Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematology > Hema Final > Flashcards

Hema Final Flashcards

1
Q

Hypoadrenocorticism and hypothyroidism cause what, how?

A

Low cortisol and low thyroxine lead to decreased epo’esis –> non-regen anemia d/t decreased production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name three types of selective BM failure

A

non-regen IMHA (targets precursors), hrEpo administration, FeLV induced eryth hypoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cause of anemia of inflammation

A

Decreased epo’esis from hepcidin cytokine trapping Fe in macs and decreasing GI absorption; cytokine direct epo’esis inhibition; concurrent fragility from ox damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lab findings of anemia of inflammation

A

normo/normo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How long until regeneration seen in peripheral blood?

A

3-5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Shorter RBC lifespan leads to (faster/slower) onset of anemia; rank dog cat horse cattle via RBC lifespan lifespan

A

Faster onset; cat (70d) –> dog (100d)–> horse/cow (150d)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Non-regenerative macrocytic anemia falls in what subcategory

A

Ineffective epo’esis (think FeLV and poodles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mechanisms of anemia in CKD; MCV/MCHC findings

A

Renal lesions = dec. epo’esis, GI hemorrhage from uremic toxins; normo/normo (typically)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

FeLV-induced eryth hypoplasia –> subcategorize

A

non-regen (dec. production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cause of anemia of Fe deficiency; MCV/MCHC findings

A

Ineffective epo’esis- microcytic (extra mitotic divisions when low in Hgb), normo- to hypochromic (decreased Hgb content), increased fragility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 causes of Fe def’cy anemia

A

diet, ext. hemorrhage, copper/B6 def’cy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ddx- microcytosis in non-anemic

A

cong. PSS, japanese breeds, some chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lead tox blood smear changes; type of anemia

A

basophilic stippling (from remnant ribosomes d/t enzyme inhibition), +/- nRBCs from marrow damage, siderocytes (pappenheimer bodies); none to mild non-regen anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of macrocytic non-regen anemia

A

FeLV-induced (from maturation defect), poodles: DNA synth defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cause of cobalamine/folate def’cy anemia; MCV/MCHC

A

DNA synth impaired in precursors –> macrocytosis, hyperseg neuts, normo/normo/non-regen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which types of blood loss is most likely to progress to Fe def’cy

A

Chronic external blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

External blood loss and PCV/TS changes

A

initial- unchanged; 6-12h - plasmadilution = decrease HCT/TP values; chronic- anemia persists, TP normalizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Extravasc hemolysis- mechanisms

A

RBCs killed by macs in spleen/liver/marrow, Hgb breakdown leads to initial conj bili in urine, excretion/liver conversion overwhelmed –> bilirubinemia –> icterus >2 mg/dL, cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Intravasc hemolysis- mechanisms

A

Lysis in vessels = Hgb in plasma –> dimers form complex via haptoglobin with protein to retain in kidney, macs eat and release bili to plasma; Haptoglobin overwhelmed –> Hgb’uria;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CS of intravasc hemolysis

A

hyperbilirubinemia (d/t mac destruction), Hgb’uria; DIC/Shock/renal compromise can follow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Lab findings of hemolytic anemias

A

poikiliocytosis, hyper-bili, leukocytosis w/L shift and tox (d/t inflammatory cytokines from RBC destruction), Hgb’emia/’uria (intra), reticulocytosis (Fe quickly recycled to precursors), splenomegaly (from macrophage hyperplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When are hemolytic dz animals icteric, dependent on?

A

> 2 mg/dL plasma bili concentration (dependent on severity of destruction, rate of clearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Erythroparasite MOAs

A

attach to membrane surface (mycoplasma), invade cell (babesia, anap, plasmodium), hemolytic toxins (clostridium), initiation of Ab-mediated destruction (any epi- or intra- cellular parasite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IMHA lab findings

A

Spherocytes, poikiliocytosis, icterus, neutrophilia, leukocytosis, CBC with marked regen, + coombs, RBC autoagglutination, +/- TCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Dz of fragmentation anemia

A

Fe deficiency, DIC, HSA/neos, vasculitis, sepsis, caval syndrome, heat stroke, splenic/hepatic dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which types of poikilocytosis in fragmentation anemia

A

Schistocytes (hallmark finding), spherocytes (resealed RBC), acanthocytes (club projection in HSA), pre- and keratocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 sites of oxidative dmg in RBC

A

Heinz bodies- globin precipitation on membrane; cross-linked cytoskel proteins (eccentrocytes and pyknocytes); Oxidation of Fe2+ –> 3+= metHgb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Effects of MetHgb’emia

A

reduced oxygen carrying capacity (Fe 3+ cant carry O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Who is more susceptible to oxidative damage, why

A

Cats: more -SH groups, non-sinusoidal spleen for clean-out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Clinical significance of feline Heinz body findings

A

<10% normal; must compare # HzBd, CS, strength of regen, likelyhood of oxidant exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Dz causing Heinz bodies in cats without concurrent anemia

