Final Exam Flashcards

(61 cards)

1
Q

Causes of anemia

A

Hemorrhage , hemolysis hypoplasia

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2
Q

The hematocrit will be inaccurate if

A

Hematocrit = MCV x RBC count / 10
◼ If there are any inaccuracies in the MCV or RBC count

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3
Q

Time period between anemia onset and bone marrow release of reticulocytes

A

Average time takes 2-5 days to generate the reticulocytes in circulation
AKA 2-5 days to see the regenerative anemia vs if its bone marrow hypoplasia

  • repeat CBC to count reticulocytes
    Absolute count =reticulocyte% x RBC
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4
Q

Melena is a form of what anemia

A

Gastrointestinal upper GI blood loss ; External hemorrhage
It is a black and tarry stool that is due to A LARGE AMT BLOOD
— this is worse than hematochezia

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5
Q

When to give transfusion and which to give

A

If affected with cardiovascular problems/poor oxygenation OR PCV<15% thats when we give blood transfusion

Three types of blood transfusions :
Fresh whole blood before refrigerating : has red blood cells, clotting factors, platelets, plasma proteins= Good for coagulopathy and blood loss anemia

Refrigerated whole blood : with red blood cells, plasma, proteins, and some clotting factors= good for blood loss anemia

Packed red blood cells : red blood cells only so good for hemolysis and hypoplasia

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6
Q

Most common dog blood type

A

DEA 1.1
- should not have naturally occurring against other DEA blood types are rare

DEA- dog only have negative blood
• can get away with DEA+ blood for the first transfusion
DEA+ dog can have negative or positive DEA blood

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7
Q

3 bad transfusion reaction

A
  1. Transfusion associated circulatory overload
  2. MOST COMMON: non-hemolytic febrile reaction
    — Fever that is due to immunologic response
  3. Hemolytic transfusion reaction
    —Life threatening -destroying the RBCs that are administered
    Fever but ALSO inc RR, inc HR, Vomit, hypotension
    PCV to check= intervascular hemolysis
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8
Q

EXTRAVASCULAR VS INTRAVASCULAR HEMOLYSIS

A

Extravascular hemolysis may occur alone but extravascular hemolysis is always present with intravascular hemolysis
EXTRAVASCULAR= yellow urine or plasma
INTRAVASCULAR= red urine or plasma

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9
Q

Things that suggest fluid therapy is needed

A

Shock
Dehydration
—PCV/hematocrit/ plasma protein concentration/ high USG
Fluid balance- fluid loss or decreased intake
— Increased fluid loss [ polyuria/ gastrointestinal disease] or less intake [not making it to waterbowl]

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10
Q

Subcutaneous vs Interveous vs Oral fluid administration

A

IV:
All fluids an option
Acute treatment

Subcutaneous:
Can be done at home with cat with CKD
Only can rehydrate the patient up to a limit
UNLIKELY volume overload
Dont use hypertonic solution subcutaneously!!

Oral: ie Nasogastric tube
Long term at home fluid and physiologic

Intraosseous :
Into the bone marrow if very young or small animal

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11
Q

Purpose of fluid therapy

A

• Increase tissue perfusion
— ie. With shock
• Repair fluid deficits
• Supply daily fluid needs
• Replace ongoing losses

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12
Q

Calculate volume of fluid administration

A

Maintenance requirement : Sensible [urine] vs insensible [fecal/repiratory loss]

Hydration deficit : Body weight x amount dehydration = Liters deficit

Contemporary loss [diarrhea and vomit]

check after 24 hours of administration -24 if chronic loss plan

Stop fluid therapy if can maintain fluid balance with oral intake of food and water - taper the fluids. By 25%-50% daily

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13
Q

Normal urine output

A

1-2 mL/kg/hr
If not enough urine made then oliguria

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14
Q

Serous nasal discharge, chemosis, restlessness, shivering, tachycardia, cough, tachypnea, dyspnea, pulmonary crackles and edema, ascites, polyuria, exophthalmos, diarrhea, and vomiting

Whats up with this inpatient??

A

Overhydration - will have reduced PCV/TP
And increased body weight

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15
Q

IMHA treatment and diagnosis

A

Minimum database to diagnose : rule out UTI and check organ function with CBC Chem and urinalysis
IMHA: packed RBC transfusion of indicated
Prednisone =2mg/kg/day to stabilize the PCV
— still takes 5-7 days
Blood transfusions

Side effect : Thinning of the cats skin
Make sure the prednisone is slowly tapered to avoid the hypadrenocortism
Increase in liver enzymes [ ALKP/GGT ] but only milf increase in ALT and AST

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16
Q

Secondary immunosuppressive

A

Azathioprine : Given in conjunction with prednisolone or prednisone or dexmethasone for IMHA
And the dose is changed after 2 weeks
— can cause bone marrow suppression and hepatotoxicity

