Exam 2 Review Flashcards

1
Q

What is the difference between vomiting and regurgitation?

A

**Vomiting is the forceful ejection of the contents (such as food, fluids, or debris) of the stomach and upper small intestine.
**Regurgitation is a passive motion that does not require effort or contraction of the abdominal muscles. Food and fluid tends to be undigested.

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2
Q

Vomiting of white fluid suggests a disorder of __ origin

A

Gastric or Esophageal

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3
Q

Vomiting of yellow fluid suggests gastric vomiting mixed with __

A

Bile from the duodenum

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4
Q

Vomiting of green fluid indicates the presence of bile that has come very recently from the duodenum.

A
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5
Q

Vomiting of both yellow and green fluid can be associated with pancreatitis.

A
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6
Q

Brown fluid suggests reflux of fecal-like material from further down the small intestine. It usually has a fecal-like odor as well.

A
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7
Q

Frank blood in the vomitus (hematemesis) typically indicates esophageal, gastric, or duodenal erosions or ulceration, although frank blood can be seen on occasion with jejunal disease.

A
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8
Q

Black flecks or “coffee grounds” indicate the blood has been present long enough in the stomach for the hydrochloric acid in the stomach to denature (digest) the hemoglobin.

A
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9
Q

Vomiting should be characterized as precisely as possible in all patients (Box 20.1). It is not uncommon for patients with complicated but also with uncomplicated GI problems to be undertreated because the vomiting has not been characterized adequately. This can lead to significant morbidity.

A
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10
Q

Metoclopramide acts by enhancing gastric emptying and increasing lower esophageal sphincter tone, and it acts centrally at the chemoreceptor trigger zone; clinically, metoclopramide appears to be most effective when given via CRI at 2mg/kg/day

A
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11
Q

Chlorpromazine (phenothiazine)

A

act at higher central nervous system centers and at the chemoreceptor trigger zone. They can cause significant hypotension, and BP should be monitored if any drugs in this class are being administered

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12
Q

Anticholinergics act by decreasing GI secretions and motility; however, these agents are almost never used because even a single dose can lead to prolonged ileus.

A
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13
Q

Serotonin antagonists such as ondansetron hydrochloride or dolasetron are very effective. Serotonin receptors are present in the chemoreceptor trigger zone, peripherally on vagal nerves, and in the GI tract; however, how the drug controls vomiting is unknown

A
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14
Q

Maropitant (Cerenia, Zoetis Inc., Florham Park, NJ) appears to be the most clinically effective antiemetic currently available. It is a neurokinin-1 (NK1) receptor antagonist. It inhibits binding of substance P (which helps initiate vomiting) in the chemoreceptor trigger zone and the vomiting center.

A
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15
Q

Butorphanol is a mild antiemetic that counteracts the nausea caused by certain medications (especially chemotherapeutic agents) and may help decrease vomiting caused by pain.

A
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16
Q

Parenteral antiemetics should be used in most vomiting patients, because oral medications can cause vomiting and GI absorption is unreliable. Whenever possible, the drugs should be given IV to ensure good blood levels.

A
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17
Q

Nonsteroidal antiinflammatory drugs should be avoided because of their negative effects on splanchnic organs (and, in some cases, coagulation)

A
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18
Q

esophageal foreign body. The animal may show signs of salivation, excessive swallowing motions, dysphagia, and apparent vomiting that on closer questioning will be determined to be regurgitation.
respiratory distress, because the foreign material may be compressing the trachea.

A
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19
Q

Early signs of a GI foreign body include nausea, vomiting, and inappetence. Vomiting usually persists until the material has been vomited, has passed, or has been removed
Abdominal pain may or may not be present

A
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20
Q

Surgery is indicated in the vast majority of these patients. If only mild clinical signs are present, then a watch-and-wait attitude may be adopted.

A
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21
Q

gastric dilation and volvulus (GDV) is not yet clearly understood. GDV has been associated with many clinical diseases and typically is seen in large, deep-chested dogs; however, it can occur in any size of dog, at any age.

