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first aid diseases > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Anisocytosis =

A

varying sizes

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2
Q

Poikilocytosis =

A

varying shapes

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3
Q

Plts contain?

- stored in?

A 
dense granules (ADP, Ca), alpha granules (vWF, fibrinogen)
- 1/3 in spleen
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4
Q

vWF R? Fibrinogen R?

A

GpIb

GpIIb/IIIa

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5
Q

Leuk’s

  • 2 types?
  • nl #
A

Granulocytes (N, Eo, Baso)
Mononuc (monocytes, lymph’s)
- 4-10k

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6
Q

Hyperseg’d poly’s =

Seen in?

A

5+ lobes in N’s

VitB12/folate defic

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7
Q

Eo’s produce what 2 substances?

Nuc is?

A

Histaminase and arylsulfatase (limit rxn post-mast cell degran)
- bilobed

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8
Q

Baso’s secrete?

A

heparin (anticoag)
hist (vasodil)
LTD4

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9
Q

Cromylyn sodium =

A

prevents mast cell degranulation

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10
Q

VitK

  • active form?
  • cofactor for
A

reduced by epoxide reductase

- 2, 7, 9, 10, C, S

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11
Q

Warfarin =

  • how long until it works?
  • which is the last factor to go away?
A

inhib’s epoxide reductase -> no VitK -> no factors 2, 7, 8, 10, C, S

  • full anticoag in 3-4d
  • prothrombin has longest t 1/2
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12
Q

vWF carries/protects which CF?

A

VIII

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13
Q

Heparin =

A

act’s antithrombin, which inact’s 2, 7, 9, 10, 11, 12

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14
Q

Factor V Leiden mutation =

A

Factor V is resistant to inhib by act’d PrC -> more clotting

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15
Q

Bernard-Soulier synd =

  • sx
  • labs
  • dx by
A

AR; no GpIb -> vWF can’t bind plts for plt plug (intrinsic cascade)

  • thrombocytopenia, giant plts (“big suckers”)
  • incr’d BT
  • Ristocetin cofactor assay (causes plts to clump only if vWF is there and its Rs work!)
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16
Q

What do plts have in them?

A

vWF, fibrinogen

Arachidonic acid -> via COX to TXA2 (more clotting)

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17
Q

Glanzmann’s thrombasthenia =

- periph smear shows?

A

AR; no GpIIb/IIIa, so plts can’t be linked together via fibrinogen -> less clotting
- no plt clumping, incr’d BT but nl plt ct

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18
Q

Aspirin =

A

inhib’s COX, so not TXA2 syn

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19
Q

Ticlopidine =

A

inhib’s ADP-induced exp’n of GPIIb/IIIa on plts -> no plt X-linking by fibrinogen and no clots

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20
Q

Clopidogrel =

A

inhib’s ADP-induced exp’n of GPIIb/IIIa on plts -> no plt X-linking by fibrinogen and no clots

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21
Q

Abciximab =

A

inhib’s GPIIb/IIIa on plts directly -> no plt X-linking by fibrinogen and no clots

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22
Q 
What are these RBCs seen in:
acanthocyte (spur cell)
basophilic stippling
bite cell
elliptocyte
macro-ovalocyte
ringed sideroblasts
schistocyte, helmet cell
spherocyte
Teardrop cell
Target cell
A
  • liver dz, abetalipoproteinemia
  • “BASte the ox TAiL” -> Thalassemias, Anemia of chronic dz, Lead poisoning
  • G6PD defic
  • hereditary elliptocytosis
  • megaloblastic anemia, marrow failure
  • sideroblastic anemia (Fe in mito -> bad)
  • DIC, TTP/HUS, traumatic hemolysis (metal heart valve)
  • hereditary spherocytosis, autoimm hemolysis
  • BM infiltration (forced out of BM home…tear tear)
  • “HALT, said the hunger to the Target” -> HbC dz, Asplenia, Liver dz, Thalassemia
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23
Q

Heinz bodies =

- seen in

A

ox’n of Hgb sulfhydryl gps -> denatured Hgb that precipitates and hurts mem -> bite cells
- G6PD defic, similar bodies in a-thalassemia

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24
Q

Howell-Jolly bodies =

- seen in

A

baso nuc remnants in RBCs, usu removed by spleen

- hyposplenia or asplenia, post-mothball ingestion (naphthalene)

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25
Q 
Anemia in:
kids? why?
adult male?
adult female?
preg female? why?
A

