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Acupuncture 1 > Hematology > Flashcards

Hematology Flashcards

1
Q

Common clotting pathway starts at

A

factor 10

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2
Q

extrinsic is cause by

A

trauma

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3
Q

factor 10 uses ___ to make _____

A

prothrombin

thrombin

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4
Q

Thrombin changes ____ to _____

A

fibrinogen to fibrin

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5
Q

Protein __ & ___ need vitamin ___

A

C & S need K

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6
Q

Vitamin is involved with which factors

A

2, 7, 9, 10

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7
Q

What factors are in the intrinsic pathway?

A

12, 11, 9, 8

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8
Q

what factors are in the extrinsic pathway

A

7

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9
Q

What factors are in the common pathway?

A

5, 2(prothrombin & thrombin), 1 (fibrinogen & fibrin), 13, Protein C, S

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10
Q

Partial prothrombin time

A

intrinsic + common, 12, 11, 9, 8, 10

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11
Q

Prothrombin time

A

extrinsic + common, 7 & 10

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12
Q

Bleeding time measures

A

platelet function

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13
Q

TT measures

A

common pathway

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14
Q

Lifespan of RBC?

A

120 days

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15
Q

RBC come from

A

common myeloid progenitor which came from hemocytoblast

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16
Q

To mature a RBC we need

A

B9, B12

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17
Q

RBC is made in the

A

bone marrow, leaves when its a reticulocyte

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18
Q

Heme has how many alpha chains?

A

2

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19
Q

each iron hold onto __ oxygen, making __ in total for each heme

A

1, 4

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20
Q

Iron is absorbed in the

A

duodenum

21
Q

folate is absorbed in the

A

jejenum

22
Q

B12 is absorbed in the

A

Ileum

23
Q

hepcidin

A

regulates iron, increases iron when needed, during infection it inhibits iron absorption from food

24
Q

Hepcidin is induced by

A

IL-6 and LPS (infection & inflammation)

25
Q

Hepdicin is inhibited

A

EPO

26
Q

EPO is released by

A

the kidneys because they can detect how much oxygen is in the blood

27
Q

Anemia means

A

low O2 carrying capacity, not low O2

28
Q

Types of hereditary hemolytic anemias:

A 
pyruvate kinase deficiency
G6PD deficiency 
abnormal membraine (spherocytosis)
Abnormal heme ( alhpa & beta thalassemia), sickle cell anemia
29
Q

Types of acquired hemolytic anemias:

A

alloimmune, drug induced, autoimmune

30
Q

Spherocytosis key features:

A

autosomal dominant
defective spectrin
splenomegaly

31
Q

G6PD deficiency

A

viral infection, fave beans, sulfa drugs, quinin

heinz bodies

32
Q

Sickel cell

A

hypoxia, dehydration, acidosis, vaso-occlusive, aplastic crisis, splenomegaly

33
Q

alpha thalassemia

A

HbH beta 4, south east asia
hydrochromic cells, target cells
hydrops fetalis
hard time passing through the spleen

34
Q

beta thalassemia

A

HbA, HbF
mediterranean & US, hypochromic cells, target cells
hard time passing through the spleen

35
Q

Glutathione is

A

powerful antioxidant that takes hydrogen peroxide and makes water uses NADPH

36
Q

G6PD is needed

A

to help RBC makes NADPH which is needed by glutathione to reduce hydrogen peroxidse and reuse glutathione

37
Q

Heinz bodies are

A

denature globin chains that are stuck to the inside of the RBC because the globin & heme bond was attacked

38
Q

Bite cells are

A

heinz bodies that were bitten by the macrophages in the spleen to get the bodies out

39
Q

bilirubin in the liver gets

A

changed from unconjugated to conjugated

40
Q

Conjugated bilirubin travels from the liver

A

to the gallbladder, mixes with bile and enters the SI

41
Q

urobilinogen is made

A

in the Si and goes to the kidney

42
Q

Spleen macrophage takes heme and makes

A

unconjugated bilirubin

43
Q

ALL Leukemia

A

Children
fever, petechiae, eccymoses, CNS infiltrate

good prognosis

Lymphoblasts

44
Q

AML leukemia

A

any age
fever, petechiae, ecchymoses, lymphadenopathy (splenomegaly)
depending on type
Auer robs in myeloblasts

45
Q

CML leukemia

A

young adults
fever, night sweats, splenomegaly

poor
Philidelphia chromosome (better prognosis if present) this gene encodes a protein with high tyrosine kinase activity
46
Q

CLL leukemia

A

elderly
insidious, few symptoms, low Ig levels, infections

Fair

lymphocytes
predominate

47
Q

Hairy cell leukemia

A

hepatosplenomegaly
poor
pancytopenia
TRAP

48
Q

Non-pitting edema

A

Lymphatic obstruction - keeps the proteins in the interstitium and retains water
-usually CHF, followed by renal complications

49
Q

Pitting edema

A

increased in hydrostatic pressure or decreased oncotic protein pressure

There is no protein in the interstitial to retain fluid

venous insufficiency

Acupuncture 1 (7 decks)

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