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Year 1/2 > Circ & Resp 2: Clin Path S1 > Flashcards

Circ & Resp 2: Clin Path S1 Flashcards

1
Q

after trauma, how long does it take for an animal to show anemia in bloodwork?

A

could take an HOUR

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1
Q

3 things seen with ACUTE BLOOD LOSS (mention how kidneys respond/timing, another notable organ/timing, and treatment-related)

A

(1) DECREASED OXYGEN (from decreased oxygen-carrying capacity)
–> kidneys respond by making erythropoietin to stimulate RBC production in bone marrow
–> response or regeneration of RBCs takes 2-3 days

(2) SPLENIC CONTRACTION
–> spleen contracts to release RBCs and platelets

(3) FLUIDS
–> either ADMINISTERED or REDISTRIBUTED
–> causes hemodilution and DECREASED PLASMA PROTEIN and DECREASED ALBUMIN/GLOBULIN (serum proteins)

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2
Q

CBC findings for acute blood loss (5, mention reasons for 2 of them)

A

(1) Decreased PCV

(2) Concurrent decrease in total protein (albumin and globulin)

(3) Decreased platelets
–> Get CONSUMED by trying to cause clotting, still circulating due to splenic contraction
–> PRIMARY = thrombopathia
–> SECONDARY = vitamin K antagonism, hepatic failure

(4) Increased BUN and NORMAL creatinine
–> Blood broken down is a PROTEIN so increase ammonia –> increased BUN (blood urea nitrogen)
–> Often seen in GI hemorrhage

(5) SEVERE THROMBOCYTOPENIA
–> Less than 25,000 platelets
–> COULD BE THE CAUSE OF BLEEDING

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3
Q

Dog RBCs description

A

normal sized WITH CENTRAL PALLOR because biconcave disc

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4
Q

Cat/Horse RBCs description

A

Smaller red cells with LACK of central pallor

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5
Q

Cow RBCs description (hint: compare to dogs)

A

SMALLER than dogs WITH CENTRAL PALLOR

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6
Q

Goats/sheep RBCs description

A

MINIMAL CENTRAL PALLOR, SOME OF THE SMALLEST RBCs

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7
Q

Camelid RBCs description

A

Have elliptical RBCs

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8
Q

Birds/reptiles RBCs description

A

odd shape/nucleated RBCs

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9
Q

which values are measured (3) vs. calculated (2) on a CBC using a hematology instrument?

A

MEASURED (directly determined)
(1) Hemoglobin concentration
(2) RBC count in millions
(3) MCV

CALCULATED (determined)
(1) Hematocrit
(2) MCHC

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10
Q

macrocytic & what can cause it

A

when MCV is ABOVE reference range, RBCs are LARGER THAN NORMAL

CAUSE?
Regenerative, accelerated erythropoiesis resulting in skipped division in larger cells

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11
Q

microcytic & what can cause it

A

when MCV is BELOW reference range, RBCs are SMALLER THAN NORMAL

CAUSE?
Iron deficiency anemia, less hemoglobin causing extra division of erythropoiesis

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12
Q

normocytic

A

MCV is within reference range

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13
Q

hypochromasia & what can cause it

A

when MCHC is BELOW reference range and LESS Hb in RBC, looks PALE (not as red)

CAUSE?
Regenerative anemia but now less Hb per cell volume because MORE RBCs

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14
Q

normochromic

A

when MCHC is WITHIN reference range

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15
Q

what does regenerative anemia look like with RBCs?

A

MACROCYTIC and HYPOCHROMASIA (large and pale)

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16
Q

what does iron deficiency anemia look like with RBCs?

A

MICROCYTIC and HYPOCHROMASIA (small and pale)

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17
Q

what does a CBC include?

A

Provides information on erythrocytes, leukocytes, platelets, and CAN include plasma proteins (albumin, fibrin, globulin)

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18
Q

where are RBCs made?

A

Produced in the bone marrow in response to erythropoietin made by the kidneys

can also be produced in extramedullary tissues like the spleen or liver

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19
Q

function of RBCs?

A

to synthesize Hb, which binds and transport oxygen

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20
Q

hemoglobin structure (include iron states)

A

each heme subunit contains a Fe ion within a porphyrin ring

Fe2+ = CAN CARRY OXYGEN

Fe3+ = METHEMOGLOBIN, CANNOT CARRY OXYGEN

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21
Q

how many Hb molecules do RBCs contain?

A

hundreds to millions

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22
Q

iron deficiency anemia and heme

A

diminished production of heme –> less RBCs/anemia

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23
Q

when is methemoglobin formed? what happens when it’s formed?

A

when RBCs undergo significant oxidative injury so they cannot carry oxygen anymore (Fe3+)

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24
Q

how long do RBCs circulate for most veterinary species (non-exotic)?

A

90-120 days

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25
Q

about __% of RBCs are ___ & ___ ___ daily due to ___

A

1, produced, broken down, senescence

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26
Q

what stimulates RBC production in the bone marrow? where is it made? what kind of tissue does it require?

A

erythropoietin

made by renal cortical cells

requires functional, adequate renal cortical tissue

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27
Q

what 3 morphological changes occur for RBCs during development?

A

(1) cells become SMALLER

(2) cytoplasm changes from blue to red with increased Hb

(3) extrusion (removal) of nucleus

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28
Q

how many RBCs are in blood on average?

A

Between 6-10 million/uL

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29
Q

stages of RBC development (7)

A
  1. rubriblast
  2. early rubricyte
  3. middle rubricyte
  4. late rubricyte
  5. metarubricyte
  6. reticulocyte
  7. mature erythrocyte
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30
Q

what stage of RBC development do they start making Hb?

A

early rubricyte (2)

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31
Q

what stage of RBC development do they stop dividing? why?

A

late rubricyte (4)

due to CRITICAL CONCENTRATION OF Hb

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32
Q

characteristics of a reticulocyte

A

NO NUCLEUS because extruded after late rubricyte stage

still contains ORGANELLES AND RNA

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33
Q

hematocrit (HCT) definition

A

% of blood volume taken up by RBCs

MEASURED BY MACHINE via RBCs and MCV

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34
Q

what two values are often used to characterize anemia? what specifically are they looking to evaluate?

A

hematocrit (HCT) and packed cell volume (PCV)

they evaluate RBC density!!

