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Year 1/2 > FTK 3: Clin Path S1 > Flashcards

FTK 3: Clin Path S1 Flashcards

1
Q

DOGS NON-NEOPLASTIC LYMPHOCYTOSIS CAUSES (number to look out for, 5 reasons)

A

NEUTROPHILS = < 20,000 cells/uL

  1. Physiologic (excitement, epinephrine)
  2. Chronic inflammation (antigenic stimulation)
  3. Young animal
  4. Rickettsial disease (granulocytic or monocytic Ehrlichia); dogs > cats
  5. Hypoadrenocorticism (Addison’s Disease)
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2
Q

CATS NON-NEOPLASTIC LYMPHOCYTOSIS CAUSES (neutrophil count, 7 causes)

A

NEUTROPHILS = < 30,000 cells/uL

  1. Physiologic (excitement, epinephrine)
  2. Chronic inflammation (antigenic stimulation)
  3. Young animal
  4. Rickettsial disease (monocytic or granulocytic Ehrlichia); dogs > cats
  5. Toxoplasmosis
  6. Hyperthyroidism or methimazole therapy
  7. Thymoma
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3
Q

What do immature lymphocytes look like compared to neutrophils? (3)

A
  1. LARGER
  2. CHROMATIN LESS CONDENSED, a different pattern (stippled)
  3. Can see NUCLEOLUS (a sign that lymphocyte wants to divide)
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4
Q

if we see mature lymphocytes on a slide, what two types of lymphocytosis causes would we be deciding between?

A
  1. chronic lymphoid leukemia = many mature leukocytes present in blood due to neoplasm
  2. reactive lymphocytosis = many mature lymphocytes present in blood due to non-neoplastic causes, such as…
    - hypoadrenocorticism (dogs)
    - toxoplasmosis (cats)
    - thymoma (cats)
    - hyperthyroidism or methimazole therapy (cats)
    - rickettsial diseases (granulocytic or monocytic Ehrlichia)
    - chronic inflammation
    - physiologic
    - young animals
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5
Q

biggest CBC difference between chronic inflammation and acute inflammation?

A

CHRONIC inflammation has >2x URL

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6
Q

physiologic leukogram CBC findings (5)

A
  1. neutrophilia (less than 2x URL) due to epinephrine
  2. NO LEFT SHIFT
  3. lymphocytosis (mild)
  4. hyperglycemia (from epinephrine)
  5. increased PCV/HCT and platelets (from splenic contraction); erythrocytosis/thrombocytosis
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7
Q

hypoadrenocorticism (Addision’s) b/w (8, what does it do in relation to cortisol, aldosterone, and one other thing); what does it do to HR? why?

A

decreased cortisol, could have decreased mineralocorticoids (aldosterone is main)

  1. neutrophils are NORMAL or neutrophilia
  2. eosinophilia (from lack of cortisol)
  3. mild, non-regenerative anemia = CHRONIC DISEASE
    regenerative anemia = GI BLEED
  4. hypoglycemia (from lack of cortisol)
  5. low total protein (from lack of cortisol)
  6. hyponatremia (due to lack of aldosterone)
  7. hyperkalemia (due to lack of aldosterone)
  8. pre-renal azotemia (elevated BUN and creatinine) from loss of sodium and water and lack of urine concentrating ability

BRADYCARDIC from being hyperkalemic and is still hypovolemic

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8
Q

what leukocyte is most important for determining pancytopenia?

A

NEUTROPHILS

even if we had leukopenia, anemia, and low platelets, this WOULDN’T COUNT

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9
Q

if we have a leukocytosis but no neutrophils, can we still suspect bone marrow issues?