A

hyperthryroidism, DM, LSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Toxic oxidants- name several

A

onion, garlic, copper, tylenol, zinc, skunk spray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MOA - Zn toxicity

A

Inhibition of RBC metabolic paths (esp protecting from oxidative dmg), direct ox-dmg, Zn as hapten for IMHA RBC binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Seen in Zn toxicity

A

Heinz bodies, eccentrocytes, spherocytes; regen anemia, negative Coombs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hemolysis as sequelae to TPN/tube feeding in lipidotic patient- MOA

A

decreased phos = dec. ATP in RBC –> fragility, ox dmg susceptibility; refeeding causes increased cell anabolism, intracell shift of P leads to low P in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Envenomation changes

A

echinocytosis (first 48h), spherocytes (hemolytic anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SA anti-coagulant of choice, why

A

EDTA- better WBC morphology, less platelet clumping than heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Underfilled EDTA tube =

A

crenation (morphology change), lower PCV/MCV, higher MCHC/TP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Changes when EDTA tube sits, timing?

A

crenation, WBC vacuolization, pyknosis, prepare slide if more than 1-2 hours before processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why use NMB; preparation

A

Confirm Heinz bodies, estimate retics; 1:1 prep sits for 30 min to allow RNA aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Perform manual retic count; dog vs cat differences; perform corrected retic%

A

retic/ 500 counted RBC= %retic; (dogs- count all, cats- count aggregate) If anemic–> [%retic x (pHCT/normHCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Why only count aggregate retic’s in cats

A

these are the ones that correlate to polychromasia and active regen (punctate circulate longer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Perform absolute retic concentration; interpret cat and dog

A

retic % x RBC/uL; cat >50k aggregates = regen; dog >80k total retic = regen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Interpret reticulocytosis in non-anemic patient

A

hypoxia, neoplasms, toxic/metabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Rouleaux- normal in? abnormal indicates? how to test?

A

normal in cats/horse/pig; abnormal indicates presence of inflammatory proteins; blood:saline 1:0.5 = disperse in rouleaux, stay clumped in agglutination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Leukergy- define; indicates?

A

Small aggregates of WBC on smear, non-specific finding (inflammatory or neoplasic), indicates automated CBC may have read clumps, lowering WBC count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

RDW- define, interpret findings

A

red cell distribution width; determines anisocytosis but not macro vs micro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MCV- define, determine artifact readings

A

mean cell volume; increased may be due to clumping, swelling d/t hyperosmolar plasma (hyperGluc/Na) with dilution in isotonic diluent; decreased may be due to hypoosmolar plasma with dilution in isotonic diluent leading to fluid efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Benign/artifact poikilocytosis

A

crenation/echinocytes- low edta ratio, delay in slide prep, normal in cats/pigs; regen anemia retics can have normal stomatocytes and codocytes due to large cell size and abrormal membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

multiple, irregularly spaced, club shaped projections; name/ddx

A

Acanthocyte; HSA, RBC membrane canges, liver/spleen dz, fragmentation disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

hemoglobinized center within central pallor (target cell); name/ddx

A

Codocyte; retics, hypothy, Fe anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

irregularly shaped spherical erythrocytes with a small cytoplasmic tag; name/ddx

A

Pyknocyte; from eccentrocyte loss of fused membrane portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

“opened” blister with 2 pinchers; name/ddx

A

Keratocyte; fragmentation hemolysis, Fe deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

teardrop shaped RBC; name/ddx

A

Dacrocyte; artifact, fragmentation, glomerulonephritis, myelofibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

RBC morphology associated with envenomation, acute Zn tox, burns, hypoP, and others

A

Spherocyte; also in IMHA!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

multiple, regularly spaced, spikey to blunt projections; name/ddx

A

Echinocyte; electrolyte depletion, envenomation, renal dz, inherited RBC disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Elliptocyte/Ovalocyte ddx; normal in:

A

liver dz, myelofibrosis, congenital RBC abnormalities: normal in llama, birds, reptiles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Clear vesicle at margin of cell, ddx

A

Prekeratocyte (aka blister cell); associated with keratocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Stomatocyte ddx:

A

retics, stomatocytosis (inherited), thick blood artifact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Peripheral fusion of opposing membranes;; name/ddx

A

Eccentrocyte; oxidative damage, rarely inherited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Varied shape RBC fragment ; name/ddx

A

Shistocyte- mechanical RBC injury in DIC, frag hemolysis, Fe anemia, vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does increased polychromasia indicate

A

Basophilic RBCs from retained RNA are retics on NMB stain, less Hgb per cell volume leads to hypochromasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Causes of hypochromasia

A

Les [Hgb] (usually Fe deficiency in mature RBC); may indicate presence of retics; can also be seen in non-regen anemia of inflam dz d/t iron sequestration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Howel-Jolly bodies- mechanism, causes