A
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22
Q

Twisting causes a one-way valve effect at the gastroesophageal junction, allowing swallowed air to enter the stomach but not leave. Carbon dioxide may also accumulate secondary to bacterial fermentation, diffusion from trapped blood, and metabolism of gastric acid and bicarbonate from the pancreas and saliva.

A
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23
Q

a history of attempting to vomit or having nonproductive retching, although occasionally all the owner reports is the dog is more quiet than normal. Abdominal distention may or may not be noted by the owner.

A

On presentation, dogs usually show some degree of circulatory shock. Ventilatory compromise may be evident because of pressure on the diaphragm from the distended stomach.

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24
Q

A right lateral abdominal radiograph will typically reveal a characteristic shelf sign with compartmentalization, supporting a diagnosis of a gastric volvulus

A
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25
Q

It is, however, very common to have extremely high lactate concentrations of 10mmol/L or higher, often as high as 20mmol/L with GDV.

A
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26
Q

Immediate treatment should consist of O2 administration if the dog is showing any signs of shock, as well as volume replacement with crystalloids with or without synthetic colloids.
A lead II ECG should be monitored, because these dogs are prone to ventricular arrhythmias

A
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27
Q

hemorrhagic gastroenteritis (HGE) usually is unmistakable because of the presence of blood (frank or digested) in the vomitus or diarrhea
foul odor to the stool is also usually present
Acute hemorrhagic diarrhea syndrome (AHDS) is characterized by a very high PCV (usually >60%) and relatively low TSs

A
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28
Q

Synthetic colloids the intravascular volume more rapidly than crystalloids IV broad-spectrum antibiotics are usually indicated.

A
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29
Q

Pancreatitis ultimately is a result of activation of the pancreatic enzymes (proteases) within the pancreas, leading to autodigestion, as well as digestion of the peripancreatic tissues, and subsequent activation of the inflammatory process through neutrophil activation and production of cytokines and free radicals.

A
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30
Q

Multiple causes of pancreatitis have been identified; however, most cases are ultimately diagnosed as idiopathic. Dietary indiscretion appears to be a common predisposing factor in dogs, and cholangiohepatitis and inflammatory bowel disease appear to be involved in many cats.

A
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31
Q

Anorexia and intermittent vomiting may be the only signs in cats. Dogs often have a history of dietary indiscretion followed by nausea, vomiting, and anorexia. Diarrhea may be present. Abdominal pain is usually present; in mild cases, pain can be localized to the upper-right quadrant of the abdomen in dogs, and in more severe cases it may be diffuse

A
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32
Q

Assays of pancreatic enzymes (amylase, lipase) do not provide any useful information in dogs and cats. Species-specific pancreatic lipase immunoreactivity (fPLI and cPLI) tests are used to help diagnose pancreatitis in both species

A
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33
Q

Bleeding in smaller vessels may be controlled by a simple response involving the vasculature and platelets, known as primary hemostasis. With larger-vessel injury, plasma coagulation factors are needed to form a stable clot, a process known as secondary hemostasis. Dysfunctions of the hemostatic system lead to life-threatening conditions through a variety of mechanisms.

A
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34
Q

The first response to blood vessel injury is vasoconstriction, temporarily diverting blood flow around the injured area.

A
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35
Q

Plasma coagulation factors (denoted by Roman numerals) are produced in the liver, many with the help of vitamin K (II, VII, IX, and X), and are enzymes or cofactors to enzymatic processes

A
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36
Q

Patients with a low platelet count, known as thrombocytopenia, experience bleeding when inadequate numbers of platelets are available to form a platelet plug (spontaneous bleeding typically does not occur unless platelet concentration is <20,000 to 30,000/μL).

A

Primary Hemo

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37
Q

Massive transfusion may cause thrombocytopenia from a combination of the rapid consumption of platelets and the dilution of platelet concentration by fluid solutions and blood components. Thrombocytopenia can also result from an increased consumption of platelets attributable to DIC, infection, neoplasia, inflammation, immune-mediated disorders, and drug interactions.

A
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38
Q

__ is a common cause of increased platelet sequestration and destruction with subsequent thrombocytopenia. __ occurs when immunoglobulin G (IgG) against platelet membrane elements are produced and bound, resulting in premature removal by the reticuloendothelial system.

A

Immune-mediated thrombocytopenia (IMT)

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39
Q

IMT can be classified into two types. These are __

A

Primary: Antiplatelet antibodies are truly autoimmune and have no apparent cause.
OR
Secondary: Disorder is warranted if antibodies are produced in response to antigenic stimuli (e.g., drugs, vaccines, infections, and neoplasia).

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40
Q

When the platelet quality is compromised, platelet adhesion or aggregation (or both) at the site of endothelial damage may be abnormal.
A platelet function defect in patients with a history of bleeding and a normal platelet count is called __.
It may be classified as an inherited or an acquired defect.

A

Thrombopathia

41
Q

Though medical management is the treatment of choice when it comes to thrombocytopenia and thrombopathia, platelet transfusion may be warranted if the patient is acutely bleeding into a vital structure. In this case, it is best to use __

A

Fresh whole blood, from which the patient will receive both platelets and oxygen-carrying support

42
Q

In situations of platelet destruction, such as IMT, it is best to treat by __

A

*Treating the underlying disease (e.g., ehrlichiosis)
*Removing the triggering agents (e.g., drugs)
*Administering immunosuppressants (glucocorticoids, azathioprine, cyclosporine, mycophenolate, vincristine, human immunoglobulins)

43
Q

When it comes to IMT, it not recommended, except in cases of severe, life-threatening hemorrhage, to administer platelets because ___

A

Survival of transfused platelets is transient

44
Q

The most common hereditary bleeding defect in dogs (recognized in more than 60 breeds) is…

A

von Willebrand’s disease (vWD)
**A deficiency of vWF (a large plasma protein produced by and stored in endothelial cells).

45
Q

__ facilitates platelet adhesion and aggregation, and acts as a carrier for factor VIII.

A

von Willebrand’s Factor

46
Q

FFP or fresh whole blood (FWB) contains viable vWF, but is not used as treatment because…

A

it carries higher risks of transfusion complications

47
Q

__ is a concentrate of specific coagulation factors (vWF, FVIII, fibrinogen, fibronectin) derived from fresh-frozen plasma (FFP), and is ideal in managing bleeding as a result of vWD.

A

Cryoprecipitate

48
Q

__ is known as clotting, the process by which blood changes from a liquid to a gel, forming a blood clot

A

Coagulation

49
Q

__ is the destruction of red blood cells.

A

Hemolysis

50
Q

__ is the process of producing red blood cells.

A

Erythropoiesis

51
Q

__ formation is a cause of hemolytic anemia. It is the result of oxidative damage to erythrocyte hemoglobin.

A

Heinz Body

52
Q

__ are the most common severe hereditary coagulopathies in the dog.

A

Hemophilias

53
Q

The __ is the site of synthesis of all coagulation factors.

A

Liver

54
Q

In certain pathologic situations, the coagulation response may become accelerated and the fibrinolytic system overwhelmed. This imbalance between bleeding, coagulation, and fibrinolysis is called __

A

Disseminated Intravascular Coagulation (DIC)

55
Q

__ is the process of a blood clot forming in the vein.

A

Thromboembolism

56
Q

__ is the lack of blood flow to a region of the body.

A

ischemia

57
Q

petechiation, ecchymosis, epistaxis, hematuria) (Figure 17.4) are usually suggestive of platelet or vascular abnormalities.

A
58
Q

A normal platelet count in dogs is 200,000 to 500,000/μL, and 200,000 to 600,000/μL in cats.

A
59
Q

Abnormal bleeding can occur in animals with platelet counts below 20,000 to 30,000/μL; however, each patient varies and some animals may not exhibit clinical signs associated with bleeding with a platelet count of 2000/μL

A
60
Q

he average number of platelets in approximately 5 to 10 oil immersion fields is counted to estimate platelet numbers

A
61
Q

The BMBT (buccal mucosal bleeding time) assesses platelet and vascular contribution to hemostasis, thereby evaluating primary hemostasis.