A

YES, can have high amounts of other white cell lineages

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10
Q

leukemoid & what 6 DDx’s (4 p’s, 2 others AND ONE OF THEM IS WEIRD)

A

when we have >50,000 neutrophils of ALL LINEAGES

by definition, a form of CHRONIC inflammation because it’s taken time for bone marrow to produce that many neutrophils

  1. pyometra
  2. pancreatitis
  3. pylonephritis
  4. pyothorax
  5. IMHA (so anemic that we can’t oxygenate tissues –> tissue necrosis –> inflammation from necrosis)
  6. hematozoon infection
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11
Q

common findings for dehydration…

A
  1. erythrocytosis/polycythemia
  2. hyperalbuminemia
  3. if BOTH plasma proteins are increased (globulin and albumin)
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12
Q

albumin

A

negative acute phase liver protein

in the face of inflammation, liver decreases its production

in the face of dehydration, it’s increased

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13
Q

stress b/w findings (7)

A
  1. mild neutrophilia (less than 2x URL)
  2. NO LS
  3. +/- monocytosis
  4. +/- eosinopenia
  5. LYMPHOPENIA IS BEST SUPPORT
  6. Hyperglycemia (from cortisol)
  7. Increased ALP
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14
Q

acute/moderate inflammatory b/w findings (9, include all WBCs, plasma proteins, large animal)

A
  1. mild neutrophilia (less than 2x URL) –> NEED TO PROVE THIS
  2. LS, could be regenerative or deep
  3. toxic change
  4. lymphocytosis
  5. monocytosis
  6. in large animals, HYPERFIBRINOGENEMIA
  7. HYPERGLOBULINEMIA
  8. HYPOALBUMINEMIA
  9. variable glucose
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15
Q

overwhelming inflammation b/w findings (5 main, one with stress)

A
  1. NEUTROPENIA
  2. other lineages like RBCs and platelets should be UNAFFECTED
  3. +/- LS –> IF PRESENT, DEGENERATIVE
  4. +/- toxic change
  5. HYPOglycemia

**LYMPHOPENIA IF CONCURRENT STRESS

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16
Q

decreased production b/w findings (4 NOT MOSTLY CBC/CHEM VALUES, including a weird one)

A
  1. NEUTROPENIA (can or cannot have)
  2. DECREASES in other lineages like RBCs such as in non-regenerative anemia or thrombocytopenia
  3. presence of IMMATURE LYMPHOID CELLS (blast cells)
  4. INFECTIOUS AGENTS (cytauxzoon in cats and distemper inclusions)
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17
Q

ruminant b/w findings (4, including ratio numbers)

A
  1. NEUTROPENIA (can be pathologic or physiologic for them)
  2. +/- mild to marked LS
  3. +/- lymphopenia
  4. HYPERfibrinogenemia that’s increased in INFLAMMATION or DEHYDRATION

cows = 10-15
horses = 15-20

ABOVE URL = DEHYDRATION
BELOW LRL = INFLAMMATION

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18
Q

plasma protein trends

A

ALBUMIN alone
- increased = dehydration
- decreased = inflammation or protein-losing nephropathy

GLOBULIN alone
- increased = inflammation that’s immune-mediated, make more globulins

BOTH
- increased = dehydration
- decreased = whole blood loss or GI protein loss

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19
Q

chronic inflammation findings (6, 1 concurrent with stress)

A
  1. neutrophilia GREATER than 2x URL
  2. monocytosis GREATER than 1.5-2x URL
  3. LS
  4. toxic change
  5. anemia
  6. hyperglobulinemia

**LYMPHOPENIA IF CONCURRENT STRESS

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20
Q

biggest reason for compensatory monocytosis?

A

decreased production in the bone marrow

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21
Q

GM-CSF is released by ___ and causes proliferation of ____ & ____, usually during _____ _____ rather than ____ _____

A

T cells, neutrophils, monocytes, chronic inflammation, overwhelming

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22
Q

eosinophils are stimulated to be produced in the ___ ___ by ___ & ___. they circulate for ___ to ____

A

bone marrow, GM-CSF, IL-5, minutes, hours

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23
Q

3 main causes of MONOCYTOSIS… (include values)

A
  1. stress (cortisol), usually LESS than 2x URL
  2. chronic inflammatory response, usually MORE than 2x URL
  3. compensatory monocytosis (decreased production of neutrophils from bone marrow)
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24
Q

what are some other factors that can stimulate eosinophil production? (2)

A

eotaxin, IL-13

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25
Q

T/F GI parasites DO cause eosinophilia

A

FALSE

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26
Q

when we don’t have cortisol, what values can we expect? (5)

A
  1. Lack of lymphopenia
  2. Eosinophilia
  3. Normal neutrophil count
  4. hypoglycemia
  5. low total protein
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27
Q

Basophilia usually follows with which parameter? In what 2 conditions?

A

Eosinophilia

  1. worms/parasitic infections (heart worm, lungworm)
  2. allergy/hypersensitivity reactions (feline asthma, eosinophilic bronchopneumopathy, inflammatory bowel disease, severe flea allergy)
28
Q

when do basophils degranulate?

A

when antigens meet membrane-bound IgE molecules

29
Q

mastocytemia is ___ in dogs and ___ in cats

A

uncommon, rare

30
Q

mastocytemia is primarily involved in ___ reactions

A

Th2

31
Q

how long do monocytes live in tissues? how long do neutrophils in tissues?

A

up to months, only 2 days

32
Q

eosinophils and basophils are very ___ in blood

A

LOW

33
Q

eosinophil functions (4, include 2 main things that are produced)

A
  1. activate mast cells, which then make IL-5 and eotaxin (which stimulate eosinophil production)
  2. work on fibroblasts to deposit collagen
  3. effects on epithelial cells
  4. stimulate lymphocytes that produce plasma cells that make IgE (binds to antigen and causes basophils to degranulate)
34
Q

plasma vs. serum?

A

plasma = supernatant of centrifuged, anti-coagulative blood that contains proteins and clotting factors

serum = liquid portion of clotted blood; substance that is left after proteins and clotting factors are used up/no longer exist there

35
Q

albumin basics (where it’s produced, 2 main functions)

A

produced in the liver

functions
1. carrier plasma protein to move things around like drugs, unconjugated bilirubin, minerals (Ca, Mg) in blood

  1. maintain oncotic pressure to keep fluid in capillaries after leaving
36
Q

globulin basics (what they are, who makes them, different types)

A

family of water-soluble plasma proteins that are mostly made by the immune system, but can also be made by the liver

ALPHA/BETA
- made by hepatocytes
- act as carrier proteins, lipoproteins, and acute phase proteins
- examples?
–> serum amyloid a (alpha 1 globulin)
–> haptoglobin (alpha 2 globulin)
–> plasminogen (beta globulin)

GAMMA
- made by the immune system
- IgG&raquo_space;> IgM + IgA
- act as antibodies produced by B lymphocytes and plasma cells
- fibronectin is a NON-IMMUNOGLOBULIN gamma globulin

37
Q

fibronectin

A

a non-immunoglobulin gamma globulin

38
Q

plasma/serum formula

A

PLASMA = SERUM + CLOTTING FACTORS

39
Q

albumin/globulin formula

A

GLOBULIN = TOTAL PROTEIN - ALBUMIN

40
Q

panhypoproteinemia (what is it, 2 causes w/ subsets)

A

when we have PROPORTIONAL decrease in albumin and globulin

causes
1. loss of albumin and globulin

  • HEMORRHAGE = WHOLE blood loss
  • GI LOSS = protein-losing enteropathy, diffuse to multifocal or neoplastic lesions on SI, often see decreased cholesterol
  • EXUDATE (EFFUSION) = losing protein-rich fluid into cavities, or as a result of dermatological insult (BURNS)
  1. hemodilution
    - when we have excessive water in plasma
    - from giving too many fluids or heart failure
41
Q

hypoalbuminemia (2 main causes, subsets)
***A LOT OF INFO

A
  1. due to LOSS OF ALBUMIN, which can be from…
  • RENAL (SELECTIVE)
    –> when there’s glomerular disease, albumin can enter Bowman’s space with ultrafiltrate
    –> glomerular disease (inflammation, Ab-complexes from inflammation, amyloid deposition)
    –> PROTEIN-LOSING NEPHROPATHY
  • GI LOSS (usually non-selective)
    –> albumin is lost in protein-losing enteropathy
  • EXUDATES (usually non-selective)
    –> albumin and globulin are often lost in exudate fluid, but in CONCURRENT INFLAMMATION we can lose MORE ALBUMIN because it’s a negative phase protein
  1. due to DECREASED PRODUCTION OF ALBUMIN by the liver
  • HEPATIC FAILURE/INSUFFICIENCY
    –> cirrhosis
    –> infiltrative neoplasia
    –> severe acute injury
  • INFLAMMATION
    –> albumin is negative acute phase protein, so decreases with inflammation
  • DECREASED INTAKE
    –> starvation
    –> malabsorption (diffuse disease of SI)
    –> maldigestion (cannot absorb nutrients)
42
Q

laboratory support for hypoalbuminemia caused by decreased albumin production by liver? (4 things produced by the liver that change, 2 things that increase, globulin?)

A
  • Decrease in analytes produced by liver
    –> Glucose
    –> BUN
    –> Cholesterol
    –> Prolonged PT & PTT

ALSO
–> Hyperammonemia
–> Increased bile acids
–> Globulin is usually normal although variable; If concurrent blood loss, both low, if inflammation globulin could increase

43
Q

laboratory support for hypoalbuminemia caused by loss of albumin due to renal disease?

A
  • POSITIVE URINE DIPSTICK
  • URINE:CREATININE PROTEIN RATIO above a certain species cutoff
44
Q

what does it mean when we say albumin is a “negative acute phase protein”?

A

produced by the liver but will DECREASE in production in response to INFLAMMATION

45
Q

laboratory support for hypoalbuminemia caused by inflammation?

A
  • INFLAMMATION on CBC (neutrophilia, LS, toxic change)
  • maybe changes to globulin (more in Ab-mediated inflammation)
46
Q

what happens if albumin is between 1.0-1.5 g/dL? (name for it, what it does and what it causes IN TERMS OF FLUID)

A

HYPOALBUMINEMIA

CANNOT MAINTAIN ONCOTIC PRESSURE

FLUID NOT REABSORBED INTO CAPILLARIES AND EITHER EDEMA OR ASCITES

47
Q

hypoglobulinemia (selective/non-selective, 2 main causes for selective, dogs and horses)

A

USUALLY NON-SELECTIVE and DECREASES WITH ALBUMIN

BUT IF SELECTIVE, can have one of two causes…
1. failure of PASSIVE TRANSFER
–> colostrum fails to properly transfer immunoglobulins to neonates

  1. combined immunodeficiency
    –> rare occurrence in dogs and horses
    –> dogs = IgA and IgG B cells do not adequately differentiate into plasma cells that secrete immunoglobulins
    –> horses = they do not make enough T and B lymphocytes, and therefore don’t make enough immunoglobulins
48
Q

panhyperproteinemia (what it’s caused by and 4 laboratory findings)

A

due to DEHYDRATION from decreased free water content in plasma

lab findings
- azotemia
- elevated Na & Cl
- increased USG
- +/- erythrocytosis

49
Q

hyperalbuminemia (what it’s caused by and laboratory findings)

A

due to DEHYDRATION from decreased water content in plasma

lab findings
- pre-renal azotemia (elevated BUN and creatinine, increased USG)
- elevated Na & Cl
- +/- erythrocytosis
- hyperglobulinemia OR normal globulin

50
Q

fibrinogen (4)

A

POSITIVE acute phase protein that is made in LARGE quantities by LIVER during inflammation; BECOMES FIBRIN TO CONTRIBUTE TO CLOT

will polymerize to help PREVENT BACTERIA from reaching INFLAMMATORY site during inflammation

also helps facilitate movement of leukocytes to site of inflammation

supports growth of new tissue

51
Q

what causes an ABSOLUTE INCREASE in FIBRINOGEN? what can this increase come before?

A

INFLAMMATION!!! (fibrin clot)

this increase can come before CELLULAR CHANGES IN NEUTROPHILS ARE APPRECIATED

52
Q

what is a big sign that B cells are undergoing neoplasia?

A

if they only produce one kind of immunoglobulin, because they should be producing many types

53
Q

give two scenarios where no further workup is needed with hyperglobulinemia, and then when we DO need further investigation

A
  1. when seen with CHRONIC INFLAMMATION INDICES (>2x URL neutrophilia, LS, etc.)
  2. when seen with specific characteristics for NON-NEOPLASTIC REACTIONS, such as in FIP

**if hyperglobulinemia cannot be explained by a reactive or non-neoplastic cause, then further investigation through serum plasma electrophoresis

54
Q

serum plasma electrophoresis

A

this can help determine if neoplasia is present among gamma immunoglobulins (differentiate between polyclonal and monoclonal)

RUN ON SERUM BECAUSE OTHERWISE CLOTTING FACTORS GET IN THE WAY

proteins will run along gel and separated according to SIZE and CHARGE, and a HISTOGRAM/ELETCROPHORETOGRAM is produced that shows each protein in its LOCATION and CONCENTRATION

has 6 different regions…
1. albumin
2. alpha-1 globulins
3. alpha-2 globulins
4. beta-1 globulins
5. beta-2 globulins
6. gamma globulins

if POLYCLONAL = immunoglobulins are diverse because B cells are diverse

if MONOCLONAL = immunoglobulins found are the SAME due to a SINGLE CLONE of plasma cells (common) or Ab-producing B lymphocytes (less common)

55
Q

causes of monoclonal gammopathy? (2 main causes, third is a pseudo-cause)

A
  1. systemic plasma cell neoplasia in bone marrow or spleen; multiple myeloma
  2. B cell lymphoma or B cell leukemia
  3. Ehrlichia (rickettsial disease) can cause one plasma cell to dominate and make it look like gammopathy
56
Q

what are acute plasma proteins/when do they change, which proteins are in which subsets (** next to ones that are most important), how they tend to behave and why

A

these are proteins produced by the liver that are either POSITIVE or INCREASE IN RESPONSE TO INFLAMMATION or are NEGATIVE and DECREASE IN RESPONSE TO INFLAMMATION

POSITIVE APPs
- ALPHA
–> serum amyloid a**
–> alpha-1 antitrypsin
–> alpha-1 glycoprotein
–> ceruloplasmin
–> haptoglobin

  • BETA
    –> C-reactive protein**
    –> fibrinogen
    –> C4 (complement factor)
    –> C3 (complement factor)

NEGATIVE APPs
–> albumin
–> beta globulins (transferrin)

since most acute-phase plasma proteins are POSITIVE and FALL WITHIN ALPHA/BETA REGIONS, ALPHA/BETA GLOBULINS WILL INCREASE IN INFLAMMATION, not necessarily in hyperglobulinemia or hyperproteinemia

57
Q

delayed phase proteins (what they do, what it means for hyperglobulinemia, and acute phase vs delayed phase responses)

A

in response to chronic antigenic stimulation, B lymphocytes and plasma cells will make more immunoglobulins (takes > 7 days)

HYPERGLOBULINEMIA IN RESPONSE TO POLYCLONAL GAMMOPATHY IS A DELAYED RESPONSE

ACUTE PHASE
- mild hypoalbuminemia
- +/- mild HYPERglobulinemia

DELAYED PHASE
- mild hypoalbuminemia
- **moderate to marked HYPERglobulinemia

–> ALWAYS EXPECT HYPOALBUMINEMIA IN THE FACE OF INFLAMMATION, BUT IF CHRONIC THEN A DELAYED PHASE HYPERGLOBULINEMIA

58
Q

3 main differentials for polyclonal gammopathy?

A
  1. inflammation
  2. chronic infection/oral disease
  3. FIP
59
Q

___ is a calculated protein, while ___ is a measured protein

A

GLOBULIN, ALBUMIN

60
Q

how is fibrinogen measured? (2 ways)

A

INDIRECTLY = heat precipitate out plasma and re-measure, and can be done in practice setting; ONLY DETECTS BIG INCREASES

DIRECTLY = most sensitive and accurate, done by reference lab

61
Q

___ & ___ are made by the liver, while ___ are made by ___ ___ which have terminally differentiated into ___ ___

A

albumin, fibrinogen, globulins, B cells, plasma cells

62
Q

what does aldosterone do? what happens in its absence?

A

usually INCREASES Na and PASSES K, also helps RETAIN WATER to CONCENTRATE URINE

without it (such as during addison’s), have LOW Na and HIGH K, can have POORLY CONCENTRATED URINE

63
Q

IL-5 helps to produce ___ & ____, but can BE produced by ____s

A

eosinophils, mast cells, lymphomas

64
Q

regenerative anemia 2 causes (2 VERY BROAD TERMS)

A
  1. BLOOD LOSS (sometimes lost with albumin and globulin)
  2. BLOOD LYSIS (hemolysis, breakdown of RBCs in bloodstream or in tissues)
65
Q

hyperglobulinemia main causes (3)

A
  1. inflammation
  2. neoplasia of B cells (cell that produces Abs)
  3. non-neoplastic reactive cause

Year 1/2 (139 decks)

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