A

retained single nuclear fragment; increased in regen anemias, splenectomized, chemo/steroid admin; low normal in cats/horses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Basophilic stippling– mechanism, causes

A

decreased heme synthesis enzyme that retains ribosomal aggregates; regen anemia (esp hemolytic, bovine), lead poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

When is peak reticulocyte response

A

7-10 days after peracute event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Heinz bodies- - mechanism, causes

A

dentaured Hgb protruding from membrane; oxidative damage to globin part of Hgb (most in cats)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Pappenhemier body- mechanism, causes

A

aka Siderotic inclusion; iron granule- lightly basophilic, some clumps; hemolytic anemia, PSS, vitamin/drug deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Refractile appearance to RBC

A

watermark artifact of slow drying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Describe canine distemper inclusions; proper stain

A

Pleiomorphic, eosinophilic or basophilic- stain with diff-quik

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

nRBC effect on total [leuk]; correct

A

Increased WBC count due to nRBCs counted; if >5 nRBC/100 WBC:

[WBC/uL x (100/ 100+ nRBC#)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe appropriate release of nRBC-

A

Released in regen anemia d/t increased epo’esis in BM and extra-med sites, highest in earliest phase of regen or in regen anemia with EMH (extramed hematopoeisis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe inappropriate release of nRBC-

A

presence does not def. indicate increased epo’esis- injury to blood-BM barrier can release; when >5/100WBC with non-regen, or non anemia could be due to marrow injury, decreased splenic clearance, hypoxia-induced RBC production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

List causes of nRBC

A

lead toxicosis; heatstroke/adderall toxicity; endotoxemia/sepsis; hypoxemia; myelophthisis: marrow neoplasm, myelofibrosis; cobalamin deficiency (Border Collies); certain breeds (e.g. Schnauzer, Dachshund); decreased splenic function; erythroid leukemia (seen most in cats); trauma; inflammatory conditions; hyperadrenocorticism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Plt slide estimate- dog and cat

A

Dog: #cells/uL = (#cells/100x oil) x 15,000
Cat: #cells/uL = (#cells/100x oil) x 20,000
(lab microscope 60x oil= x6000)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Causes of increased MPV

A

Younger plt (megaplts) are larger, clumping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Leukocyte slide estimate and differential

A

Differential: at monolayer 100x oil, coulnt 200 cells in 10 fields= avg #per field x obj^2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe neut toxicity

A

Cytoplasmic changes (only in neuts) from maturation arrest: 1+ dohle or basophilic cytoplasm; 2+ both; 3+ both and foamy cyto vacuolization; 4+ all + gigantism or toxic granulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How is toxicity different from degenerative change

A

degen: nuclear changes that occur in peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Causes of neut hypersegmentation

A

> 5 segments- d/t steroids, dysplastic BM dz, delay in smear prep, heat stroke/adderall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe features of lymphocyte reactivity

A

Basophilic cytoplasm, eccentric nucleus, perinuclear clear zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Monocyte response to inflammation

A

very b’philic cytoplasm, vacuolated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Process by which immune system removes self-reactive lymphocytes

A

Central and peripheral tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

3 roles of complement in auto-immune cell destruction

A

combine with Ab or bind to microbe to trigger 1) release of comp fragments which are chemotactic for inflammatory cells and 2) activation of MAC (membrane attack complex) to lyse cell wall; 3) bound complement can flag an RBC for phagocytsosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Why are RBC more likely to be target of type II hypersensitivity

A

Many surface molecules, high concentration of circulating exposed to lymphocytes and Ab, more prone to adsorb drugs/infxn components to their surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

In IMHA, macs recognize Ig’s or complement on RBCs to target for phagocytosis- what type of hemolysis is this associated with

A

Extravascular (within mononuclear phagocyte system of spleen, liver, BM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Why/how are spherocytes formed

A

Often in IMHA; macrophages remove portions of membranes and membrane seals creating smaller surface to area volume ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What do ghost RBCs indicate, how do they form in dz process

A

indicate intravascular hemolysis; in IMHA- complement binds and creates a pore in RBC membrane through which cell is lysed and contents (including Hgb) are leeched out, leaving just the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Pathophysiology of intravascular hemolysis; why is it a poor prognostic indicator?

A

Requires complement cascade activation to form MAC and lyse cell= Hgb’emia/uria, ghost cells; worse bc breakdown products (Fe, heme) cause oxidative damage once hapten transport systems are overwhelmed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe intravasc hemolysis oxidative damage MOAs

A

NO in blood maintains homeostasis, free Hgb oxidizes NO and prevents it from maintaining vasodilation and stop plt agg’gn. Also release of phospholipid pieces of RBC allow coagulation factor pathways to propagate, creating conditions for DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Differences between intra- and extra-vascular hemolysis

A

extra-: within MPS, conserves Iron/AAs; intra-: outside of MPS (loss of Fe/AAs), greater DIC/shock risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Causes of secondary IMHA