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35
Q

packed cell volume (PCV) definition

A

% of blood volume taken up by RBCs

MANUALLY CALCULATED using a microhematocrit tube and microcentrifuge

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36
Q

hemoglobin count definition (on laboratory)

A

grams of Hb/100 mL of blood MEASURED BY ANALYZER

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37
Q

RBC count (on laboratory)

A

amount of RBCs/unit of blood MEASURED BY ANALYZER

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38
Q

if we have blood loss/hemolysis or decreased oxygen tension, what occurs in regards to RBC development? (**hint, mention what specific part of the organ does the first step, the process, and how long it takes)

A

renal cortical cells secrete EPO and tell bone marrow to undergo reticulocytosis within 2-3 days once these changes occur

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39
Q

how long do reticulocytes remain in blood? what happens after this period?

A

1-2 days, then become mature RBCs

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40
Q

horses and related species do not have ___ released

A

reticulocytes

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41
Q

no reticulocytosis = we do not have regenerative anemia (T/F and explanation)

A

FALSE

can have anemia with lackluster regenerative response

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42
Q

reticulocytosis definition

A

erythroid regeneration/increased erythropoiesis

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43
Q

reticulocyte vs. polychromasia

A

SIMILARITIES?

(1) BOTH are the stage before mature RBC
(2) BOTH appear bluish on microscopic stains

DIFFERENCES?

(1) Reticulocytes are enumerated by MACHINES, polychromatophils are semi-quantitatively determined on blood smears
(2) grading scales are subjective and variable for polychromatophils (slight, mild, moderate; marked 1+, 2+, 3+); % and absolute counts in reticulocytes
(3) DEGREE OF POLYCHROMASIA AND THEREFORE REGENERATION DEPENDS ON THE AMOUNT OF ORGANELLES/RNA PRESENT IN RETICULOCYTES; whereas reticulocytes are given in an exact number to determine regeneration

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44
Q

All ____ RBCs are ____, but not all ____ have enough ____ & ____ to be _____

A

polychromatophilic, reticulocytes, reticulocytes, RNA, organelles, polychromatophilic

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45
Q

AUTOMATIC vs MANUAL reticulocyte enumeration

A

AUTOMATIC
–> occurs with most hematology analyzers
–> absolute count

MANUAL
–> equal parts blood and new methylene blue for 10-15 minutes to aggregate organelles/RNA in RBCs to make a blue-speckled reticular pattern
–> 1000 RBCs counted and reticulocytes are a % out of these RBCs

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46
Q

absolute reticulocyte number (definition, formula, and what we do with the value)

A

number of reticulocytes per uL of blood

absolute reticulocyte number = reticulocyte % x RBC count (in millions)

COMPARE THIS TO REFERENCE RANGE TO DETERMINE IF REGENERATIVE ANEMIA IS OCCURRING

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47
Q

CORRECTED reticulocyte % (CRP, how often it’s used, formula, normal ___ values for dog/cat/cow)

A

NOT OFTEN USED, incorporates PCV

CRP = reticulocyte % x (patient PCV/normal PCV)

normal PCV values
dog = 45
cat = 35
cow = 35

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48
Q

2 reasons we could have reticulocytosis WITHOUT anemia?

A

(1) SUBCLINICAL BLEEDING
ex = intermittent intraabdominal bleed
- patient hasn’t developed clinical signs but still hemorrhaging somewhere, erythropoiesis was activated

(2) PATIENT’S NORMAL VALUES FOR RETICULOCYTES FALLS OUTSIDE REFERENCE RANGES

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49
Q

mean corpuscular volume (MCV)

A

MEASURED average volume of circulating RBCs

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50
Q

mean corpuscular hemoglobin concentration (MCHC)

A

CALCULATED average concentration of Hb within circulating RBCs

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51
Q

cellular hemoglobin concentration mean (CHCM)

A

MEASURED more accurate MCHC with in vivo or in vitro hemolysis or lipemia

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52
Q

mean corpuscular hemoglobin (MCH)

A

NOT TYPICALLY USED

CALCULATED concentration of Hb per cell NOT AN AVERAGE

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53
Q

iron deficiency anemia findings (4)

A

(1) Decreased MCV AND MCHC

(2) Can be REGENERATIVE or NON-REGENERATIVE
–> Reticulocytes can be NORMAL OR INCREASED

(3) Can see MICROCYTES and HYPOCHROMASIA

(4) Can also see SCHISTOCYTES, KERATOCYTES, AND ACANTHOCYTES

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54
Q

differential for RBCs that are NORMOCYTIC and NORMOCHROMIC?

A

ANEMIA OF CHRONIC DISEASE, or many other types of anemia

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55
Q

INCREASED MCV differentials (5)? another word for increased MCV?

A

MACROCYTIC, RBCs are larger than normal (immature likely)

(1) Erythroid regeneration
SUPPORT: RETICULOCYTOSIS, +/- concurrent DECREASED MCHC

(2) RBC agglutination (artificially high MCV)

(3) Cobalamin or folate deficiency

(4) Poodle

(5) FeLV infection

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56
Q

INCREASED MCHC differential (with 3 causes)? another term increased MCHC?

A

HYPERCHROMASIA/HYPERCHROMIC

IN VITRO (outside cells) or IN VIVO (in cells) ARTIFACT

(1) Intravascular hemolysis –> Hb is in blood because HEMOLYSIS

(2) Numerous Heinz bodies

(3) Lipemia (spectral interference)

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57
Q

Why do we see microcytic cells (LOW MCV) in iron deficiency anemia?

A

because we need IRON to make HEMOGLOBIN, so WITHOUT ENOUGH IRON = NOT ENOUGH HEMOGLOBIN, and that means WE DON’T REACH CRITICAL CONCENTRATION OF HEMOGLOBIN AT LATE RUBRICYTE STAGE to tell cell to STOP DIVIDING

often see MICROCYTIC AND HYPERCHROMIC CELLS (smaller and pale)

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58
Q

Why do we see macrocytic cells (HIGH MCV) in erythroid regeneration?

A

if we have ACCELERATED ERYTHROPOIESIS, then we might have RBCs that have SKIPPED DIVISIONAL STAGES and are LARGER THAN NORMAL

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59
Q

causes of iron deficiency anemia (2, first one has 3 subclasses)

A

(1) Chronic external blood loss
–> GI or external parasitism
–> GI neoplasia causing loss of blood
–> GI ulcers

(2) Nutritional deficiency (RARE)

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60
Q

should we classify anemia as hyperchromic if increased MCHC? why or why not? what would be 3 reasonable explanations for this finding?

A

NO, RBCs cannot be oversaturated with Hb, so this must be due to INCREASED Hb in the PLASMA!

Could be from something like a traumatic blood draw, intravascular hemolysis, or even the presence of heinz bodies

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61
Q

what are normoblasts?