< 11.5 (high phos -> incr’d 2,3BPG -> R shift OBC -> more O2 released, so don’t need as high Hgb)
< 13.5
< 12.5
< 11 (2x incr in pl vol than RBC mass)

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26
Q

Hemochromatosis =

A

HFE gene prod -> binding of pl transferrin to mucosa cell R -> incr’d transferrin reab’n by GI cells -> more mucosal cell Fe so more released into the pl to bind w/ transferrin -> high pl Fe

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27
Q

Plummer-Vinson synd

  • caused by?
  • manifestations?`
A

chronic Fe defic -> eso web (dysphagia for solids but not liquids), achlorhydia, atrophic glossitis, koilonychia (spoon nails), pica

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28
Q

Hepcidin =

A

Antimicrobial peptide released by liver in response to inflamm (acute phase rct) -> enters Mphage in BM -> prevents release of Fe to transferrin bc binds ferroportin on intestinal mucosa cells and Mphage so Fe can’t get out -> incr’d ferritin syn and Fe stores but little released

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29
Q

Fanconi synd =

sx?

A

renal tubular damage (from Pb)

- RTA type II (prox loss of bicarb), aminoaciduria, phosphaturia, glucosuria

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30
Q

Stages of Fe defic:

A 
No Fe stores
Decr'd serum ferritin
Decr'd serum Fe
Incr'd TIBC
Decr'd Fe sat'n
Normocytic normochromic anemia
Microcytic hypochromic anemia
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31
Q 
Decr'd MCV
Decr'd serum Fe
Incr'd TIBC
Decr'd % sat
Decr'd serum ferritin
Incr'd RDW
Decr'd RBC count
Hb electrophoresis nl
A

Fe defic bc sm RBC, less Fe so incr’d TIBC, decr’d ferritin bc less stored, incr’d RDW bc diff in sizes

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32
Q 
Decr'd MCV
Decr'd serum Fe
Decr'd TIBC
Decr'd % sat
Incr'd serum ferritin
Nl RDW
Decr'd RBC count
Hb electrophoresis nl
A

ACD (anemia of chronic dz) - diff than Fe defic bc decr’d TIBC from incr’d serum ferritin, nl RDW
- first is normocytic normochromic anemia -> can become microcytic hypochromic

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33
Q

Decr’d MCV
Nl serum Fe, TIBC, % sat, serum ferritin, RDW
Incr’d RBC count

A

a-thal or b-thal minor

Hgb electrophoresis nl in a-thal trait

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34
Q 
Decr'd MCV
Incr'd serum Fe
Decr'd TIBC
Incr'd % sat
Incr'd serum ferritin
Nl RDW
Decr'd RBC count

Also have?

A

Lead poisoning bc have enough Fe, everything is nl, but decr’d RBC ct
AND
ringed sideroblasts (bc can’t turn Fe into heme, NZ doesn’t work) and coarse basophilic stippling (ribosomes)

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35
Q

Lead poisoning -> inhibits? interferes w/?

- high risk in?

A

inhibits ferrochelatase and ALA DH -> decr’d heme syn (ringed sideroblasts bc have Fe in mito but no heme)
inhib’s ribonuclease so can’t brkdwn ribo’s in RBCs -> basophilic stippling
interferes w/ growing cartilage -> see deposits in bones and lines on gums (Burton’s lines)
- houses built before 1978

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36
Q

Sx of lead poisoning?

Trtmt?

A

LEAD:
Lead Lines on gums (Burton’s lines) and on metaphyses of long bones on XR
Encephalopathy and Erythrocyte basophilic stippling
Ab colic and sideroblastic Anemia
Drops - wrist/foot
Trtmt by chelation: EDTA and succimer for adults, succimer (EDTA, dimercaprol) for kids

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37
Q

How is VitB12 ab’d?

A

Eaten ->
Pepsin (from pepsinogen via gastric acid from parietal cells) frees it from pr’s ->
Binds R-binders from salivary gl’s ->
Panc NZs in duo free B12 -> binds IF (from parietal cells) in duo ->
B12-IF reab’d in term ileum -> B12 binds transcobalamin II -> secreted into pl -> used or stored in liver for 6-9yrs

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38
Q

Folic acid

  • circ’ing form?
  • reab’n blocked by?
  • supply in liver lasts?
A
  • methylTHF
  • EtOH, OCPs; phenytoin blocks intestinal conjugase which converts it into ab’able form
  • 3-4mo
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39
Q 
Lab findings in VitB12 defic:
Decr'd...
Incr'd...
See in periph bl?
See in BM?

Determine cause by?

A
  • Decr’d serum B12
  • Incr’d serum homocysteine and methylmalonic acid
  • pancytopenia, oval macrocytes, hyperseg’d Ns (>5 lobes)
  • megaloblastic nucleated cells w/ open (lacy) chromatin pattern
  • Schilling test (PO radioactive B12 +/- IF or panc extract)
40
Q

VitB12 defic -> demyelination of what?

A

Post columns (decr’d vibratory sensation and proprioception)
Lat corticospinal tract (spasticity)
Dorsal spinocerebellar tract (ataxia)

41
Q

Haptoglobin =

A

acute phase rct, combines w/ Hgb to form complex that Mphage eat -> decr in serum haptoglobin

42
Q

Target cells =

sign of?

A

excess RBC mem

- hemoglobinopathy (like HbS) or EtOH excess (incr’d choles -> incr’d cell mem)

43
Q

5 ox’ing drugs:

A

CD-NPS

chloroquine, dapsone, nitrofurantoin, primaquine, sulfonamides

44
Q

Hemolytic anemias:
extravasc hemolysis -> ?
IV hemolysis -> ?

A

EV: Mphage phagocytosis, unconj’d hyperbilirubinemia -> jaundice, incr’d LDH
IV: decr’d serum haptoglobin, hemoglobinuria, incr’d LDH

45
Q

Does the hemolysis occur EV or IV? What type of defect (intrinsic vs. extrinsic)

  • Hereditary spherocytosis
  • PNH
  • Sickle cell
  • G6PD
  • Pyr kinase defic
  • IgG-mediated
  • C’-mediated
  • IgM-mediated
  • MHA (macroangiopathic hemolytic anemia)
  • Malaria
A
  • EV (intrinsic defect)
  • IV (intrinsic)
  • EV (intrinsic)
  • IV (intrinsic) or EV
  • EV (intrinsic) (PK defic)
  • EV
  • IV or EV
  • IV usu, some EV
  • IV (extrinsic) (MHA)
  • IV (extrinsic)
46
Q

Hereditary spherocytosis:

  • defect in?
  • aplastic crisis from?
  • (+) ? test
A
  • AD: ankyrin, band 3, pr 4.2, spectrin
  • Parvov. B19 infec
  • (+) osmotic fragility test (bc bad mem)
47
Q

What yields hemolytic anemia in a newborn?

Which is an acq’d defect -> hemolytic anemia?

A

Pyr kinase defic

PNH

48
Q

HbC =

- if you have HbSC?

A

Glu -> Lys mutation at residue 6 in b-globin

- you have milder dz than HbSS

49
Q

PNH triad?

  • Flow cytometry shows?
  • Trtmt
A 
Hemolytic anemia
Pancytopenia
Venous thrombosis
- CD55/59 (DAF, protectin) are NOT on RBCs on flow cytometry
- Eculizumab (term C' inhib)
50
Q

Sickle cell trtmt?

A

Hydroxyurea bc incr’s HbF, which doesn’t sickle; BM transplant

51
Q

Direct vs. Indirect Coomb’s tests?

- (+) direct Coomb’s test in?

A

Direct: anti-Ig Ab added to pt’s bl -> RBCs aggregate if coated w/ Ig
Indirect: nl RBCs added to pt’s serum and add anti-IgAb -> RBCs aggregate if anti-RBC Ig in pt’s serum
- AIHA (hot and cold)

52
Q

When do you see schistocytes on periph bl smear?

A

W/ micro/macro-angiopathic hemolysis

53
Q

Drug-induced hemolytic anemia, MoA for:

  • Pn
  • Quinidine (Class IA anti-arrhythmic)
  • a-methyldopa (a-agoinst)
A
  • a-Pn IgG attaches to RBC mem
  • drug-IgM imm complex deposits on RBC -> IV hemolysis
  • drug alters Rh Ag on RBCs -> autoAbs to new Rh
54
Q

Infectious mononucleosis

  • caused by? infects how?
  • sx?
  • imm response is what?
  • test for it how?
A
  • EBV (less commonly CMV) first rep’s in epi cells in oropharynx -> spreads to B cells in LNs (attaches to CD21 on B cells) -> incr’d syn of IgM [atyp lymphocytosis!]; also goes to liver (-> hepatitis)
  • severe fatigue, exudative tonsilitis, HSM (periart lymphatic sheath in spleen enlarged) (spleen can rupture), painful lymphadenopathy (incr’d CD8 T cells in paracortex of LN), rash if trted w/ Amp
  • atyp CD8 T cells (big nuc and lots of blue cyto), which are reactive T cells
  • Monospot test: pos. heterophil Ab test (detects IgM Abs to animal RBCs) is screening test -> confirm w/ VCA test (viral capsid Ag)
55
Q

How to tell acute vs. chronic leukemia?

A

Do BM aspirate w/ blast count:
Acute has >20% blasts in BM
Chronic has >10% blasts in BM

56
Q

ALL

  • Age
  • Markers?
  • Can manifest at?
  • Better prog w/?
A
  • <15yo
  • CALLA (CD10) and TdT
  • B cell types goes to CNS/testes, T cell type (CD10-) can be mediastinal mass
  • t(12;21)
57
Q

SLL/CLL = ?

  • Age
  • Periph bl smear shows?
  • Assoc’d sx?
  • Diff btwn SLL and CLL?
A

Virgin B cell leukemia (no pl cells, no Igs and incr’d risk for infec)

  • > 60yo
  • smudge cells
  • asymp, autoimm hemolytic anemia (IgG and IgM), lymphadenopathy in old ppl
  • SLL is confined to LNs, CLL has leukemic phase (incr’d periph bl lymphocytosis or BM involvement)
58
Q

Hairy cell leukemia = ?

  • Age
  • Stains?
  • Sx? Pos/neg
  • Trtmt
A

Mature B-cell tumor

  • Middle-aged men
  • TRAP(+)
  • Splenomegaly from prolif of B cells in red pulp, trapped in BM -> fibrosis and dry tap; NO lymphadenopathy
  • Purine (adenosine) analogs = Cladribine (2-CDA)
59
Q

Adult T cell leukemia

  • Markers?
  • Sx?
  • Due to?
  • Assoc’d w/?
A
  • CD4+ Tdt-
  • skin infiltration (RASH); lytic bone lesions -> hyperCa
  • act’n of TAX gene -> inact’n of p53
  • HTLV-1
60
Q

AML

  • Age?
  • Periph smear shows?
  • stain is (+) for?
  • M3 AML subtype =
  • What do you usu see w/ M3?
A
  • 15-59yo, avg 65yo
  • incr’d circ’ing myelobl’s (-> Ba, Eo and N)
  • peroxidase
  • t(15;17) -> PML, trt w/ all-trans retinoic acid to induce differentiation of myeloblasts
  • DIC, Auer rods (when released in trtmt can cause DIC)
61
Q

CML

  • Age
  • Cause?
  • Periph bl smear shows?
  • Sx?
  • Labs show?
  • Trtmt?
A
  • 30-60yo
  • Philadelphia chr, t(9;22), bcr-abl gene
  • Basophlilia w/ NO Auer rods
  • HSM, painless lymphadenopathy, thrombocytosis sometimes present (only leuk w/ this!!!)
  • Low leuk alk phosphatase (via high in leukemoid rxn to infec)
  • Imatinib (sm-molec inhib of bcr/abl TK)
62
Q 
Where do you see these translocations?
t(9;22)
t(8;14)
t(11;14)
t(14;18)
t(15;17)
A
  • CML
  • Burkitt’s lymphoma (c-myc act’n)
  • Mantle cell lymphoma (NHL, cyclin D1 act’n)
  • Follicular lymphoma (NHL, bcl-2 act’n)
  • PML (M3 type of AML)
63
Q

Where are these found:
B cells
T cells
Histiocytes

A
  • LN germinal follicles, periph areas of white pulp of spleen
  • LN paracortex (parafollicular), periart sheath in spleen, thymus
  • LN subcapsular sinuses, skin (as Langerhans cells)
64
Q

Hodgkin’s lymphoma

  • arises from?
  • characterized by?
  • age of onset? M/F?
  • which is assoc’d w/ EBV?
  • worst prog w/?
  • best prog w/?
  • sx?
A
  • single gp of nodes w/ contiguous spread, usu starts in neck region
  • Reed-Sternberg cells (binuc/bilobed, owl’s eyes, CD30+, CD15+), secrete cytokines to bring in other cells which define type of HL
  • bimodal: yg adults and >55yo; M>F except nodular sclerosing F>M
  • mixed cellular
  • lymphocyte mixed or depleted forms
  • lymphocyte-rich type
  • constitutional, low-gr F that comes and goes, night sweats, wt loss
65
Q

Non-Hodgkin’s lymphoma

  • arises from?
  • usu involves?
  • age of onset?
  • may be assoc’d w/?
  • sx?
A
  • mult periph nodes, extranodal involvement or starts extranodal; non-contiguous spread
  • B cells, some have T cell origin though
  • 20-40yo
  • HIV, immsupp’n
  • less constitutional sx than HL
66
Q

Burkitt’s lymphoma =

  • assoc’d w/? presents as?
  • age of onset
  • genetics
  • histo shows?
A

NHL

  • EBV, jaw lesion in Africa or GI/para-Ao’ic nodes in America
  • yg adults
  • t(8;14) -> act’s c-myc
  • “starry sky” of lymph’s w/ star Mphage clearings
67
Q

Diffuse large B cell lymphoma =

  • age of onset
  • derives from
  • common?
A

NHL

  • older adults, 20% in kids
  • germinal center
  • Yes, most common adult NHL
68
Q

Mantle cell lymphoma =

  • age of onset
  • genetics
  • marker
  • prognosis
A

NHL

  • older males
  • t(11;14), act’n of cyclin D1
  • CD20+ B cells, and CD5+
  • poor
69
Q

Follicular lymphoma =

  • age of onset
  • genetics
  • prognosis
A

NHL

  • adults
  • t(14;18), act’s bcl-2 (anti-apoptosis gene)
  • hard to cure, indolent course
70
Q

Mycosis fungoides/Sezary syndrome =

  • marker
  • course
  • why might you mistake it for MM?
A

Mature T cell neoplasm, CD4+

  • Starts as skin rash -> plaque -> nodular masses
  • Sezary when reaches leukemic spread (see cells w/ cerebriform nuc)
  • has lytic bone lesions w/ hyperCa, like MM, but also has RASH
71
Q

MM =

  • on histo?
  • Sx?
  • cell makes?
  • Light chains can do what?
  • RBCs looks like?
  • bone lesions are ? why?
A

monoclonal pl cell (IgG > IgA) ca from bone

  • fried egg appearance
  • CRAB: hyperCa, Renal insuff, Anemia, Bone lytic lesions and Back pain
  • monoclonal M pr
  • become amyloid (1* amyloidosis), make BJ pr’s in urine
  • Rouleaux formation
  • lytic bc pl cells make IL-1 = osteocl act’ing factor
72
Q

Waldenstrom’s macroglobulinemia =

  • don’t have?
  • does have?
A

has M spike on electrophoresis like MM

  • no lytic bone lesions
  • does have hyperviscosity sx and BJ pr
73
Q

MGUS =

  • sx?
  • progresses to?
  • does not have?
A

monoclonal gammopathy of undetermined significance = monoclonal expansion of pl cells w/ M spike

  • asymp
  • MM at rate of 1-2% per yr
  • BJ pr
74
Q

Langerhans cell histiocytosis =

  • presents as?
  • do the cells work?
  • marker?
  • characteristic look on EM?
A

prolif d/o of DCs (Langerhans histiocytes)

  • in kid as lytic bone lesions and skin rash
  • cells are functionally immature, don’t stim T cells via Ag presentation (not func’ing APCs)
  • S-100 (neural crest origin) and CD1a
  • Birbeck granules (tennis rackets)
75
Q

PT

  • measures what?
  • use for?
A
  • Extrinsic coag system

- Pt’s on Warfarin, eval liver func, defect F VII defic

76
Q

PTT

  • measures what?
  • use for?
A
  • intrinsic coag system

- Pt’s on heparin (not needed for LMWH)

77
Q

D-dimer assay

  • detects what?
  • use for?
A
  • X-linked insol fibrin monomers in fibrin clot

- evidence of degradation of fibrin clot: CA thrombosis, screening for PE or DIC

78
Q

4 anti-thrombi mech’s in sm vessels?

A

1) heparin-like molec’s that enhance AT III activity which neutralizes Ser protease coag factors (7, 11, 9, 10)
2) PGI2 (prostacyclin)
3) prC/S (inact F V and F VIII)
4) tPA (act’s plasminogen to plasmin)

79
Q

3 pro-thrombus mech’s in sm vessels?

A

1) TXA2 (made by plts, inhib’d by COX inhib’s)
2) vWF (made in Weibel-Palade bodies in endo cells and megakaryocytes, carried in plts)
3) FIII = TF = tissue thromboplastin (released by injured tissue, act’s F VIII)

80
Q

Where is F VIII:c made?
What stabilizes it?
What does it act on?

A
  • in liver and reticuloendo cells
  • vWF prevents its degradation in pl
  • when act’d, helps IXa act Xa
81
Q

Factors consumed in a clot to produce serum are?

A

I, II, V, VIII

82
Q

How do plts make a temp plug?
What changes in the stable plt plug?
How do you test formation of the temp plug?

A
  • Adhesion -> release rxn (of ADP) -> TXA2 syn -> temp plug that is held together by fibrinogen (btwn GpIIb/IIIa Rs on plts)
  • held together by fibrin monomers made by clotting cascade
  • bl’ing time
83
Q

INR =

A

standardizes PT for warfarin tx, nl is 2-3

84
Q

How does renal failure -> prolonged bl’ing?

- Reverse w/?

A

Inhib of plt phospholipid by toxic products -> plt aggregation defect (incr’d BT)
- dialysis and desmopressin acetate (incr’s vWF release from endo cells)

85
Q

Von Willebrand dz =

  • dx by?
  • trtmt
  • assoc’d sx?
A

AD; plt adhesion defect bc no vWF -> decr’d VIII:c
Is combo plt and coag factor d/o (incr’d BT and nl/incr’d PTT)
- Ristocetin cofactor assay (causes plts to clump ONLY if vWF is there)
- DDAVP (desmopressin) bc incr’s vWF release from endo cells; OCP (incr’d CFs and decr’s ATIII)
- MVP, Marfans, angiodysplasia

86
Q

Lead poisoning has what affect on heme formation?

- sx?

A

Inhib’s ferrochelatase and ALA DH -> accum of protoporphyrin and d-ALA
- microcytic anemia, GI and kidney dz

87
Q

Acute intermittent porphyria =

  • sx?
  • trtmt?
A

AD; defect in porphobilinogen deaminase -> build-up of porphobilinogen, d-ALA, uroporphyrin (urine)

  • 5P’s = painful ab, port wine-colored urine (when exposed to sunlight), polyneuropathy, psych disturbances, precipitated by drugs (which enhance P450, like EtOH -> decr’d heme and thus more ALAS activity so more build-up)
  • glc (carbs) + heme -> inhib ALA synthase
88
Q

Porphyria cutaneous tarda =

- sx?

A

no uroporphyrinogen decarboxylase -> incr’d uroporphyrin (tea-colored urine)
- blistering cut photosensitivity; most common porphyria

89
Q

Hemophilia A/B =

A

defect in F VIII / F IX -> incr’d PTT

90
Q

VitK defic ->

A

decr’d syn of F II, VII, IX, X, prC/S -> incr’d PT and PTT

91
Q

ITP (idiopathic thrombocytopenic purpura) =

  • occurs when?
  • labs show?
A

IgG Abs to GpIIb/IIIa -> splenic Mphage eat Ab:plt complex -> decr’d plt ct

  • 1-3wks post viral infec in kids, in adults usu 2* to SLE
  • incr’d megakaryocytes
92
Q

Thrombotic thrombocytopenic purpura (TTP) =

  • occurs in who?
  • labs show?
  • sx?
A

no ADAMTS 13 (vWF metalloprotease) -> less degradation of vWF multimers -> have more vWF and more plt aggregation and thrombosis

  • adult F (usu is Ab to ADAMTS13)
  • schistocytes, incr’d LDH
  • 5 sx: F, decr’d plt ct, neuro and renal sx, and microangiopathic hemolytic anemia w/ schistocytes (damaged by plt thrombi)
93
Q

HUS =

  • occurs in who?
  • sx?
A

endo damage at art-cap jxn by Shiga-like toxin of O157:H7 E. coli (undercooked beef) -> plt thrombi, shearing of RBCs
- usu in kids y D; sx like TTP but less CNS sx: F, low plts, renal failure, microangiopathic hemolytic anemia w/ schistocytes

94
Q

Causes of DIC =

A

“STOP Making New Thrombi”

Sepsis (Gm-), Trauma (rattlesnake bite), Obstetric comp’s, acute Pancreatitis, Malig (APL, adenoca), Nephrotic synd, Transfusion

95
Q

If given, what do these incr?

  • Packed RBCs
  • Plts
  • FFP
  • Cryoprecipitate
A
  • Hb and O2 carrying capacity
  • plt ct (~5000/unit)
  • coag factors
  • fibrinogen, F VIII, XIII, vWF and fibronectin
96
Q

Leuk’s:

60yo

A

ALL if <15yo
Hairy cell leuk, CML, or AML(PML) if adult
SLL/CLL or AML(PML) if older

first aid diseases (16 decks)

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