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issues and policy > hematoligic disorders > Flashcards

hematoligic disorders Flashcards

1
Q

hgb

A

14-18g/100ml

12-16g/100ml

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2
Q

HCT measures the % of a given volume of whole blood, that is occupied by erothrocytes

A

40-54%

37-47%

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3
Q

TIBC

A

250-450ug/dl

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4
Q

serum Iron

A

50 to 150ug/dl

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5
Q

MCV- average size of the indivual erythrocyte

A

80-100fl

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6
Q

MCH average amount and weight of HGB in a single erythrocyte

A

26-34pg

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7
Q

microcytic

A

less than 80 MCV

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8
Q

normocytic

A

80 to 100 MCV

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9
Q

macrocytic

A

over 100 mcv

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10
Q

Mean corpuscular HGB concentration MCHC

A

32-36% expression of average hgb concentratio or proportion of each RBC occupied by HGB as a percentage more accurate than MCH

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11
Q

hypochromic MCHC

A

less than 32%

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12
Q

normochromic MCHC

A

32 - 36%

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13
Q

hyperchromic MCHC

A

over 36 contraversial

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14
Q

Low MCV less than 80

A

iron defficiency anemia and thalassemia

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15
Q

high MCV anemia greater than 100

A

b12 or folate defficiency, etoh, liver failure and drugs

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16
Q

normocytic MCV 80-100 anemia

A

anemia of charonic disease, sickle cell, renal faiure, blood loss, hemolysis

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17
Q

iron defficiency anemia

A

low MCV less than 80
most common cause
decreased IRON for RBC formation
caused by blood loss, inadequate iron intake or impaired absorption.

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18
Q

Iron defficiency anemia S and S

A 
few sx with HCT over 30
pica
dypsnea with mild exercise
HA
postural hypotensioin
pallor 
palpitations tacchy
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19
Q

IRON deff anemia Labs

A

MCV less than 80
low MCHC less than 32
“micro hypo”
High TIBC- 240 to 450 micrograms per deciliter (mcg/dL).
serum ferritin is low 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.

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20
Q

iron defff not most common anemia in one pop

A

gero (anemia of chronic disease)

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21
Q

Iron defficiency anemia tx

A

oral ferrous sulfate- 300-325 1-2hrs after meals
dont take with antacids
take with vitamin C
rasins, geen vegies, red meats, citrus products,

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22
Q

Thalassemia def

A

genetically inherited disorders resulting in abnormal HGB production resulting in microcytic MCV less than 80 hypochromic MCHC less than 32.
mediterianina african, indian etc

normal TIBC 240 to 450 micrograms per deciliter (mcg/dL).

Normal serum ferritin 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.

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23
Q

thalassemia treatment

A

not much, dont give iron, RBC way later on

splenectomy way way down the road

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24
Q

Folic acid deficiency def

A

macrocytic MCV over 100, normochromic 32-36 due to folic acid deficiency or mal absorption

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25
Q

Folic acid deficiency anemia s and s

A

NO NEUROLOGICAL SIGNS ARE SEEN WHICH IS DIFFERENT FROM B12
glossitis
fatigue,
low folate levels Adults - 2-20 ng/mL, 2-20 μg/L, or 4.5-45.3 nmol/L.
he lists red blood cell folate less than 100ng/ml
HCT and RBC decreased

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26
Q

folic acid deficiency anemia treatment

A

folate 1mg orally daily

bananans, peanut butter, fish green leafy veggies, iron fortified breads and cereal

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27
Q

pernicious anemia def

A

macrocytic MCV over 100, normochromic MCHC 32-36 anemia due to deficiency of intrinsic factory which results in mal absorption of B12

28
Q

pernicious anemia def

A 
glossitis- big beefy red tongue 
lss of vibratory sense
loss of fine motor control
positive romberg
positive babinski 
dizzy annorexhea
29
Q

pernicious anemai labs

A 
low hgb, hct, adn RBC's
MCV is increased over 100
serum b12 is less that 01 mcg/ml
anti-IF and antipareietal cell atntibody test affirms a deficiency 
schilling test may help determine cause
30
Q

pernicious anemia treatment

A

B12 100mch im daily for one week

lifelong monthly admin may be indicated

31
Q

anemia of chronic disease

A

chronic MCV 80-100 MCHC 32-36 associated with chronic inflammation, infection, renal failure or malignancy - associated with decreased erythrocyte life span.
SECOND MOST LIKELY CAUSE OF ANEMIA

SERUM IRON AND TIBC LOW serum Ferritin is high serum ferritin 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.

and TIBC is low normal TIBC 240 to 450 micrograms per deciliter (mcg/dL).

32
Q

sickle cell anemia

A

chronic hemolytic anemia that is genetically transmitted by sickle shaped RBC

an acute periodic exacerbation in which RBC’s become sickle shaped and cause obstruction

cellular hypoxia, results in acidosis and tissue iscemia
pain occurs from tissure ischemia, and blood hyperviscoisty

33
Q

factors that percipitate sickling

A

hypoxia, infections, high altitudes, dehydration, physical or emotional stress, surgery, blood loss, acidosis.

34
Q

sickle cell s and s

A

increased succeptability to infection
sudden onset pain in chest back and abdomen
joint pain

35
Q

sickle cell labs

A

HGB down, preipehral smear shows sickle shaped RBC’s

celulose acetate and cirate agar gel electrophoresis to confirm HGN genotype

36
Q

sickle cell treatment

A

acute - fluids for dehydration

analgesics for pain, o2 for hypoxemia

37
Q

von villebrand disease

A

reduced ability to produce blood clots (genetic) deficiency in clotting factory VIII 8

S and S
frequent prolonged or sever episodes of bleeding
easy brusing

management isdesmopressin, adding factor 8

38
Q

leukemia

A

neoplasms arising from hematopoietic cells in bone marrow

39
Q

leukemia

A

more frequent in males,

40
Q

leukemia ANL/AML

A

acute nonlymphocytic anemia/ acute myelogenous leukemia

80% of leukemia in adults
remission from 50% to 80%
long term survival is 40%

41
Q

leukemia ALL

A

acute lymphocytic lukemia
more difficult to treat in adults than in kids
HALLMARK OF DISEASE IS PANCYTOPENIA WITH CIRCULATING BLASTS

42
Q

leukemia CLL

A 
chronic lymphocytic leukemia 
most common leuk in adults
occurs in middle and old age
median survival is 10 years
LYMPHOCYTOSIS IS HALLMARK OF THE DISEASE
43
Q

Chronic myelogenous leukemia

A

CML
most often 40 or older
median survival is 3-4 years
HALLMARK IS PHILADELPHIA CHROMOSOME seen in leukemic cells

44
Q

leukemia s and s

A

may be asymptomatic
cancer stuff
generalzed lymphadenopathy

45
Q

leukemia labs

A

CBC with subnormal RBCs and neurtrophils
elevated ESR
peripheral blood smear differentiates between acute and chronic
NEED BONE MARROW ASPIRATION TO CONFIRM DIAGNOSIS

46
Q

leukemia management

A

chemo- use allopurinot to reduce tumor lysis syndorme in high risk patients

bone marro transplant
control of symptoms

47
Q

Lymphoas

A

lymphocytic malignancy

diagnoses by biopsy of enlarged lymph nodes

48
Q

lymphoma stage 1-4

A

lymphoma stage 1: localized to single node or group
2 more than one node or group, confined to one side of diaphragm
3nodes or spleen involved, both sides of the diaphragm
4. liver or bone marrow involvmentt.

49
Q

when to generally biopsy a node

A

any node greater than one cm, not associated with infection lasting more than 4-6weeks

50
Q

non hodgkins lymphoma

A 
may be viral cause, unknown
presents with lymphadenopathy 
most common neoplasm between 20-40 years of age
less predictable patten of spread
advanced stage is usually apparent
51
Q

hodgkins disease

A

cause is unknown
more commmon in males around 32 years of age
usually presents iwth cervical adenopathy and spreads in a predictable fashion along lymphy node groups\

CHARACTERISTIC REED STERNBERG CELLS DIFFERENTIATE FROM NON HODGKINS DISEASE

52
Q

HODG AND NON HODGE DX

A

ct, xray, mri used to locate and stage

BIOPSY AND HISTOPATHOLOGIC EXAM USEED TO CONFIRM DX

53
Q

hodg and non hodge treatment

A

radiation, chemo, bone marro transplant.

54
Q

ITP

A

thrombocytopenia resulting from autoimmune destruction of platelets with or without supression of thrombopoiesis

55
Q

ITP concepts

A

usually chronic, only occasionally requiring hospitilaization, women outumber men 3-1

56
Q

ITP labs and diagnostics

A

bone marro analysis
low platelet count 150,000 to 450,000 platelets
with other causes of thrombocytopenia ruled out,

57
Q

ITP management

A

may not need to treat untill plt is less than 20K
high dose steroids can push up count in a few days
iv gamma globulin, works quickly as well
gamm glob is preferred inHIV patients
patlet transfuison may help as well

58
Q

ITP thrombocytopenic precautions

A

avoid constipaiton
no floos or shaving
hold pressure for 5 mins on cuts or line insertion

59
Q

HIT

A

argatroban, lipirudin (refuldan

60
Q

how to differentiate ITP from SLE as both have thrombocytopenia

A

bone marrow aspiration will tell u

61
Q

DIC - acuired coagulation defficiency intravascular activation of coag and fibrinolytic systems thrombin and plasmin are activated, causing

A

simultaneous thrombus and hemorrhage- mortality is 50-85%

62
Q

DIC is associated with

A 
malignant neoplasm
burns
shock
obestrical complicaitons
acute leukemia 
liver disease
63
Q

DIC pathophys

A

thrombin causes conversion of fibrinogen to fibrin, producing fibrin clots and microcoagulation

coagulation factors IE fibrinogen, prothrombin, platelets, factor 5, and 8 are thus reduced

criculating plasmin, activates the firinolytic system which lyses fibrin clots tion fibrin degradation products

hemmorhage results from the anticoagulant activity of Fibrin degradation products and the depletion of coagulation factors

64
Q

DIC s and S

A

DIC variens greatly in severity

petechiae and mucous membrane bleeding

65
Q

DIC labs

A

thrombocytopenia Plat less than 150k
decreased RBCs
hypo fibrinogen less thant 170mg/dl
increased fibrin degradation products over 45mcg/ml or rpresent at over 1:100 dilution
pt over 19 seconds
ptt over 42 second
d dimer positive at 1:8 dilution reflects simultaneous activation of thrombin and plasmin
increased FDP’s gives a predictive accuracy of 96% for diagnosing DIC

66
Q

DIC treatment

A

treat the underlying condition and control the bleeding
platelet transfusions for thrombocytopenia
FFP for clotting factors
cryoparticiate to maintain fibrinogen levels are givenif bleeding is severe
use of heparin remains contriversial
therapy is aimed at cessation of bleeding and increasing plasma fibrinogen, and platelet count and decreasng FDP’s

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