A

NUCLEATED RBCs, or METARUBRICYTES

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62
Q

nRBCs = REGENERATION, true or false?

A

NO, nRBCs whether INCREASED OR NOT does not indicate regeneration, although it CAN

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63
Q

why do we need corrected WBC counts for in-house hematology analyzers?

A

because they count WBCs as all NUCLEATED CELLS, but this accidentally includes nucleated RBCs (metarubricytes/normoblasts)

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64
Q

metarubricytosis definition

A

presence of nRBCs >1/100 WBCs in peripheral blood

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65
Q

APPROPRIATE metarubricytosis (what condition is it present with, 1 main support)

does this mean we have regenerative?

A

presence with REGENERATIVE ANEMIA

SUPPORT
- reticulocytosis

**METARUBRICYTOSIS ALONE DOESN’T MEAN WE HAVE REGENERATION!!

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66
Q

INAPPROPRIATE metarubricytosis (2 conditions it’d be in, 5 causes with the FIRST CAUSE HAVING A BUNCH OF REASONS FOR OCCURRING)

A

CONDITIONS
(1) presence of nRBCs (>1/100 WBCs) WITHOUT RETICULOCYTOSIS; no evidence of regenerative anemia

(2) NORMAL PCV (we have enough RBCs in blood volume)

CAUSES
(1) Damage to the MEMBRANE that separates HEMATOPOIETIC SPACES from MARROW SINUSES
–> HEAVY METAL TOXICITY (lead)
–> SEVERE ANEMIA (hypoxic bone marrow injury)
–> NEOPLASIA IN BONE MARROW
–> MARKED HYPERTHERMIA (heatstroke, malignant hyperthermia)
–> ENDOTOXEMIA/SEPSIS
–> MARROW INFECTION WITH INFILTRATES OF INFLAMMATORY CELLS

(2) SPLENIC injury

(3) Recent FRACTURE or BONE INJURY

(4) ERYTHROID LEUKEMIA (CATS)

(5) STEROID THERAPY

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67
Q

red cell distribution width (RDW) definition, formula

A

this measurement provides instrument estimate amount of variation in RBC size

RDW = (SDMCV / MCV)

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68
Q

when does RDW increase? what does it mean when it increases?

A

INCREASES when we have anemias with microcytosis (smaller than normal RBCs present), macrocytosis (larger than normal RBCs present), or reticulocytosis

HIGHER RDW = MORE VARIABILITY IN RBC SIZE

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69
Q

which 4 b/w values are most commonly used to evaluate RBC DENSITY/numbers? which two are both nearly identical and MOST COMMONLY USED to provide relevant clinical information (and why not the other two?)?

A

4 values?
PCV, HCT, HGB, RBC

2 most important/similar values?
PCV (manual), HCT (measured)

HGB = 1/3 of RBC count
RBC count = in MILLIONS, hard to appreciate change unless it’s less RBCs we’re observing

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70
Q

which b/w value should we evaluate to determine if there’s ERYTHROID REGENERATION?

A

RETICULOCYTES

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71
Q

rouleaux appearance of RBCs

A

stacked RBCs like stacks of coins

common in cats and horses during inflammation

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72
Q

agglutination appearance of RBCs (& 2 reasons)

A

grape-like clusters of RBCs due to either…

(1) AUTO- or ALLO-ANTIBODY BINDING

(2) ARTIFACT

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73
Q

ghost cell RBC appearance

A

remnant of an RBC, can be due to artifact or intravascular hemolysis

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74
Q

polychromatophil appearance on smear

A

POLYCHROMATOPHILS ARE RETICULOCYTES WITH ENOUGH ORGANELLES/RNA TO SHOW PATTERN (POLYCHROMASIA)

LOOKS BLUE

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75
Q

microcyte appearance on smear

A

SMALLER than usual RBC

Often has central pallor

if there’s enough microcytes could correspond to DECREASED MCV

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76
Q

macrocyte appearance on smear

A

LARGER than usual RBC

Often appears POLYCHROMATOPHILIC (immature RBC)

if there’s enough microcytes can correspond to INCREASED MCV

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77
Q

acanthocyte

  1. Disease if with schistocytes and keratocytes?

2; Disease if with keratocytes, schistocytes, microcytes, and hypochromasia?

A
  • SPLENIC AND HEPATIC DISEASE
  1. schistocytes + keratocytes + acanthocytes = intravascular trauma/RBC shearing
  2. keratocytes + schistocytes + microcytes + hypochromasia = IRON DEFICIENCY ANEMIA
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78
Q

eccentrocyte (when do they form?)

A

forms SECONDARY to RBC OXIDATIVE INJURY from FUSED HB

79
Q

4 causes of echinocytes, which one is most common?

A
  1. dehydration
  2. electrolyte disturbance
  3. POISONOUS snake bite
  4. ARTIFACT MOST COMMON
80
Q

keratocyte

  1. give two alternate names
  2. what two diseases is this most commonly associated with?
A
  1. blister or helmet cell
  2. splenic or hepatic disease, including hemangiosarcoma and other infiltrative diseases
81
Q

pyknocyte

  1. remnant of a ___
  2. why does it form?
  3. what happens to its membrane?
  4. what kind of cell does it resemble?
A
  1. remnant of an eccentrocyte
  2. from oxidative injury
  3. remnant membrane detaches from cell
  4. spherocyte
82
Q

schistocytes

  1. is actually fragments of a ___
  2. formed due to… (and give 3 examples of diseases that’d cause this)
  3. commonly found in what kind of anemia?
A
  1. RBC
  2. RBC trauma/shearing from endocarditis, vasculitis, glomerulonephritis, etc.
  3. iron deficiency
83
Q

spherocyte

  1. how is it formed?
  2. why is it round?
  3. what disease is indicated if there’s increased spherocytes?
A
  1. formed via Ab binding to RBC
  2. once Ab binds, loses membrane and becomes round
  3. IMHA
84
Q

target cell

its formation is caused by what 2 explanations?