A

Infectin ( ana, FeLV, FIV, etc), ITP, LSA, HSA, drugs acting as haptens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Evan’s syndrome

A

IMHA and ITP concurrent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Warm agglutinin dz- describe, CS

A

CS and agglutination occurs at body temp; non-specific generalized CS, more common PTE/DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Cold agglutinin dz- describe, CS

A

Occurs at temps below body temp, often armless, more likely in peripheral sites; CS- cyanosis, necrosis, extremity gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Dx IMHA

A

At least one of: marked spherocytes (dog), positive direct coombs, autoagglutination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Other causes of spherocytes

A

fragmentation hemolysis, Zn tox, envenomation, hypoP, burns, transfused RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Clin Path findings of IMHA

A

Low: RBC, PCV, Hgb
Increased: MCV, anisocytosis
+/- Retics , L-shift toxic neutrophilia, monocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Why run direct Coombs?

A

Only way to test for anti-RBC-Ab’s when concentration too low to auto-agglutinate; not useful in patients who already auto-agglutinate; cannot tell difference between primary and secondary IMHA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Reasons for false negative coombs

A

Lab error, low qty bound Ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Poor prognostic indicator in IMHA dog

A

Bili >10 mg/dL; intravasc hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Cat IMHA signalment trends

A

Younger more likely to be primary and have good outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Cat primary IMHA: negative and positive prognostic indicators

A

Neg: older age, higher bili; Pos: lymphocytosis or hyperGlobulinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Most common cause of cat 2* IMHA

A

Neoplasia (> mycoplasma, FeLV, FIP, inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Pathophys of primary ITP; signalment

A

IgG binds to plt surface to mark for destruction by spleen/liver; middle aged cockers, dogs&raquo_space;> cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Pathophys of secondary ITP; causes

A

Ag binds to surface of plt and Ab then targets cell

107
Q

Non-pathologic low plt count on machine- causes

A

Plt clumping, breed variation (larger, fewer), greyhounds/shiba inu - normal size but decreased number; may-hegglin anomaly

108
Q

Causes of 2* ITP

A

Infectious dz (ricketsiosis, FIV, FeLV, histo, HWD, babesia), neoplasms (MCT, HSA, nasal adeno, fibrosarc, LSA); drugs (heparin novel exposure, previous exposure, Abx, aspirin/anti-inflammatories); 3-5 days post modified live vaccines (distemper, parvo, panleuk)

109
Q

Clin path findings of ITP

A

low plt, +/- increased MPV, increased BM megakaryocytes

110
Q

ITP signalment

A

Middle age (wide range); Cocker, mini poo, sheepdog;

111
Q

IMHA signalment

A

COCKERS! Young-mid age; mini schnauz, collie, springer, OE Sheepdog

112
Q

Why should cats be cross-matched when typing is not available

A

Cats have pre-formed anti-RBC Ab’s, so transfusion reactions can be very dangerous

113
Q

Which cats could be killed by the wrong transfusion

A

Type B cats given type A blood- 95% have preformed anti-RBC-Ab

114
Q

How can Mik incompatibility be tested? What will results show?

A

Cross matching- ____________

115
Q

What cats have high type B prevalance?

A

exotic shorthairs, rexes, abyssinians, persians

116
Q

What cats have low type B prevalance?

A

Siamese, burmese, russian blue- 0% prevalance

117
Q

What is the most clinically significant DEA type in dogs

A

1- 60% are DEA-1 positive, so 40% can have severe reaction

118
Q

What is the universal dog blood donor

A

DEA 4; a DEA 1 negative dog can be used in emergencies

119
Q

Components of major crossmatch

A

Recipient serum with donor RBCs

120
Q

Components of minor crossmatch

A

Recipient RBC with donor serum

121
Q

What does + crossmatch indicate

A

Hemolytic reaction likely to occur

122
Q

Interpret autocontrol in cross-match

A

Minor results will not be interpretable bc agglutination already present in DONOR before minor reaction, cant determine if reaction occurs

123
Q

Cytauxzoonosis- which domestic species

A

Cats

124
Q

How is cytauxzoonosis different in bobcats/panthers compared to domestic cats

A

Mild to subclinical manifestation of dz in reservoir hosts

125
Q

Describe cytauxzoonosis in exotic felids (lions/tigers)

A

can be fatal but asymptomatic with + PCR has been seen

126
Q

How has cytauxzoonosis changed in domestic cats over time

A

previously almost completely fatal, increasing recovery from initial stage to move to carrier status (d/t organism genetic variation, awareness, improved tx)

127
Q

T/F chronic carrier cats with cytauxzoonosis cannot act as reservoir hosts

A

False

128
Q

Diagnosis of cytauxzoonosis

A

blood smear: piroplasm organisms in RBC that stain light blue with purple nuc

129
Q

CS of cytauxzoonosis, source of CS

A

depression/anorexia –> fever (in first 3-4 days) –> +/- dyspnea/organomegaly –> end-organ damage of liver and BM by schizonts (CS not from piroplasm form)