Another to give in conjunction with pred : Mycophenolate [v/d]
— less likely to cause bone marrow suppression

Another is cyclosporine to use like Atopica [NOT use vegetable oil base]

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17
Q

Main complication with IMHA

A

KEY : Pulmonary Thromboembolism

Also AKD, DIC, infections

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18
Q

Key way to test for infectious hemolysis of mycoplasma in cats

A

PCR to detect true infection

Tx. Floroquinolone and doxycycline

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19
Q

Canines specific to the babesia

A

Greyhound babesia canis
Imidocarb dipropionate

American pit bull terrier babesia
Gibsoni
Atovaquone + azithromycin

Esp test for babesia if hemolytic anemia on top of the thrombocytopenia

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20
Q

Heinz body anemia can be caused by

A

◼ Onion
◼ Garlic
◼ Tylenol (acetaminophen)
◼ Propylene glycol (semi-moist cat foods)
Zinc ingestion (pennies)
◼ Systemic disease (Cats - diabetes mellitus, hyperthyroidism, hepatic lipidosis, chronic renal failure, and lymphoma)
— If it is due to systemic disease in cat then there may not be anemia even

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21
Q

What are the clinical signs of anemia in horses?

A

• Tachycardia
• Tachypnea
• Weakness
• Depression
• Colic

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22
Q

Horse vs Small animal anemia

A

PCV of horse: PCV can increase or decrease by >10% with epinephrine or acute stress bc of splenic contraction
• big stress = transportation
No reticulocyte production - cant use to tell is reg or non-regen
Regeneration takes 9 days too
Use immature red cells in horses : slightly paler and bigger cells than normal RBC
Macrocytosis
As they get smaller the RBC will have the heme all come together so they get darker

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23
Q

How to tell if equine anemia is regenerative or not

A

RDW most accurate
Increased RDW is regenerative =increase in variation of size of RBC

Increased reticulocytes in bovine is regenerative

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24
Q

How much blood loss can the animal lose before death??

A

30-33% of the blood volume can be lost
Blood volume itself is 8% body weight

With internal hemorrhage the body is losing less

We are taking 25% of the donor’s blood volume

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25
What species Has the most hemoglobin concentration
Camelid
26
When to transfuse anemia with donor blood [ruminant or horse
• Acute anemia: 18% • Chronic anemia: 12% • Clinical signs of tissue hypoxia
27
Types of shock and most common
Hypovolemic - fluid loss from blood **most common** Cardiogenic- when the pump has failed Obstruction to blood flow • LDA or GDV- stomach twists and the vessels are obstructed • Pericardial - the pressure in the pericardium is so high that the heart cant work [ the heart is NOT the problem] Maldistributive - Significant sudden increase of blood in vasculature • usually 2/3 in veins Massive systemic vasodialation where the blood quantity overall isn’t lower or higher but there is a lot in the vasculature
28
Physiology of shock Where the tissue isn’t getting what they need
1. Maintain pressure: preserve and reabsorb water/plasma, reduce venous compliance [increase tone of vessel] 2. Optimize cardiac performance —If a patient is in early shock they may have normal BP bc the heart is compensating for the BP!! 3. Redistribute to vital organs 4. Promote offloading oxygen -improve utilization of o2
29
Does size matter for a normal heart rate
No it does not, it is not size of the dog but it is the genetics and age! All dogs have same range
30
Differentiate shock and anemia
White gums= anemia or shock PCV/TS to differentiate Increased lactate in shock ; because under anaerobic conditions and then the citric acid cycle wont happen but itll get shunted to different metabolism that results in lactate Fast CRT with maldistribution **Except in cardiogenic shock caused by a bradyarrhythmia, an increase in heart rate is often the earliest recognizable sign of shock in a patient**
31
four basic arrhythmias commonly observed during cardio pulmonary arrest and treatment
ventricular fibrillation =Shockable ventricular tachycardia =Shockable asystole =chest compression - Atropine pulses less electrical activity =chest compression - Atropine Every other cycle of CPR - every 4 minutes; atropine and epinephrine **no** fluid bolus usually recommended except for the hypovolemic patients
32
CPR alone
Close dogs mouth and seal the dogs nose with your mouth and give 2 breathes then 30 chest compressions
33
CPR how to position if >10kg vs <10kg/cat
>10kg then there is the thoracic pump model and pump and the highest point of the chest <10kg then cardiac pump model and compress over the heart Always elbows locked Compress to the 30% of the chest wall 100bpm Cycles of 2 minutes
34
ETCO2 what does it mean in CPR settings
Correct placement of ETT and the higher the ETCO2 the more likely there is spontaneous perfusion again **in arrest ETCO2 reflects perfusion!!!** not ventilation
35
Most common cause of death in dogs
Cancer And lymphoma is the most common hematopoietic neoplasm in dog —> 1-2 months for dogs without treatment Most frequently treated round cell timer — high incidence
36
Etiology of lymphoma
Immune deregulation—> increase risk of getting lymphoma Ie. Rheumatoid arthritis, any other autoimmune diseases that we are also treating with immunosuppressives The more the immunosuppression—> the more risk of lymphoma **Ie organ transplant is high risk** Ie. Cyclosporine, or herbicides licked over time Ie. Hair dyes or Smoke licked
37
Type of lymphoma classified by incidence in breed and ago
Sporting breeds= B cell lymphoma Toy breeds= T cells Cocker spaniels and Doberman pinschers get the T cell lymphoma Boxers= T cell lymphoma Over the age of dog Young dogs = T cell lymphoma Adults= B cell lymphoma Over all ages = both have same incidence **so you have to actually test dog to differentiate** a lot of factors [genetic, age]
38
Lymphoma patient should never go on prednisone because
It will upregulate the Pgp pump- increasing the cells exposure to toxic stuff—> then which the cancer comes back and we want to do chemo it wont work because multi drug resistance!!! Chronic steroids —>only if will never do chemo AND owner understands that the lymphoma that comes back will be very drug resistant
39
Stages of lymphoma in dogs
 Stage I – Involvement limited to a single lymph node, or lymphoid tissue in a single organ (excluding bone marrow).  Stage II – Involvement of many lymph nodes in regional area, in the same part of the diaphragm.  Stage III – Generalized lymph node involvement.  Stage IV – Liver and/or spleen involvement (±stage III). **common**  Stage V – Manifestations in the blood and involvement of bone marrow and/or other organ systems (± stages I-IV).  Substage a – Clinically Healthy b – Symptomatic due to LSA [Worse]
40
Diagnosis of lymphoma in dog
**FNA cytology and Flow cytometry [Proteins on lymphocytes - which type of B or T cell lymphocytes]** Blood work - check hypercalcemia [ Ionized Ca] PARR = check if the cells are clones which would push towards cancer via PCR • if they are polyclonal then push the diagnosis away from cancer • Just a supportive test not a true test Symptoms  Hypercalcemia  Anemia  Fever  Cachexia  Hypoglycemia **Reach remission and replase within 1 year of diagnosis**
41
Diagnosis of feline lymphoma
Blood work and FeLV test Chest rads and abdominal ultrasounds CATS: CT to look at head for nasal or CNS lymphoma In CATS No hypercalcemia related to cancer FNA cytology and bone marrow aspirate Diagnosis in CATS is also going to have biopsy - bc rare lymphomas can pull in different lymphocytes to the site of cancer so to identify which cell is actually cause of lymphoma Hard to tell if cytology is cancer or not IN CATS —> so use PARR [clonality to determine] **Staging is not prognostic in cats**
42
What is prognostic in CAT lymphoma
Substage - if the clinical signs are due to the lymphoma FeLV status — If positive then… **they get large cell lymphoma [agressive] AND we CANNOT treat it aggressively as we need to** — We can treat bc with normal chemotherapy and neg FeLV bone marrow will regenerate —BUT if the bone marrow is damaged by the FeLV infections then it doesn’t have the reserve so the cats cant get the chemotherapy they need Anatomical location Grade/Size matters- **the large cell lymphoma negative prognostic!!** *Doesn’t matter:* — stage [1-5] — immunophenotype [b vs t]
43
Cats lymphoma: grade, diagnosis, survival and treatment Alimentary Lymphoma Nasal lymphoma Renal Lymphoma
Alimentary Lymphoma GRADE -small cell [better] DIAG- biopsy via endoscopy of GI upper and lower OR exploratory surgery **to differentiate from IBD** SURV- years with small cell [vs **BAD/perforation of GI with large cell GI lymphoma!!** Not able to measure response with chemo - 1-3 months ] TX- prednisolone and chlorambucil [steroid and chemotheraputic] Nasal lymphoma GRADE: large cell lymphoma - LOCAL DIAG- **biopsy through the nose** SURV- >5 years if treated with radiation, everything else is palliative TX- Radiation therapy can cure because of local tumor ; chemo if disseminated Renal Lymphoma GRADE: large cell lymphoma —> lymphoma cause **Emergency acute kidney failure** DIAG: **Renal failure and big kidney —> do FNA— > progresses to neurological signs** SURV- months TX- fluids and chemotherapy - push lymphoma back and treat kidney after rescission
44
Define Anisocytosis
Varying shapes of RBC
45
Healthy platelet plug formation is made of
Platelets healthy ndothelium fibrinogen and vWF
46
Primary hemostasis vs secondary hemostasis Whats the problem?
Primary hemostasis : platelets- multi focal —assess quantity of platelets —spontaneous bleeding with 30000-50000 platelets —Buccaneers mucosal bleeding time: are the platelets working? Secondary hemostasis : clotting factor problem - localized — cavitation bleeding —Prothrombin time= extrinsinc and common pathway —Partial thromboplastin time [PTT] = intrinsic and common pathway
47
Congenital macrothrombocytopenia
Inherited and common in cavalier King Charles spaniels : DOES NOT CAUSE BLEEDING
48
Causes of the thrombocytopenia
SPUD Destruction- severe -IMTP Consumption/utilization - mild to moderate —DIC and hemorrhage Decreased production or hypoplasia - mild to severe — primary bone marrow : if other cell lines are affected —liver failure Sequestration - mild — no bleed: spleen / liver
49
IMMUNE-MEDIATED THROMBOCYTOPENIA (IMTP)
**0 to 20000 platlets** Spontaneous primary hemostasis disorder Regenerative anemia - hemorrhage or hemolysis IMHA Concurrent : where there is hemolysis and immune reaction against platlets too —> bad [ hyperbilirubinemia] Trigger: Primary idiopathic!! Secondary due to drugs and vaccination and **Rickettsial disease: Ehrlichiosis, anaplasmosis, Rocky Mountain Spotted Fever (RMSF), and borreliosis** and neoplasia Goal initially is to get to the spontaneous hemorrhage range!! 30k-50k ITP treatment : **Doxycycline** even if negative on rickettsia 4dx and **immunosuppressive dose of corticosteroids** and **One time immunosuppression with chemotherapy vincristine to speed up the platelet increase** — vomit [with cerenia] and transient leukopenia and can cause tissue damage if outside vessel!!! Scary vancristine
50
Thrombocytopathia
Primary hemostasis disorder When bleeding occurs (impaired platelet function) with the normal platelet count and normal clotting times [PT/PTT] Screen for drugs and erlichiosis Congenital von Willebrands disease BMBT test : endothelial and platelet function
51
VwDisease is because of ____and breeds affected are___
Lack of vWF = **most common primary hemostatis disorder** VWF helps with platlets adhering to the damaged endothelium **Doberman pinscher, German shepherd** Tx= cyroprecipitate
52
Factor difficiency :**hemophilia A vs hemophilia B**
Secondary hemostasis disorder = intrinsic [long ptt] Hemophilia A= factor 8 deficiency Tx Cryopercipitate Hemophilia B = factor 9 deficiency Tx. Fresh frozen plasma
53
Acquired coagulopathy Secondary hemostasis problem
Vitamin K deficiency coagulopathy = PT affected first then PTT affected Vitamin K is required for production and activation of the vitamin K-dependent coagulation factors (II, VII, IX, X) **factor 7 shortest half life** Not bleeding: Happens with anticoagulant rodenticide which **inhibits vitamin K reductase** —Clinical signs 2-5 after —**PT prolonged after 36hrs-72 hours ==> shows if there is vitamin K deficiency** Cavoatry bleeding: blood component therapy —> fresh frozen plasma Tx. Start SQ then oral vitamin K1 therapy initially **with food**
54
Liver disease can cause multi factorial acquired coagulopathy what effects?
Thrombopoitein tells bone marrow to make new platelets [production of platlets] Pimary hemostasis • this comes from the liver so with liver injury there can be thrombocytopenia The liver also makes coagulation factors so has impact on secondary hemostasis
55
DIC pathophysiology
**Hypercoagulable then hypocoagulable at the end of it** Diagnosis: **no definitive test** Consumption/utilization thrombocytopenia Prolonged PT/PTT Schistocytes - damaged RBC Increased D-diners Treat : Fluid therapy Prevent thrombosis in hypercoagulable stage Replenish clotting factors if hypocoagulable
56
If intravascular hemolysis then the hemoglobin
Hemoglobin normally = 1/3 Hematocrit If this is not correct and hemoglobin is increased
57
Equine transfusion cutoff
13% PCV for chronic 18% PCV for acute
58
Where is the majority of the body fluid stored?
Intracellular fluid compartment The least is the intravascular compartment that is extracellular
59
Which fluids to give and when?
Crytalloids : Isotonic , hypotonic, hypertonic — enter all compartments because electrolyte and no electrolyte solutes Replacement: Shock Maintenance Hypertonic saline: Not used commonly- used to rapidly increase intravascular volume **never use hypertonic Subcutaneously =burns** Colloids - *plasma compartment [intravascular]* • Severe hypoalbuminemia • Inadequate response to crystalloids • Shock • Hypotension during anesthesia • Less risk of edema in patients with intact endothelium
60
Spontaneous bleeding for platlets
Spontaneous bleed happens at 30k-50k
61
No bleeding tendencies but born with low platlets
Congenital macrothrombocytopenia