A
  1. ACCELERATED ERYTHROPOEISIS causes excess MEMBRANE for the volume, makes target shape
  2. hepatic disease
85
Q

basophilic stippling

3 causes (hint: dogs, cattle, cats)

A

(1) precipitation of ribosomes in CATTLE

(2) regenerative anemia in DOGS, CATTLE, AND CATS

(3) lead poisoning which causes inhibition of enzymes in heme synthesis pathway

86
Q

Howell jolly bodies in blood smears

  1. what are they?
  2. what causes them? (4, ONE with steroid use, MULTIPLE with HEMATOPOEITIC ORGAN)
A
  1. nuclear remnants in RBCs (little dots)
  2. CAUSES =

(1) regenerative anemia
(2) splenic disease
(3) splenectomy
(4) steroid use

87
Q

water artifact in blood smears

A

found when cells aren’t dried sufficiently for blood smears

88
Q

infectious erythrocyte organisms in CATS

**Hint, one of these isn’t in the USA!

A

(1) Mycoplasma hemofelis (+ small forms)

(2) Cytauxzoon felis

(3) Babesia sp. (not in the USA)

89
Q

infectious erythrocyte organisms in DOGS (5)

A

(1) Babesia gibsoni

(2) Babesia canis

(3) Babesia microti

(4) Theileria sp

(5) Mycoplasma hemocanis

90
Q

infectious erythrocyte organisms in CATTLE (3)

A

(1) Anaplasma marginale

(2) Anaplasma centrale

(3) Theileria spp.

91
Q

infectious erythrocyte organisms in HORSES (2)

A

(1) Theileria spp

(2) Babesia equi

92
Q

infectious erythrocyte organism in CAMELIDS (1)

A

(1) M. hemollamae

93
Q

infectious erythrocyte organism in PIGS (1)

A

(1) M. suis

94
Q

anemia DEFINITION

A

reduced HGB, RBC, and HCT (or PCV)

95
Q

common associated clinical signs with anemia? (8)

A

(1) Pale mucous membranes (pallor)

(2) Weakness

(3) Exercise intolerance

(4) Lethargy

(5) Tachypnea

(6) Tachycardia

(7) Syncope

(8) Sudden death

96
Q

response by the body to anemia?

**hints:
start with DECREASED O2 TENSION DETECTION in WHAT ORGANS, then how many days to see increase in reticulocytes, blood smear changes, MAXIMUM time for regeneration?

A

(1) Lowered oxygen tension in arterial blood is detected by renal cortical cells, which then produce and release EPO

(2) EPO stimulates erythropoiesis in bone marrow (sometimes also spleen or liver) and EARLY RELEASE of already produced RETICULOCYTES (24 hours earlier than normal); not necessarily causing reticulocytosis yet though

(3) Within 2-3 days, numbers of circulating reticulocytes should increase (due to increased PRODUCTION being able to take place) and we should see INCREASE in polychromasia on routinely-stained blood smears

(4) Maximum bone marrow response is at 7-10 days

97
Q

3 main causes of anemia

A

(1) blood loss/hemorrhage

(2) decreased production of RBCs

(3) hemolysis

98
Q

4 SPECIFIC causes of blood loss/hemorrhage causing anemia (WITH A LOT OF EXAMPLES)

A

(1) BLOOD VESSEL DAMAGE
–> Trauma
–> GI ulcers
–> Neoplasia
–> Inflammation
–> Wounds

(2) HEMOSTATIC ABNORMALITIES (can’t clot)
–> Acquired or congenital COAGULATION FACTOR DEFICIENCIES
–> Severe THROMBOCYTOPENIA (<25,000/uL)
–> Platelet function defect (vWD)

(3) PARASITISM
–> Hookworms
–> Haemonchus
—> Ostertagia
–> Coccidiosis
–> Severe external parasitism with fleas/ticks

(4) IATROGENIC
–> Repeated sampling in small patients
–> Blood donation

99
Q

regenerative vs. non-regenerative causes of anemia?

A

NON-REGENERATIVE = DECREASED PRODUCTION OF RBCS, literally not being able to regenerate RBCs adequately

REGENERATIVE =
1. HEMOLYSIS
2. BLOOD LOSS/HEMORRHAGE

100
Q

anemia definition

A

decrease in number of RBCs in the body

101
Q

8 things to determine cause of anemia

A

(1) SEVERITY
can be MILD, MODERATE OR MARKED

(2) PROTEIN
- ALBUMIN AND GLOBULIN DECREASED = GI BLEED

(3) REGENERATIVE status
- Regnerative = blood loss or hemolysis, RETICULOCYTES
- Non-regenerative = decreased production
**NOT IN HORSES

(4) PATIENT information
- YOUNG ANIMAL = have lower PCV or decreased MCV, OR GI bleed
- OLDER ANIMAL = neoplasia

(5) RBC MORPHOLOGY
- Evidence of regeneration, iron deficiency, hemic parasites, evidence of oxidative injury, immune-mediated RBC targeting

(6) RBC INDICES
o IF NORMAL (MCV and MCHC), SUGGESTS ANEMIA OF CHRONIC DISEASE/OR NOT RELEVANT
- Macrocytic, hypochromic + reticulocytosis = regenerative
- Microcytic, hypochromic = iron deficiency

(7) Serum bilirubin
- BREAKDOWN PRODUCT OF HEME, so increases can be due to HEMOLYSIS

(8) BUN, creatinine, USG
- KIDNEY FUNCTION

102
Q

what 3 things can cause lowered oxygen tension in body?

A

(1) ANEMIA (not enough RBCs)

(2) Decreased PiO2 (less oxygen available in INSPIRED air)

(3) Heart failure (poor circulation)

103
Q

erythroid hyperplasia vs erythroid hypoplasia

A

in response to decreased RBCs, there is either INCREASED erythropoiesis (PROPER RESPONSE, HYPERPLASIA) or not (HYPOPLASIA)

104
Q

routine RBC stain is called?

A

DiffQuik

105
Q

horses and reticulocytes

A

HORSES DO NOT RELEASE RETICULOCYTES

106
Q

difference between impedance analyzers and optical analyzers?

A

impedance cannot tell difference between any nucleated cell (will count nRBCs as WBCs), while optical can!

107
Q

most common causes of iron deficiency anemia? (3)
**Patient ages, human causes?

A
  1. Younger patients = PARASITES, HOOKWORMS causing HEMORRHAGE
  2. Older patients = NSAID therapy, neoplasia
  3. IATROGENIC CAUSES
108
Q

how do we get iron in our bodies? **hint: young animal and unlikely cause of iron deficiency?

A

most of it is RECYCLED upon HEMOLYSIS, small amount is NUTRITIONAL

In YOUNGER animals with lower PCV, they may be more dependent on NUTRITIONAL sources of iron, but not a likely cause

109
Q

what happens in EXTREME cases of iron deficiency?

A

we LOSE THE ABILITY TO REGENERATE RBCs, likely to see NON-REGENERATIVE ANEMIA

110
Q

effect of low iron on the INTEGRITY of RBCs?