130
Q

Clin path findings of cytauxzoonosis

A

non-regen anemia, icteric plasma, +/- pancytopenia and/or thrombocytopenia (d/t BM infiltration and DIC)

131
Q

cytauxzoonosis- infected cells/organism life stages

A

Sexual repro in tick (amblyomma americanum), sporozoites infect macs/monos in MPS system; Piroplasms in RBC replicate via binary fission

132
Q

cytauxzoonosis- cause of severe/fatal manifestations of dz

A

Schizogony within macs- end organ damage

133
Q

Tx/prevention cytauxzoonosis

A

atovaquone and azithromycin; tick prevention and indoor housing prevents

134
Q

What is limitation of PCR for cytauxzoonosis

A

Slow turnaround time

135
Q

Babesiosis- species in US (*= most clinically relevant)

A

B. vogeli; B. coco B. gibsoni, B. conradae, B. microti

136
Q

Describe the differences in morphology between the two most clinically relevant babesia species

A

B. vogeli: larger, pear shaped; B. gibsoni: smaller, signet ring shape

137
Q

What cell is infected in mammals with babesia

A

Erythrocytes

138
Q

Mode of transmission, signalment- babesia

A

Large: puppies, immunocompromised, greyhounds; Small: dog bites, staffordshire terriers

139
Q

Dx- babesia

A

PCR most sensitive to speciate, light micro may not be definitive ID

140
Q

CS and severity- babesia

A

Range from inapparent dz to chronic to severe: thrombocytopenia (immune mediated destruction and consumption) +/- hemolytic anemia, splenomegaly + non-specific CS; less commonly hepatopathy, renal failure, CNS signs

141
Q

hepatozoon: species in dogs, clinically relevant species, geographical area

A

Dogs: H. canis; H. americanum- SE and S. central US

142
Q

How is hepatozoon transmitted

A

INGESTION of tick (not tick bite like babesia, cytaux)

143
Q

Mechanism of disease- H. canis vs H. americanum

A

merozoites invade monos and neuts where gamonts are formed in both; H. canis- mild/inapparent, rarely severe (typically immunocompromised) meronts develops in hemolymphatic and other organs; H. americanum- severe dz, meronts develop in skel and cardiac mm.

144
Q

Labs/imaging findings- H. americanum

A

Neutrophilic leukocytosis, long bone periosteal reaction, cysts within muscle from inflammatory rxn

145
Q

Dx hepatozoon

A

Dx: gamonts in leukocytes (more readily found in h. canis), buffy coat concentration may help find. PCR avail, but may get flase negative in H. am.

146
Q

Tx hepatozoon

A

H. am: TMS, clinda, primethamine, decoquinate; H. canis: imidocarb

147
Q

Where does rangeliosis occur

A

Southern Brazil

148
Q

What cell types will rangeliosis be found in

A

Piroplasms in RBC, neut, monos

149
Q

CS- rangeliosis

A

icterus, organomegaly, GI hemorrhage, regenerative anemia

150
Q

Infective species of cats and dogs in mycoplasmosis

A

Cats: m. haemofelis, m. haemominutum, m. turicensis; Dog: m. canis, h.

151
Q

Most pathogenic cat mycoplasmosis

A

H. haemofelis

152
Q

Which mycoplasmas can be seen on blood smears

A

haemofelis and haemominutum

153
Q

Transmission of mycoplasmas

A

blood sucking arthropods like fleas; queen to kitten (m. haemofelis), iatrogenic via transfusion

154
Q

CS/Lab findings- m. haemofelis

A

weakness/depression/etc, splenomegaly; parasites in peripheral blood, mild to moderate anemia that may be regenerative, +/- bilirubinemia/uria

155
Q

Risk factors for m. haemofelis

A

bite abscess, FeLV/retroviral +, outdoors, < 3y old, male, (dogs: splenectomized)

156
Q

How is dz of m. haemofelis different from cytauxzoon

A

Cats less sick in m. haemofelis, m. h. has more male predisposition; attach to surface and destruction is immune mediated in m. haemo

157
Q

Dx mycoplasma

A

light microscopy or PCR

158
Q

How should mycoplasma samples be shipped

A

fresh smears right away so EDTA doesnt remove orgs within tube in transport

159
Q

Tx- mycoplasma

A

tetracylines in dogs; doxy or enro in cats +/- supportive care

160
Q

Species of monocytic erlichiosis and SA species affected

A

E. canis and e. chaffiensis are both found in dogs

161
Q

CS- monocytic erlichiosis; unique features of E. canis

A

Asymptomatic to fever, thrombocytopenia, nasal/ocular discharge, non-specific; E. canis: chronic infxn at 40-80d- bone marrow hypo/aplasia (myelosuppression), hyperglobulinemia, plasmacytosis, lymphocytosis, bleeding, uveitis, CNS, organomegaly

