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PANRE > hematology > Flashcards

hematology Flashcards

1
Q

Heme component

A

FE is part of heme- functions to bind and release oxygen as needed

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2
Q

globin component

A

5 subunits- in adult hemoglobin- 2 alpha and 2 beta chains- make up the ADULT hemoglobin

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3
Q

cheleation therapy

A

patients who receive frequent transfusion to remove excess FE

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4
Q

Transferrin and total iron binding capacity (TIBC)

A

Transferrin binds to free Fe —> transferring trasnports FE throughout the body-
TIBC is indirect way of measuring transferring level:
INCREASED transferring and TIBC : Fe deficiency
Decreased Transferrin and TIBC: Anemia of chronic disease

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5
Q

Ferritin

A

decreased in FE deficiency
Increased in anemia of chronic disease
Iron is stored in the ferritin protein molecule- IRON IN STORAGE!

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6
Q

Hemolytic anemia (intrinsic)- inherited disorders)

A

sickle cell anemia, Thalassemia, G6pd deficiency, Hereditary spherocytosis

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7
Q

Extrinsic hemolytic anemia (aquired)

A

autoimmune hemolytic anemia, DIC, TTP, HUS, hypersplenism

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8
Q

LDH

A

enzyme found in RBC- too much rbc destruction leads to increase in serum LDH

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9
Q

indirect bili

A

if too much rbc distruction - causes jaundice

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10
Q

direct bilirubin

A

dark urine production

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11
Q

sickle cell anemia

A

hgb S on hemoglobin electrophoresis

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12
Q

Thalassemia

A

microcytic anemia with normal or increased iron - no tx response to Fe tx.
alpha thalassemia: hgbA, A2 and F- normal hemoglobin ratios
beta thalassemia: hemoglobin electrophoresis shows decreased A, increased A2 and Increased F

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13
Q

G6pd deficiency

A

episodic- sulfa drugs, fava beans, infections- hemolytic anemia

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14
Q

hereditary spherocytosis

A

coombs negative and +osmotic fragility test

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15
Q

autoimmune hemolytic anemia

A

coombs POSITIVE!- microspherocytes

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16
Q

TT{ and HUS: both normal coags

A

TTP: thrombocytopenia, hemolytic anemia, kidney damage ++++++++ neurological symptoms and fever

HUS: TRIAD!= thromboycotpenia, hemolytic anemia and kidney damage- seen in children- kidney inovelemnt higher than in TTP.

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17
Q

DIC

A

prolonged PT and PTT

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18
Q

rouleaux formation

A

stack of coins- multiple myeloma

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19
Q

auto agglutination

A

clumping of RBC- cold agglutinin autoimmune hemolytic anemia

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20
Q

howell jolly bodies

A

decreased splenic function !!!

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21
Q

hemolytic cells

A

bite cells, schistocytes, keratocytes

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22
Q

basophilic stippling

A

SIDEROBLASTIC ANEMIA, THALASSEMIAS, heavy metal poisioning

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23
Q

target cells

A

sick cell, thalassemia

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24
Q

hypersegemented neutrophils

A

B12 and folate deficiencies

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25
Q

Auer rods

A

Acute myelogenous leukemia

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26
Q

reed sternberg cells

A

hodkin lymphoma

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27
Q

b12 deficiency

A

animal food is main source.
b12 binds to IF - absorbed in terminal ileium
-b12 def causs abnormal synthesis of DNA
pernicious anemia- loss of gastric parietal cells- these secrete IF
strict vegans
ETOH

neuro: paresthesia, gait abnormalities, memory loss, dementia, anorexia, diarrhea, glossitis
increase serum omocysteine and methylonic acid
IM b12 repplacement

28
Q

folate deficiency

A

needed for DNA syntehsis- no neuro symptoms.

replace folate

29
Q

iron defi anemia

A

mc due to bleeding
chronic blood loss- colon cancer or hookworm
pregnancy

crave ice, pica, angular cheilitis, koilonychia (nail spoon)-
decreasedferritin, increased TIBC, decreased iron, decreased transferrin sat

give iron, vitamin C increases FE absoroption

30
Q

plummer vinson sndreom

A

dysphagia, esophageal webs, atropic glossitis and fe deficiency

31
Q

lead poisoining

A

abd pain with constip, neurologic symptoms, basophilic stippling
cheleation therapy

32
Q

thalassemia

A

decreased production of globin chains
after 6 months of age- adult HGB is predominant produced
adult: hgb A: 2 alphas, 2 betas
A2: 2 alphas, 2 DELTAS
fetal: 2 alphas: 2 gamma (tracE)- looks like yY

33
Q

alpha thalassemia

A

MC in SE asians
target cells
decreased alpha globin chain production- 4 genes determine it

mild: no treatment
blood transfusion, iron chelating agents

34
Q

beta thalassemia

A

decreased production of beta globins chains—>excess alpha chains
minor- 1/2
major: 2/2

minor- no symptoms
cooley’s : major: become symptomatic at 6 monthshepatosplenomagly, severe hemolytic anamie,a jaundice
TARGET CELLS!
increased hgba2 and hgbF

periodic blood transfusions, vitamin C, folate, iron chelating agents.

35
Q

chronic disease anemia

A

increased ferritin- iron storage due to acute phase reactant, decreased TIBC, decreased serum Fe

36
Q

G6pd def

A

affects mostly males- african american males- heiz bodies-
g6pd usually protects rbc enzyme against oxidative stress- without it- hgb becomes methemoglobin- which does not carry oxygen well. —>these denatured hgb are destructed by splenic macrophages: episodic hemolytic anemia

EPISODIC: splenomegaly- infections, FAV bbeans, SULFA drugs, antimalarials

avoid offending food and drugs
iron/folic acid supp, blood transfusions if needed

37
Q

sickle cell disease

A

micro thrombsois- due to rbc sickling because when someone is hypoxic, decreased solubility- so it causes throbosis- sickeld cells then destroyed by the spleen

infections: osteomyelitis: salmonella- aplastic crisis associated with parvovirus!

h shaped ventrebra, splenic sequestration, painful occlusive crisis (acute chest syndrome, back, abd , bone pain)- priapism common
howell jolly- functional asplenia- due to splenic infarction!

38
Q

TX for sickle cell

A

IV hydration and OXYGEN!- pain crisis
hydroxyurea: reduces frequency of pain crses
folic acid
immunized for s. neumo, h flu, and n.gonrrhea
STEM CELL TRANSPLANT: cure

39
Q

hereditary spherocytosis

A

+osmotic fragility test, hypercrhomic microcytosis, coombs neg, sphre shaped RBC

Tx: folic acid for mild`
splenectomy for severe disease

40
Q

autoimmune hemolytic anemia

A

+direct coombs test: distinguishes from hereditary spherocytosis
warm agglutininis: autoimmune- SLE
cold: at colder temp- mycoplasma, EBV

warm: cortico
cold: avoid cold

41
Q

hemostasis

A

vascular injury causes platelet aggregatin

activation of that: ADP and thromboxane A2- forms platelet plug

42
Q

clotting factors- secondary hemostasis

A

FIBRIN stands- strengthens the platelet plug
Disease: hemophillia, DIC and von willebrand disease
extrinsic path( prolongs PT), intrinsic path (prolongs PTT)

43
Q

PTT

A

heparin, DIC, vwD, hemophilia A and B

factors 1,2,5,8,9, 11 and 12

44
Q

heparin overdose treatment

A

protamine sulfate

45
Q

PT

A

extrinsic pathway: warfarin, vitamin K deficiency, DIC

2, 5,7,10

46
Q

ttp

A

thromboycopenia- petechiae, mucocutaenous bleeding- skin, oral,nose bleed,
2. MICROANGIOPATHIC hemolytic anemi
+neurological symptoms and FEVER!

decreased ADAMTS13- vwf cleaving protese: vwf is not cleaved- so it stays there blocking - small vessel thrombosis- RBC become damaged when they circulate in the occluded small vessels- hemolytic anemia
normal coag
splenomeg

47
Q

TX for TTP

A

plasmapheriesis- TOC- removes antibodies vs.. ADaMTS13

CORTICOSTEROIDS, cylclophosphamide

48
Q

HUS

A

hemolytic uremic syndrome
no fever, or neuro symptoms
preceded by E.coli- shigella or salmonella gastroenteritis
platelet activation by exotoxins: hemolytic anemia, thrombocytopenia

OBSERVATION MOSTLY
TX: plasmapheresis
NO ABX

49
Q

DIC

A

bleed and coag
infections!: gram neg sepsis most common reasons, malignancy, or obstetric

thrombosis and widespread hemorrhage
decrease thrombin, decreased fibrinogen, increased PTT/PT/INR- severe thrombocytopenia, increased fibrinolysis, increased D dimer

TReat underlying….FFP if severe bleed- replaces coag factors

50
Q

ITP

A 
autoimmune thrombocytopenia- mc in children after a viral infection
-mucocutaneous bleed- no splenomegally
normal COAG TESTS!
children: observation, IVIG
adults: cortico +IVIG
51
Q

hemophilia A

A

only in males- x linked
affects intrinsic of clotting

+HEMARTHROSIS, +excessive hermorrhage in trauma or surgery,

prolonged PTT!!- normal platelet levels
TX: factor 8 infusion
desmopressin - increases factor 8 and vwf

52
Q

factor 9-deficiency- christmas disases

A

prolonged PTT- deep tissue bleeding, demopressing IS NOT SUEFUL!!
GIVE FACTOR 9 infusion

53
Q

Von willebrand disease

A

ineffective platelet adhesion- - MOST COMMON HEREDITARY bleeding disorder
it is needed for initial platelet adhesions and prevents factor 8 degradation.
mucocutaenous bleed- menorrhagia, epistaxis, easy bruising- PETECHIAe common in VWF
prolonged PTT, bleeding time and ptt prolongation worse with aspirin
mild: no treatment
severe:DEsmopressin

54
Q

hodgekin’s

A

bimodal- peaks at 20 and then 50: upper body lymph nodes affected- neck, axilla, sholuder, abdomen
Epstein barr virus
painless lympadenopathy, night sweats weight loss and fever- if advanced
reed-sternberg cells!- mediastinal lymphadenopathy

55
Q

non-hodgkin’s lymphoma

A

painless lymphadenopathy
extranodal sites common: GI, skin, CNS MC!!
PERIPHERAL LYMPH NODES MOST COMMON!

56
Q

multiple myeloma

A

plasma cells, african american men, bone pain, recurrent infections, elevated calcium, anemia, kidney failure
monoclonal M rotein spike, bence jones proteins, rouleaux formation, punched out lytic lesions
STEM CELL TRANSPLANT!- curative

57
Q

ALL

A

C childhood malignancy
FEVER MC symptoms
CNS symptoms too
hepatosplenomegaly, lymphadenopathy!!!
bone marrow: hypercellular with more than 20% blasts!!!, anemia, thrombocytopenia, wbc: 5-100,000
oral chemo: hydroxyurea, stem cell trasnplant

58
Q

CLL

A

B cell clonal malignancy
MC leukemia in ADULTS overall
fatigue, lymphadenopathy, hepatosplenomeg
DIFERNTIATED lymphocytes with scattered “SMUDGE cells”, lymphocytosis more than 20k
pancytopenia: thryombocytopenia, anemia
chemo: fludarabine

59
Q

AML

A

MC acute form of leukemia in adults
splenomegaly, gingival hyperplasia, LEUKOSTASIS: wBC is more than 100k

AUER RODS!!!! more than 20% blasts!

60
Q

CML

A

philadelphia chromosome: splenomegaly!!
more than 100k wbc
more than 30 % blasts

61
Q

primary erythrocytosis- polycythemia vera

A

jak 2 mutation
no hypoxia, incresed hemotaocrit- hyperviscosity, pruritis, splenomeg, flushed face
phlebotomy is management of choice

62
Q

secondary erythrocytosis

A

hypoxia - pulmonary disease- COPD, high altitude, cyanotic heart disease- reactive!- normal WBC/platelets distinguishes 2nd from 1st.

63
Q

factor V leidan

A

MC inheritied cause of hypercoagulability,

- resistant to breakdwon of factor V by cativated protein C- ypecoag- dvt and pe in young patients.

64
Q

protein c deficiency

A

vitamin K dependent anticoagulant- stimulates fibrinolysis and clot lysis.
recurrent DVT and pulm emobilism
tx: heparin- anti coag for LIFE

65
Q

antithrombin III def

A

venous thrombosis!! recurrent DVT or pulmonary emoboli.
high dose IV heparin!
can lead to heparin resistance because it is activated by heparin

66
Q

chloromphenicol

A

chemo tx

SIDE EFFECT: APLASTIC ANEMIA

PANRE (18 decks)

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