A

they’re more FRAGILE, likely to exhibit POIKILOCYTOSIS

111
Q

reactive thrombocytosis (2 causes)

A

(1) IL-6 and IL-12 –> INFLAMMATION for INCREASED PLATELET PRODUCTION

(2) Chronic EXTERNAL blood loss

112
Q

in ACUTE blood loss, ___ may or may not develop
(**this is a weird one)

A

ANEMIA

113
Q

clinical signs of ACUTE blood loss (with low PCV? give 5)

A

signs of LOW OXYGEN CARRYING CAPACITY

(1) sudden lethargy
(2) syncope
(3) tachycardia
(4) tachypnea
(5) weak pulse

114
Q

in acute blood loss/hemorrhage, why don’t we see PCV decrease until hours to days after hemorrhagic event

A

because we lose blood components PROPORTIONALLY, so that after plasma fluid redistributes from the TISSUES into the VASCULAR SPACE, we see DILUTION OF NOW LOWER, REMAINING RBCs

115
Q

what do platelets do in acute blood loss?

A

VARIABLE

INCREASED = splenic contractions

DECREASED = being used up to stop the bleeding

or normal :)

116
Q

what 3 things can cause iron deficiency anemia to occur? VERY BASIC

A

(1) decreased erythropoiesis

(2) increased RBC fragility

(3) ongoing chronic bleeding that was never amended

117
Q

lab findings for hemolysis-caused anemia? (5)

A
  1. reticulocytosis if REGENERATIVE
  2. hyperbilirubinemia/uria
  3. abnormal RBC morphology
  4. NORMAL proteins
  5. +/- hemoglobinemia
118
Q

signs of IVH and EVH (extra- and intra-vascular hemolysis) on labs?

A

IVH
- bilirubinuria
- hyperbilirubinemia
- hemoglobinemia
- hemoglobinuria

EVH
- bilirubinuria
- hyperbilirubinemia
- TOTAL PROTEIN SHOULD BE NORMAL BC NO BLOOD LOSS

119
Q

how long do RBCs live? how much is killed per day?

A

3-4 months, ~1% killed per day NORMALLY

120
Q

which organ mostly gets rid of senescent RBCs? what are the other 2 organs?

A

SPLEEN

liver, bone marrow

121
Q

steps for breakdown of RBC? (7, think about pigments of excrements)

A
  1. Heme + globin separated
  2. GLOBIN recycled
  3. Heme broken down into IRON AND BILIRUBIN
  4. IRON recycled
  5. BILIRUBIN is NON-SOLUBLE but is a waste process, so it GOES TO LIVER to get CONJUGATED (to make it soluble)
  6. Bilirubin leaves through biliary tree and through INTESTINES, converted through actions of bacteria and MAKES POOP BROWN
  7. Some bilirubin is reabsorbed and enters blood, goes to kidney and MAKES PEE YELLOW
122
Q

dogs will have both SERUM bilirubin INCREASED when we see them have INCREASED URINE SPECIFIC GRAVITY of +1 or +2 (T/F)

A

FALSE.

SERUM BILIRUBIN SHOULD NEVER BE INCREASED

123
Q

3 basic causes of hemolysis?

A

(1) immune-mediated
(2) infectious RBC disease
(3) OXIDATIVE RBC injury

124
Q

rate-limiting step of RBC breakdown?

A

bilirubin getting out of hepatocyte into bile canaliculi

if it’s not able to pass through, BACKS UP AND GETS BACK INTO BLOOD –> hyperbilirubinemia

CAUSES INCREASE IN CONJUGATED BILIRUBIN (water-soluble)

125
Q

haptoglobin system? (what is it used in, how does it work, what does it cause in b/w?)

A

USED IN INTRAVASCULAR HEMOLYSIS

haptoglobin “ties up” free Hb in blood since it’s potentially toxic, takes it to liver to be broken down

STILL CAUSES HYPERBILIRUBINEMIA AND BILIRUBINURIA

once haptoglobin is USED UP and cannot capture hemoglobin, then we have HEMOGLOBIN FREELY IN BLOOD and will PASS THROUGH TO KIDNEYS and we see HEMOGLOBINURIA and HEMOGLOBINEMIA

126
Q

when do we expect to see ghost cells?

A

when we have INTRAVASCULAR HEMOLYSIS, “exploded” RBCs

127
Q

what do we see in hemoglobinuria? what causes this?

A

red urine with NO RBCs and a BLOOD DIPSTICK

INTRAVASCULAR HEMOLYSIS

128
Q

infectious causes of hemolysis in dogs, cats, horses, cattle, camelids? (name morphology with dogs, one with cats

A

DOGS
1. mycoplsma hemocanis
–> often from SPLENECTOMY or STEROID USAGE

  1. babesia
    –> CANIS = in greyhounds, tear-drop shaped thing in RBC
    –> GIBSONI = looks like a signet ring-shaped thing in RBC

CATS
–> Mycoplasma hemofelis
–> Cytauxzoon = causes NON-REGENERATIVE ANEMIA)

HORSES
–> Babesia equi
–> Theileria

CATTLE
–> Mycoplasma wenyonii
–> Babesia
–> Theileria

CAMELIDS
–> Hemollama

129
Q

lab findings that indicate RBC oxidative injury? (6, including RBCs found on blood smear)

A
  1. INCREASED MCHC (from increased Hb or Heinz bodies)
  2. hemoglobinemia (INTRAVASCULAR ONLY)
  3. hemoglobinuria (INTRAVASCULAR ONLY)
  4. bilirubinuria
  5. hyperbilirubinemia
  6. RBCs on blood smear –> eccentrocytes, Heinz bodies, pyknocytes
130
Q

CAUSES of oxidative RBC injury in dogs, cats, horses, sheep/goats?

A

DOGS
- onions
- garlic
- ZINC (found in OLD PENNIES)

CATS
- onions
- garlic
- tylenol/acetaminophen

HORSES
- dry red maple leaves

SHEEP/GOATS
- COPPER (found in OLD FEED)

131
Q

what is the most common cause of hemolytic anemia?

A

IMMUNE-MEDIATED

132
Q

difference between PRIMARY and SECONDARY IMHA?

A

PRIMARY = idiopathic, often in dogs

SECONDARY = from DRUGS or ALLOANTIBODIES against RBCs

133
Q

IMHA using the COMPLETE phagocytosis mechanism and lab findings (where are RBCs broken down, how it happens, lab findings)

A

NORMAL RBC BREAKDOWN (EXTRAVASCULAR)

Broken down in SPLEEN, liver, or bone marrow

RBC broken into heme + globin –> globin RECYCLED, heme broken down into BILIRUBIN

Lab findings
- hyperbilirubinemia
- bilirubinuria

134
Q

IMHA using PARTIAL phagocytosis mechanism and lab findings (mention appearance of RBCs, intra vs extra vascular?)