162
Q

Dx- monocytic erlichiosis

A

Morula sometimes seen within monocytes in smear or splenic aspirates. Speciate via splenic PCR ( blood PCR may give false negative). IFA can diagnose but cannot speciate due to cross rxn

163
Q

Tx- monocytic erlichiosis

A

Tetracyclines

164
Q

What agents are responsible for granulocytic rickettsial infection

A

E. ewingii, Anaplasma phagocytophilum

165
Q

CS- granulocytic rickettsial infection

A

E. ewingii: non-specific, nero, swollen joints (neutrophilic polyarthropathy); Anaplasma: fever, lethargy, anorexia

166
Q

Lab findings of - granulocytic rickettsial infection

A

Thrombocytopenia, non-regen anemia, leuko and lymphopenia, morulae in neutrophils

167
Q

Dx - granulocytic rickettsial infection

A

4DX differentiates ana from erl; Morulae in neutrophils, speciate via PCR, 16SrRNA

168
Q

What agent causes thrombocytic anaplasmosis

A

A. platys

169
Q

CS- thrombocytic anaplasmosis

A

Typically subclinical, mild fever, minor hemorrhage/ecchy/petech of MM possible

170
Q

Dx- thrombocytic anaplasmosis

A

Dx- org in platelet (not often seen), PCR, 16SrRNA. 4DX and IFA cross-react with other species

171
Q

Tx- thrombocytic anaplasmosis

A

tetracyclines

172
Q

Indications for bone marrow eval

A

Unexplained cytopenias/persistent cytoses (except neuts), /clinical chemistry findings, FUA, suspicion of systemic infection in marrow, dx/stage marrow neoplasms

173
Q

Marrow collection sites- dog/cat

A

iliac crest, trochanteric fosa of the femur, prox humerus (in skeletally immature)

174
Q

Supplies needed for marrow aspirates

A

Illinois or rosenthal needle with stylet, analgesia (lidocaine), scalpel, sterile prep supplies, saline/EDTA lined 6-12cc syringe for suction, sterile gloves, slides, petri dish

175
Q

How is M:E ratio quantified

A

Count 500 nucleated cells total. M= ALL stages of granulocytes (eos, neuts, basos); E= nucleated RBC precursors

176
Q

Interpret M:E > 2 with hypercellular marrow

A

Granulocytic hyperplasia

177
Q

Interpret M:E < 1 with hypercellular marrow

A

Erythroid hyperplasia

178
Q

Interpret M:E > 2 with hypocellular marrow

A

Erythroid hypoplasia

179
Q

Interpret M:E < 1 with hypocellular marrow

A

myeloid hypoplasia

180
Q

Erythroid hyperplasia- ddx

A

Matur’n WNL (effective): strong regen anemia (hemolysis, blood loss);

Matur’n arrest (ineffective): immune mediated attack on later RBC precursors, MDS, iron deficiency

181
Q

Erythroid hypoplasia- ddx

A

(decreased production) inflamm dz, ckd, endocrine dz, endocrinopathies (less common), myelofibrosis, MDS, etc (other cells taking over bone marrow)

182
Q

Myeloid hyperplasia- ddx

A

(Usually in response to neut demand) Effective: hemolysis, blood loss, polycythemia vera; Ineffective: IMHA against later precursor, MDS, low Fe, low cobalamine, congenital dyserythropoiesis

183
Q

Dog and cat- BM cellularity normal range

A

25-75% (older = lower)

184
Q

Dog and cat - %small lymphocytes normal range

A

Dog- <5-10%; Cat- <15-25%

185
Q

Dog and cat BM normals: % immature erythroid, % immature myeloid, % plasma cells, %macs/monos

A

eryth/myeloid each <5%; plasma/macs/monos each <3%

186
Q

megas/particle- dog and cat

A

1-3

187
Q

T/F - stainable iron is present in dog bone marrow but not in cats

A

T

188
Q

What are the most common causes of megakaryocytic hyperplasia

A

Consumption/destruction/loss, inflammation response, iron deficiency

189
Q

What are the cuases of megakaryocytic hypoplasia

A

ITP directed at megakaryocytes, generalized marrow hypoplasia

190
Q

Describe general marrow hypoplasia/aplasia

A

hypocellular at <25%, aplastic if all cell types are severely reduced/absent

191
Q

Ddx- generalized marrow hypo-/aplasia

A

Drug induced (TMS, alben/fenben, azathioprine, chemo), estrogen tox, parvo/panleuk, chronic erlichia, imm-med/idiopathic

192
Q

What is myelofibrosis

A

Deposition of connective tissue in marrow secondary to injury which releases TGF-B cytokine.