A
62
Q

Normal bleeding time is less than 4 minutes in dogs, and 3 minutes in cats

A
63
Q

Blood samples for hematologic testing are ideally collected directly into a plastic syringe containing 3.2% or 3.8% trisodium citrate at a ratio of 1:9 with blood to be collected. It is collected in a light blue tube

A
64
Q

“PT” is an abbreviation for __

A

Prothrombin Time - How long it takes blood to clot

**A prolongation in PT can be caused by liver failure, vitamin K antagonism, malabsorption, hereditary factor deficiencies, or consumptive factor deficiencies.

65
Q

Small surface bleeds (e.g., petechiation, ecchymosis, epistaxis, hematuria) (Figure 17.4) are usually suggestive of platelet or vascular abnormalities. Larger bleeds or bleeding into body cavities (e.g., hematoma formation, hemarthroses, deep muscle hemorrhage, hemothorax, hemoabdomen) are suggestive of clotting factor deficiencies. A combination of these clinical signs is not uncommon. The presence of blood in more than one general location is suggestive of a bleeding disorder.

A
66
Q

“PIVKA” is an abbreviation for __

A

Proteins Induced by Vitamin K Antagonism
**developed and used to detect anticoagulant toxicity. detect any coagulation factor deficiency of the extrinsic and common pathways and are not specific for the detection of anticoagulant rodenticide poisoning. no advantage in using the PIVKA test over the PT aside from possibly having higher sensitivity in certain species.

67
Q

“aPTT” is an abbreviation for __

A

Activated Partial Thromboplastin Time
**The intrinsic and common pathways are assessed by aPTT.
Prolongation of aPTT indicates deficiencies in coagulation factors in the intrinsic or common pathway. Some causes are liver failure, vitamin K antagonism, malabsorption, hereditary factor deficiencies, consumptive deficiencies, and vWD.

Prolongation of PT and aPTT will be seen when clotting factors are depleted below 30% of normal.

68
Q

“ACT” is an abbreviation for __

A

Activated Clotting Time
**The ACT test is a simple, inexpensive screening test for severe abnormalities in the intrinsic and common pathways of the clotting cascade. It evaluates the same pathways as aPTT but is less sensitive at detecting factor deficiencies

69
Q

Anemia, most accurately described, is a deficiency in the blood’s oxygen-carrying capacity attributable to a reduction in the circulating red cell mass

A
70
Q

Classification is helpful in differentiating blood-loss and hemolytic anemias (which are generally regenerative) from bone marrow depression anemias (which are generally nonregenerative).

A
71
Q

IMHA may be a primary disease, also known as idiopathic or autoimmune hemolytic anemia, in which autoantibodies are produced against the unaltered RBC membrane.

A
72
Q

the greater the stimulation of marrow erythropoiesis, the greater the reticulocytosis. This is not the case with nonregenerative anemias; therefore the degree of reticulocytosis must be viewed in concert with the degree of anemia. The technician can do this by calculating a corrected reticulocyte count (percent [%]) or an absolute reticulocyte count (numbers/microliter [μL] of blood). The absolute reticulocyte count is calculated by multiplying the percentage of reticulocytes by the RBC count.

A
73
Q

RBC autoagglutination indicates anti–RBC antibodies are present and therefore strongly suggests IMHA. Agglutination appears as grapelike clustering of erythrocytes in the blood smear and can be distinguished from rouleaux formation by examining a wet-mount preparation of a blood sample. The veterinary technician should mix one drop of blood with one drop of isotonic saline on a clean microscope slide, cover it with a coverslip, and examine it under the microscope.

A
74
Q

Normal adult canine PCV is 37% to 55%, with lower values in puppies and higher values in sighthound breeds such as greyhounds. Normal adult feline PCV is 30% to 45%, also with lower values in young kittens

A
75
Q

When evaluating RBC morphology you must note the ____________, _____________ and ___________ of the RBCs

A

Size, Shape, and Color

76
Q

Serum is the liquid that remains after the blood has clotted. Plasma is the liquid that remains when clotting is prevented with the addition of an anticoagulant

A
77
Q

Diabetic ketoacidosis (DKA) is a complicated form of diabetes mellitus that can have fatal consequences in dogs and cats. Patients with insulin-dependent diabetes mellitus have an absolute or relative insulin deficiency.
Starvation, or the perceived lack of glucose, initiates lipolysis (the breakdown of stored body fat into fatty acids) and promotes the conversion of the released fatty acids into glucose precursors in the liver by a process called β-oxidation. From a simplistic view, in the state of starvation, the body will convert these free fatty acids into ketones.