A

Only a PORTION of RBC broken down, causes biconcave disc –> SPHEROCYTE appearance

occurs in EXTRAVASCULAR HEMOLYSIS

135
Q

IMHA using INTRAVASCULAR hemolysis (is it common? what happens? what do we often see on a bigger whole blood scale?)

A

LESS COMMON CAUSE OF IMHA

occurs when IgM (large antibody) binds to RBCs and causes HEMOLYSIS

often also see AGGLUTINATION

136
Q

how can we test for IMHA? what does it do?

A

AUTO-AGGLUTINATION OR COOMB’S TEST

it tests for the ANTIBODY present on the RBC

137
Q

4 causes of NON-regenerative anemia?

A

(1) iron deficiency
(2) chronic renal failure
(3) anemia of chronic disease
(4) bone marrow disease

138
Q

chronic renal failure and non-regenerative anemia (causes, MCV/MCHC characteristics, lab findings INCLUDING USG)

A

can be caused by LACK OF FUNCTIONAL CORTICAL TISSUE or LACK OF FUNCTIONAL NEPHRONS

ALMOST ALWAYS NORMOCYTIC AND NORMOCHROMIC

lab findings
- AZOTEMIA = increase in nitrogenous waste products, BUN and creatinine

  • LACK OF CONCENTRATING ABILITY = kidneys can’t concentrate, decreased USG
  • ISOSTHENURIA = concentration of urine is no more than concentration of PLASMA
  • USG findings?
    –> Less than 1035 in cats
    –> Less than 1030 in dogs
    –> Less than 1025 in large animals
138
Q

in pancytopenia, order of cells lost time-wise? how long do they usually live? where are they made?

A

NEUTROPHILS –> PLATELETS –> RBCs

Neutrophils = 12 hours
Platelets = 5-7 days
RBCs = 3-4 months

made in BONE MARROW

139
Q

bone marrow disease and non-regenerative anemia (how is it diagnosed, MCV/MCHC characteristics, diseases and the most common disease that causes it, most important lab finding)

A

must be diagnosed through BONE MARROW EXAMINATION, not blood smear

ALMOST ALWAYS NORMOCHROMIC AND NORMOCYTIC

Diseases?
- lymphoma
- fibrosis
- infections
- MOST COMMON = INFILTRATING NEOPLASIA

Lab finding that’s most important?
- PANCYTOPENIA

140
Q

erythroid hypoplasia (what it is, 2 main causes)

A

a type of NON-REGENERATIVE ANEMIA that targets RBC production in bone marrow

either idiopathic or immune-mediated

141
Q

anemia of chronic disease (MCV and MCHC characteristics, how common it is, most common form/cause, lab findings that suspect, and what CONCURRENT lab findings would suspect)

A

ALMOST ALWAYS NORMOCYTIC AND NORMOCHROMIC

MOST COMMON TYPE OF NON-REGENERATIVE ANEMIA

USUALLY FROM INFLAMMATORY DISEASE; the body sequesters iron so that bacteria cannot get to iron and this causes lower RBC production

lab findings?
- NON-REGENERATIVE
- NORMOCYTIC
- NORMOCHROMIC
- NOT VERY SEVERE ANEMIA (greater than or equal to 23/24% in dogs/cats)

LOOK FOR INFLAMMATION, STRESS, OR SIGNS OF SYSTEMIC ILLNESSES

142
Q

3+ blood in urine?

A

(1) RBCs –> CHECK SEDIMENT FOR RBCs

(2) Hb -

143
Q

what do we expect if we suspect IMHA?

A

SPHEROCYTES

144
Q

why might we see increased platelets? this is sort of random

A

INFLAMMATION

145
Q

polycythemia definition

A

INCREASED PCV/HCT

AKA ERYTHROCYTOSIS

146
Q

RELATIVE vs. ABSOLUTE polycythemia? (name 2 causes of each)

A

RELATIVE = APPEARS that there’s a PROPORTIONAL INCREASE IN RBCs, but really only due to…

(1) dehydration

(2) redistribution –> splenic contraction

ABSOLUTE = INCREASE in QUANTITY OF RBCs

(1) PRIMARY –> RARE, INCREASED production of RBCs from BONE MARROW due to NEOPLASTIC CELLS

(2) SECONDARY –> 2 TYPES

I. APPROPRIATE = increase in RBCs due to LOW O2 (chronic hypoxia)
–> High altitude
–> Chronic lung disease
–> Heart failure (R –> L shunt, CHF)

II. INAPPROPRIATE = RBCs made in response to EPO produced by the kidneys INAPPROPRIATELY

147
Q

dehydration CBC/chem findings? what is the main finding that defines this?

A

RELATIVE CAUSE OF POLYCYTHEMIA/ERYTHROCYTOSIS

Increases of other values, such as…

(1) INCREASE IN TOTAL PROTEIN
–> Albumin and globulin proportionally increases

(2) INCREASE IN Na/Cl
–> Primary electrolytes in plasma

(3) INCREASE IN USG
–> This means URINE IS MORE CONCENTRATED
–> > 1.035 in cat, > 1.030 in dog, > 1.025 in LA
–> IF USG IS HIGHER THAN THESE VALUES, then the KIDNEY IS WORKING PROPERLY/concentrating urine

(4) +/- AZOTEMIA (increased BUN and creatinine)
–> Could be due to decreased blood flow being filtered by kidney

148
Q

redistribution CBC/chem findings? what is the main finding that defines this?

A

RELATIVE CAUSE OF POLYCYTHEMIA

splenic CONTRACTION
(1) INCREASE RBCs

(2) INCREASE platelets

(3) INCREASE in mature neutrophils
–> Pushed off of walls/margination

(4) INCREASE in LYMPHOCYTES

(5) INCREASE in GLUCOSE
- Who does this happen to?
–> YOUNG ANIMALS
–> CATS
–> HORSES
–> **Cats, horses, and young animals are highly spirited and more likely to release epinephrine!

149
Q

polycythemia vera definition & what animals it’s most common in

A

this is an example of ABSOLUTE polycythemia

PRIMARY = when bone marrow increases production of RBCs to make quantity of RBCs increase, NEOPLASM

COMMON IN OLDER ANIMALS, BUT RARE OVERALL

150
Q

if we have erythrocytosis/polycythemia and NOTHING ELSE, then what is the likely cause?