193
Q

Primary conditions associated with myelofibrosis

A

leukemias, marrow neos, IMHA, marrow necrosis, drugs, PK deficiency

194
Q

What is myelophthisis

A

Crowding out of bone marrow

195
Q

What are the causes of dysplastic features in hematopoietic cell lines

A

MDS, lead tox, low Fe, low cobal/folate, FeLV, drugs (chemo, anti-convulsants, sulfa), IMHA/ITP, Leukemia, LSA

196
Q

Supplies for core bx

A

Jamshidi needle with stylet, scalpel, sterile prep supplies, saline/EDTA lined 6-12cc syringe for suction, sterile gloves, 10% formalin, slides

197
Q

Where is EPO made

A

interstitial fibroblasts within the kidney

198
Q

What is the function of EPO

A

Increases survival of RBC by diminishing normally high apoptosis

199
Q

Where is CSF made, what is it

A

Produced by various cells in response to inflammation, colony stimulating factor stimulates proliferation of neut and/or mono stem cells by inhibiting apoptosis of precursors and helping survival

200
Q

What is the function of CSF-GM?

A

enhances function of mature neuts and maxs

201
Q

Where is TPO made?

A

Constantly synthesized by hepatocytes

202
Q

Fxn of TPO

A

Stimulates platelet production- increased concentration (less platelets to bind to) increases megakaryocyte differentiation and fragmentation

203
Q

What cytokine is responsible for eosinopoiesis

A

IL-5

204
Q

what is the progression of the erythroid lineage?

A

rubriblast –> prorubricyte –> rubricyte –> metarubricyte –> reticulocyte –> erythrocyte

205
Q

what is the progression of the granulocyte lineage?

A

myeloblast –> promyelocyte –> myelocyte –> metamyelocyte –> band –> segmented neut

206
Q

Marrow transit time for erythrocytes, granulocytes, platelets

A

erythrocytes 5 days, granulocytes 7 days, platelets 5 days

207
Q

What cell line will begin increasing first in bone marrow recovery and why

A

Monocytes, 3 day transit time

208
Q

Causes of increased and decreased iron stores in BM

A

Inc: anemia of inflammation, hemolytic anemia, previous transfusions; Dec: cats (none present normally), iron deficiency

209
Q

Define leukemia

A

Neoplasm of one or more lines of hematopoeitic cells

210
Q

Differentiate acute and chronic leukemia via lab findings and diagnosis (cbc/bone marrow results)

A

Acute: typically with peripheral cytopenias (esp. anemia), abnormal blast cells, >20-30% blasts in marrow; Chronic: marked cytopenia of affected line in periphery, <20-30% blasts, neoplastic cells appear more mature

211
Q

T/F- chronic leukemias have poorer prognosis than acute

A

F

212
Q

Besides acute leukemia, why else could >20-30% blasts be found in marrow aspirate

A

Rebound toxicity- New recovery from toxic insult to marrow which caused hypoplasia

213
Q

How can rebound toxicity be differentiated from leukemia?

A

rebound tox animals wont have CIRCULATING blasts

214
Q

Chronic leukemias must be differentiated from what process? How?

A

Reactive cytosis; presence of dysplastic change in blood or BM indicates leukemia

215
Q

Why wont bone marrow eval help diagnose chronic leukemias

A

Cells may look well-differentiated, so may be hard to determine if they are neoplastic

216
Q

What makes chronic lymphocytic leukemia different from all other discussed leukemias

A

May not arise from BM (check spleen- T cell can arise here)

217
Q

What is primary MDS

A

Primary myelodysplastic syndrome (neoplastic) is from abnormalities in early precursor cells in marrow +/- changes to microenvironment; hypercellular marrow, peripheral cytopenias, >10% dysplastic features in one or more cell lines, blast count <20%; may progress to leukemia

218
Q

Ddx for marrow dysplasias

A

MDS, acute leukemia, lead tox, low Fe, drugs, 2* to immune/neoplastic

219
Q

What is the prognosis for MDS

A

Varies depending on form

220
Q

Define multiple myeloma

A

malignant tumor from plasma cells in BM

221
Q

Dx multiple myeloma

A

2 of 4: monoclonal gamopathy, Bence Jones proteinuria, >20% plasma cells in marrow, osteolytic bone lesions

222
Q

Differences in K9/fel MCT (marrow involvement, prognosis)

A

cat&raquo_space;> dog marrow involvement, poorer px in dogs, good px in cats with splenectomy

223
Q

What is histiocytic sarcoma? What forms can be present in marrow?

A

Malignant tumor of histiocytes; disseminated dendritic cell form and hemophagocytic macrophage cell form; both rapidly fatal

224
Q

What marrow disorders can cause peripheral pancytopenias

A

Double check this: acute leukemia, myelodysplasia, myeloid hypoplasia

225
Q

Species and breeds- LAD

A

Dogs and cattle; GSD, irish setters, mixed breeds

226
Q

CS- LAD

A

recurrent unexplained bacterial infections of skin, lung, GI in young dogs; GSD may have bleeding d/t plt affects

227
Q

Tx/Px- LAD

A

Symptomatic support and Abx, poor Px

228
Q

Blood film and lab findings- LAD

A

bacteria and inflam cells (usually macs) with little to no neuts; labs: marked neutrophilia +/- non-regen anemia, “pus-poor” infections