A
78
Q

Ketones are a by product of __

A

Lipolysis

79
Q

Potassium supplementation is required in all DKA patients. Diabetes mellitus, and especially ketoacidosis, causes total body potassium depletion attributable to shifting of potassium out of the cells into the serum in an effort to replenish renal losses and help offset acid-base imbalances. Treatment of DKA will result in a further decrease in serum potassium concentrations because of dilution from fluid therapy, insulin-mediated uptake of potassium by the body cells, correction of acidemia, and continued renal losses.

A
80
Q

Calcium-containing fluids (lactated Ringer’s) should not be used for administering phosphorus because of the risk of precipitation.

A
81
Q

Hypoadrenocorticism (Addison’s disease) is a deficiency in the production of mineralocorticoids (primarily aldosterone), glucocorticoids (primarily cortisol), or both, by the adrenal glands.

A
82
Q

A lack of aldosterone results in sodium, chloride, and free water loss in the urine with retention of potassium, hydrogen ions, and calcium. The resultant severe electrolyte imbalances and dehydration contribute to the shock and cardiac effects seen in an addisonian crisis.

A
83
Q

Lack of cortisol results in loss of GI integrity and lack of ability to prevent shock.

A
84
Q

Eventually the P waves become smaller and wider and, in severe hyperkalemia, will disappear altogether

A
85
Q

Correcting hypovolemia and hypotension and addressing electrolyte imbalances are the primary goals. The fluid of choice is 0.9% sodium chloride administered at a maintenance volume plus dehydration deficit volume

A
86
Q

Dexamethasone sodium is inexpensive and readily available; therefore most clinicians consider it the initial glucocorticoid of choice. Dexamethasone sodium phosphate is a water-soluble, rapid-onset steroid, and it does not cross-react with the cortisol assay required for the ACTH stimulation test.

A
87
Q

Once the patient has been stabilized, those with primary hypoadrenocorticism can have mineralocorticoids added to their treatment. Desoxycorticosterone pivalate (DOCP) is the most economical way to replace mineralocorticoids. DOCP (Percorten-V, Novartis)

A
88
Q

The most commo cause of hypercalcemia isn

A

Most common cause is hypercalcemia of malignancy
Lymphoma by far the most common cause

89
Q

IV 0.9% NaCl or other non-Ca containing crystalloid 100-180 mL/kg/day to promote diuresis (usually need K supplementation in fluids)

A
90
Q

UA to evaluate for renal casts, BUN, creatinine daily to monitor kidney fxn

A
91
Q

The most common cause of Hypocalcemia is

A

hypoalbuminemia

92
Q

State of decrease serum glucose concentration
Disorders that promote rapid removal of glucose from plasma
Otherwise, parenteral Ca salt therapy if caused by hypoparathyroidism, puerperal tetany, or enemas Calcium gluconate 10% - safer Calcium chloride 10% - more potentSlow IV infusion
Continuous ECG monitoring during administration - pause infusion if bradycardia and Q-T segment shortening

A
93
Q

Fresh Frozen Plasma is used to treat __

A

Used for DIC, liver disease, anticoagulant toxicities and hereditary coagulopathies

93
Q

Packed Red Blood Cells are used to treat __

A

Severe Anemias

94
Q

Monitor BG q 2 hours
Target 60-150 mg/dL

A
94
Q

What are the components of blood?

A

RBC, Plasma, and Platelets

94
Q

Late term pregnancy
Fanconi syndrome - loss of glucose through kidneys
Severe prolonged seizures
Neonatal/toy breed hypoglycemia
Starvation or malabsorptive GI disease
Prolonged exercise without food
End-stage liver disease
Addison’s disease

A
95
Q

Frozen Plasma is used to treat __

A

Hypoproteinemia

96
Q

Most severe reactions occur with DEA 1 antigen. Testing for this blood type is strongly recommended

A