A

DEHYDRATION

151
Q

pre-renal azotemia causes? (3)

A

HYPOVOLEMIA

DEHYDRATION

GI BLEED (causes HIGH AMOUNTS OF RBC/PROTEIN TO BE BROKEN DOWN)

152
Q

what animals are most likely to have PHYSIOLOGIC/REDISTRIBUTIVE reason for polycythemia/erythrocytosis? (3)

A

YOUNG ANIMALS

CATS

HORSES

THEY ALL FREAK OUT

153
Q

where do platelets come from? (2 locations, and development)

A

BONE MARROW & SPLEEN

MegakaryoBLASTS –> MegakaryoCYTES

Megakaryocytes have PLATELETS IN CYTOPLASM, so once they are destroyed, BLEB OUT PLATELETS INTO CIRCULATION

154
Q

how many platelets in spleen vs. circulation?

A

1/3 in spleen compared to blood

155
Q

thrombopoeitin (where is it made, who binds it, what does it do)

A

made in bone marrow, liver, and spleen

bound up by megakaryocytes and platelets

when FREE (not a lot of platelets or megakaryocytes around to bind it), then PUSHES DEVELOPMENT OF MEGAKARYOCYTES to generate platelets

156
Q

platelet enumeration (what machine does it, issues it can have, what we should do instead)

A

done automatically by a hematology analyzer on EDTA tube blood

machine will treat CLUMPS or LARGE PLATELETS as RBCs

we should do BLOOD SMEAR at 100X HIGH POWER field, multiply number found by 15-20,000

157
Q

thrombocytopenia definition, normal range, mild, moderate, and severe

A

decrease in PLATELETS

NORMAL = 120,000 - 150,000

MILD = 80,000 - 120,000

MODERATE = <50,000

SEVERE = <25,000

158
Q

what does moderate thrombocytopenia indicate vs. severe in terms of platelets or bleed being the primary cause?

A

MODERATE = BLEED IS THE PRIMARY CAUSE AND PLATELETS ARE BEING USED UP

SEVERE = DECREASED PLATELETS CAUSED THE BLEED

159
Q

clinical signs of thrombocytopenia?

A

SURFACE BLEEDING (oozing of mucosal surfaces)
- GI
- Oral
- Bladder

PETECHIAE/ECCYMOSES

160
Q

4 MAIN DIFFERENTIALS FOR THROMBOCYTOPENIA

A

(1) ARTIFACT

(2) CONSUMPTION

(3) PERIPHERAL DESTRUCTION

(4) DECREASED PRODUCTION

161
Q

artifact in thrombocytopenia (what we see on smear, why it appears, and HOW we measure it/determine if it’s present)

A

CLUMPING OR LARGE PLATELETS

Hematology analyzer will count it incorrectly

MEASURE VIA PLATELET NUMBER x 15-20,000 and SEE IF IN NORMAL RANGE; ALSO ASSESS BLOOD SMEAR

162
Q

consumption in thrombocytopenia (what kind of thrombocytopenia we expect, 3 diffs and CBC expectations)

A

associated with MILD to MODERATE thrombocytopenia

3 differentials
(1) BLEEDING EVENT
- MILD thrombocytopenia (bleeding first)
- LOW serum proteins
- PRE-REGENERATIVE/REGENERATIVE anemia

(2) DISSEMINATED INTRAVSCULAR COAGULATION (DIC)
- VARIABLE thrombocytopenia
- INCREASED PTT, +/- INCREASED PT
- Schistocytes (from RBC shearing)
- INCREASED D-Dimers

(3) VASCULITIS
- MILD thrombocytopenia
- INFLAMMATORY signs

163
Q

peripheral destruction in thrombocytopenia, 2 differentials, 2nd differential has 4 subs

A

SEVERE, IMMUNE-MEDIATED THROMBOCYTOPENIA

  1. IDIOPATHIC
  2. SECONDARY to another disease…

(1) Infection (Rickettsial)
- Ehrlichia/anaplasma
- can still have NEGATIVE SNAP test because they can be in neutrophils/macrophages
- VARIABLE THROMBOCYTOPENIA

(2) Neoplasia

(3) Drugs

(4) Vaccines?

164
Q

decreased production in thrombocytopenia, 2 differentials

A

due to BONE MARROW issue, uncommon

differentials –> DEPEND ON WHAT’S TARGETED

  1. Megakaryocytes TARGETED specifically, can’t make as many platelets
  2. WHOLE MARROW…

(1) Myelophthisis = marrow CAN’T MAKE MORE CELLS BC SOMETHING ELSE IS THERE (other cells, fibrosis)

(2) Hypoplasia = bone marrow just not making enough cells, so expect to see…
- Neutropenia
- Anemia
- Severe thrombocytopenia

165
Q

thrombopathia basic definition

A

ABNORMAL platelet function

166
Q

EXTRINSIC thrombopathia

A

caused by VON-WILLEBRAND FACTOR DEFECTS

vWF = helps platelets bind to subendothelial collagen to form platelet plug

CBC/chem findings
- NORMAL platelet numbers
- NORMAL PTT/PT
- ABNORMAL buccal mucosal bleeding time
- ABNORMAL platelet function assay
- ABNORMAL special vWF tests

167
Q

molecular components inside of platelets (3)

A
  1. ALPHA granules
  2. DENSE granules
  3. TRANSMEMBRANE proteins
168
Q

INTRINSIC thrombopathia (2 differentials, examples for second one)

A

CONGENITAL
- issues with GRANULE or TRANSMEMBRANE protein function INSIDE PLATELETS
- RARE

ACQUIRED
- from DISEASE or DRUGS
- DISEASE = RENAL FAILURE
- DRUGS = acetominophen

169
Q

3 main things that would point us toward thrombopathia?

A
  1. BLEEDING with NO INDICATORS OF TRAUMA
  2. NORMAL SECONDARY HEMOSTASIS (not mediated by platelets)
  3. EVIDENCE OF PLATELET ABNORMAL FUNCTION (vWF test, buccal mucosal bleeding time, etc.)
170
Q

Thrombocytosis (3 differentials)

A

= INCREASE in number of platelets

  1. REACTIVE
    - from diseases involving INFLAMMATION
    - from CHRONIC EXTERNAL BLOOD LOSS (release EPO, resembles thrombopoietin)
    - Ex = IRON DEFICIENCY ANEMIA
    –> can cause IL-6 and EPO release, mimicking THROMBOPOIETIN and causing increase
    –> On CBC/chem, look for DECREASED MCV/MCHC and SIGNS OF CHRONIC INFLAMMATION
  2. REDISTRIBUTION
    - Ex = SPLENIC CONTRACTION secondary to EPINEPHRINE RELEASE
    –> Neutrophilia
    –> Lymphocytosis
    –> Thrombocytosis
    –> Polycythemia
    –> Increase in blood glucose
  3. CANCER
    - platelets become neoplastic, RARE
171
Q

3 things that secondary hemostasis depends on?