229
Q

Species and breeds- defective neutrophil function

A

Weimaraner, dobie

230
Q

CS- defective neutrophil function

A

chronic recurrent respiratory tract infections

231
Q

Tx/Px- defective neutrophil function

A

Symptomatic support and Abx, poor Px

232
Q

Species and breeds- Cyclic Hematopoiesis

A

Grey collies

233
Q

CS - Cyclic Hematopoiesis

A

non-specific

234
Q

Blood work findings- Cyclic Hematopoiesis

A

cyclic neutropenia q 12-14d; thrombocytosis, reticulocytosis, monocytosis when in neutropenic episode

235
Q

Tx/Px- Cyclic Hematopoiesis

A

Abx, bone marrow transplant; poor px

236
Q

Species/breed- trapped neutrophil syndrome

A

border collies (ferrets?)

237
Q

CS/bloodwork- trapped neutrophil syndrome

A

persistent neutropenia despite myeloid hyperplasia within BM, recurrent infections, +/- born narrow skull and extremities

238
Q

Species/breed- Pelger-huet

A

dogs (es.p australian shep) > cats

239
Q

Dx- Pelger-huet

A

Microscopy- bilobed, dense chromatin clumping, non-toxic mature neutrophils (functionally normal with normal cytoplasm)

240
Q

PE/CS- - Pelger-huet

A

None! great Px

241
Q

Tx- Pelger-huet

A

None needed

242
Q

Rule outs- Pelger-huet

A

left shift, pseudo-PH (drugs, leukemia, MDS)

243
Q

Species/breed- Chediak-Higashi

A

Persian cat

244
Q

Dx- Chediak-Higashi

A

Blood film with enlarged abnormal granules/inclusions in neutrophils in “smoke blue” Persian

245
Q

PE/CS- Chediak-Higashi

A

photophobia, bleeding (plt defect), hypopigmentation, +/- increased infxn risk

246
Q

Reasons for leukocyte inclusions

A

organelles, toxic change granules, genetically-abnormal cell components, phagocytized material, infectious agents

247
Q

What might reddish granules in neutrophils of Birman cat indicate?

A

Nothing- genetic variation. Also seen in himalayan and siamese

248
Q

Species/breeds- macrothrombocytopenia

A

CKCS, norforlk, cairn terriers

249
Q

Clinical significance- macrothrombocytopenia

A

no increased bleeding bc plt size makes up for lower numbers, 30-50% CKCS affected, genetic testing available

250
Q

Species/breeds- hereditary stomatocytosis

A

Mini and standard schnauzers, poms, malamutes, Drentse patrijshonds

251
Q

Of hereditary stomatocytosis breeds, in which breeds are other conditions associated

A

Malamutes also have chondrodysplasia; Drentse dogs have polysytemic dz (growth retardation, D, pu/pd, weakness, somnolence (NO CS in schnauz, pom)

252
Q

Px - hereditary stomatocytosis

A

Not life threatening in malamutes, Drentse usually euthanized young due to progressive deterioration

253
Q

Non-hereditary causes of stomatocytosis

A

regenerative anemias, liver dz, lead poisoning

254
Q

Why does hereditary elliptocytosis occur? What is the clinical significance

A

abnormalities in RBC skeletal membrane proteins that maintain normal shape; No clinical signs

255
Q

Important differences between acquired and inherited methemoglobinemia; name similarities

A

Acquired d/t toxicity, so CS= V, D, anorexia, anemia, etc; no other oxidative damage, signs of toxicity in hereditary. All forms have brown blood, + spot test, and cyanotic MM

256
Q

What enzyme is deficient in hereditary methemoglobinemia

A

methemoglobin reductase (cytochrome B5 reductase)

257
Q

Species/breed- PK deficiency

A

Dog/cat: Basenji and beagle, Abyssinian, Somali, DSH

258
Q

Compare dog/cat differences in PK deficiency

A

Dogs: young, more severe regen. anemia, fatal in 1-5 y d/t sequelae of osteosclerosis and myelofibrosis;
Cats: older at dx, more mild anemia, less CS, good Px

259
Q

Testing options- PK deficiency

A

Measure low total RBC PK acitvity or basenji or cat genetic test- no test works all the time in dogs

260
Q

Species/breed- PFK deficiency

A

Springers, Cockers, whippets, Wachtelhund

261
Q

CS/lab findings- PFK deficiency

A

Persistent hemolytic anemia +/- occasional intravasc hemolysis w/ Hgb’uria, also general non-specific illness signs, mild hepato-splenomegaly, muscle wasting (less myopathy than in people)

262
Q

Testing options- PFK

A

Measure RBC PFK activity in homozygous >3m old; PCR DNA test for heterozygous carriers and normal animals (but doesnt work in wachtelhunds)

263
Q

Px/Tx for PFK

A

Normal life if managed well: avoid stress, excitement, high temps; tx with aspirin for fever in hemolytic episodes

Hematology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions