which provides a measure of ventilation and which better reflects oxygenation?

A

Pao2 is a measure of oxygenation, not ventilation.

PaCo2 provides the best measure of a patient’s ability to ventilate and determines whether respiratory acidosis or alkalosis
is present. Remember that co2 is approximately 20× more diffusible than o2, making it easier for a patient to maintain normal co2 concentrations in the presence of lung disease.

• PvCo2 is the partial pressure of carbon dioxide dissolved in venous blood. When the sample has been obtained properly, it measures a patient’s ability to ventilate, similar to Paco2.

78
Q

Define Base Excess/Deficit and what information it provides

A

Base excess/deficit (BE)
» reflects the metabolic portion of the acid–base balance, which takes into account all of the body’s buffer systems
» estimates how much base needs to be added or subtracted to achieve a normal ph at normal temperature
» evaluates for metabolic acidosis or alkalosis.

79
Q

Explain the difference between osmolatity and tonicity

A

While osmolality is a measure of all solutes in solution, tonicity refers only to the effective solutes in solution; that is, those that cannot cross a membrane and so exert an osmotic pressure.

80
Q

Define isotonic fluid loss

A

Isotonic losses, such as those observed with vomiting and diarrhea, occur when the fluid being lost has an osmolality similar to that of plasma. With isotonic !uid loss, sodium concentrations are typically normal; however, if the animal is able to drink water, hyponatremia may result from replacement with a hypotonic fluid

81
Q

Define hypotonic losses

A

Hypotonic losses occur when the type of fluid being lost has a higher concentration of water than plasma, such as with diabetes insipidus and panting. The loss of a hypotonic !uid, or water in excess of sodium, can result in hypernatremia. Although isotonic replacement !uids may bene$t some patients with hypotonic losses, others benefits from !uids that contain more free water.

82
Q

Define Hypertonic losses. Give possible causes

A

Hypertonic losses, or loss of sodium in excess of water, are uncommon but can be seen with hypoadrenocorticism, third-space loss of fluid (such as pleural or peritoneal efusion), and diuretic administration.1 Excess loss of hypertonic fluid can result in hyponatremia.

83
Q

List 6 possible signs of iatrogenic overhydration

A

Signs of overhydration include chemosis, serous nasal discharge, increased skin turgor, peripheral edema, ascites, pleural eusion, and pulmonary edema.

84
Q

What are the four main routes of fluid administration? Which is considered ideal?

A

IV
SQ
intraosseous
Enteric (considered ideal since most physiological. Even if through ET tube or similar)

85
Q

How much of an isotonic crystaloid solution will leave the Intravascular space within 30 min?

A

More than 60% to 80% of a crystalloid solution distributes out of the intravascular space within 20 to 30 minutes.

86
Q

Is LRS a good choice for neonates? Why?

A

Neonates are able to use lactate as a fuel source, making LRS the preferred fluid choice for young patients.

87
Q

Is LRS a good fluid choice for patients with liver disease? Why?

A

Lactate in LRS is metabolized by the liver; thus, it is a suboptimal choice for patients with hepatic dysfunction or diabetic ketoacidosis because they will not be able to convert lactate to bicarbonate.

88
Q

Percentage of body weight composed by fluids in aduts Vs neonates

A

Adults: 60%
Neonates: 80%

89
Q

Intracellular fluid acccounts for 2/3 of body weight. Of the remaining 1/3, how much is intersticial Vs Intravascular?

A

75% intersticial
25% Intravascular
Small amout is transcellular (synovial, CSF)

90
Q

What is the normal lifespan of RBC’s in dogs and cats?

A

dogs: 110 days
cats: 70 days

91
Q

Explain the role of Thromboxane and COX-2 on the coagulation system?

A

Upon vascular injury, platelets will release arachidonic acid which is converted into thromboxane by thromboxane synthase via COX-1. Thromboxane promotes vasoconstriction and coagulation. At the same time endothelial cells will use prostacyclin synthase to synthesize prostacyclin through COX-2, leading to vasodilation and anti-coagulation. This balance is fundamental to prevent excessive coagulation and thrombosis.