A

(1) Vessels/integrity
(2) Platelets
(3) Clotting factors

172
Q

clotting factors (where they’re made, what they work alongside of, function, what’s needed for them to work properly)

A

made by the LIVER

work alongside PLATELETS

help to form fibrinogen –> fibrin CLOT, make it NON-SOLUBLE

need adequate AMOUNT and NORMALLY FUNCTIONING clotting factors

173
Q

what clotting factors are in the intrinsic pathway? how is it tested WITH THE COMMON PATHWAY?

A

12, 11, 9, 8

PTT/ACT

174
Q

what clotting factors are in the extrinsic pathway? how is it tested WITH THE COMMON PATHWAY?

A

tissue factor (TF), 7

PT

175
Q

what clotting factors are in the common pathway?

A

10, 5, 2

176
Q

vitamin-K activated clotting factors (4)

A

2, 7, 9, 10

177
Q

clotting disorders and hypocalcemic animals?

A

HYPOCALCEMIC ANIMALS WILL NOT HAVE CLOTTING DISORDERS

Ca is only a co-factor for clotting

178
Q

coagulation tests are generally ___

A

INSENSITIVE, we need a big loss of clotting factors to show PROLONGATION

179
Q

PTT increase?

A

caused by >75% loss in INTRINSIC/COMMON PATHWAY factors

12, 11, 9, 8, 10, 5, 2

180
Q

PT increase?

A

caused by >75% loss in EXTRINSIC/COMMON PATHWAY factors

TF, 7, 10, 5, 2

181
Q

TT (thrombin time) increase?

A

DISSEMINATED INTRAVASCULAR COAGULOPATHY or issue with fibrinogen

182
Q

3 differentials for RED urine dipstick?

A

(1) RBCs

(2) Hb

(3) Myoglobin

183
Q

Hb and Myoglobin will NOT clear with ___

A

Sedimentation

184
Q

measurement of FIBRINOGEN in relation to CLOTTING?

A

Fibrinogen = clotting factor

Can either do a PRECIPITATE (precipitates fibrinogen out of blood) or AUTOMATED**

185
Q

ACT increase? (there’s an extra reason for increase here, and difference between this test and other clotting tests)

A

> 95% of INTRINSIC or COMMON PATHWAY factors GONE to see ELEVATION

TF, 7, 10, 5, 2

ALSO INCREASED IF PLATELET NUMBER IS LESS THAN 10,000

Done MANUALLY, gray-top tube that’s checked every 5 mins for clotting; diatomaceous earth inside tube!

186
Q

INCREASED PTT & NORMAL PT?

A

**STILL NEED >75% FACTORS GONE TO SEE ELEVATION

ABNORMAL INTRINSIC (12, 11, 9, 8)

12 = deficiency in cats seen, NO BLEED/NOT CLINICALLY SIGNIFICANT

11 = RARE, in some Holsteins/dogs

8/9 = COMMON, hemophilia A (8) and B (9)
–> 8 more common
–> Often X-linked and congenital (more common in young males)
–> we could do FACTOR LEVELS to determine which one it is

187
Q

ACT INCREASED but NORMAL PTT? (weird one)

A

PLATELET COUNT LESS THAN 10,000, REGARDLESS IF SECONDARY COAGULATION FACTORS ARE NORMAL OR NOT

188
Q

PT INCREASED but NORMAL PTT?

A

likely JUST EXTRINSIC PATHWAY ABNORMAL

TF and 7

Factor 7 deficiency more common, no real problems in TF

(1) INHERITED in beagles
(2) ACQUIRED** MORE COMMON
–> VITAMIN K ANTAGONISM, think of RODENTICIDES!
–> Factor 7 has the shortest half-life and is vitamin K-dependent

189
Q

BOTH PTT and PT INCREASED? (what can’t it be, 3 differentials w/ CBC inclusions in one particular organ-related differential)

A

cannot be INHERITED because we can’t have MULTIPLE FACTORS involved

(1) VITAMIN K ANTAGONISM/RODENTICIDE
- affects vitamin K-dependent factors (2, 7, 9, 10), which are in BOTH INTRINSIC AND EXTRINSIC PATHWAY

(2) LIVER FAILURE
- liver makes clotting factors
- also see DECREASE in things that liver is responsible for… (ABC GLUCOSE)
–> ALBUMIN
–> BUN
–> CHOLESTEROL
–> GLUCOSE

(3) DISSEMINATED INTRAVASCULAR COAGULOPATHY
- CLOTTING SYSTEM IS OVERACTIVE/UNREGULATED
- expect to see…
–> increased PT/PTT
–> SCHISTOCYTES (sheared RBCs) from clots shearing them
–> D-Dimers (clots broken down)
–> Thrombocytopenia (mild to severe) due to CONSUMPTION to MAKE CLOTS

190
Q

thrombin function & what clotting factor it is

A

converts FIBRINOGEN –> FIBRIN

THIS IS CLOTTING FACTOR 2 (common pathway)

191
Q

what should we be looking at when searching for DIC? (6)

A

+/- CBC/chem = signs of INFLAMMATION

Blood smear = SCHISTOCYTES

Platelets = THROMBOCYTOPENIA, using up platelets for clots

DECREASED fibrinogen

INCREASED D-DIMERS

DECREASED antithrombin

192
Q

DIC (why it’s “death in cage,” what it causes pathophys)

A

“death in cage”
Causes such severe ISSUES WITH CLOTTING that POOR PERFUSION –> CELL DEATH –> ORGAN DEATH

Causes?
UNREGULATED MAKING AND BREAKING OF CLOTS

193
Q

protein-losing nephropathy vs. enteropathy?

A

expect to see BOTH ALBUMIN AND GLOBULIN lost in ENTEROPATHY but NOT NEPHROPATHY

This is because bigger “holes” for globulin, then larger protein

194
Q

IMHA can sometimes cause INCREASED LIKELIHOOD OF ___, so we might expect to see increased ____

A

clotting!

D-Dimers

195
Q

keratocytes, acanthocytes, and schistocytes DDxs?

A

(1) iron deficiency anemia

(2) DIC

(3) hemangiosarcoma

(4) Glomerulonephritis

(5) Heart disease

(6) Microangiopathy (capillaries become thick and weak and bleed out contents)

Year 1/2 (139 decks)

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