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Clin Med > Heme/Onc basics > Flashcards

Heme/Onc basics Flashcards

1
Q

RBCs

  • nuclei +/-
  • shape
  • filled with what
  • life span
A

no nuclei
biconcave– filled with hemoglobin
life span=120 days

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2
Q

Neutrophils

  • Nucleus +/-
  • contain?
  • function
  • life span
A
  • 3-5 nuclear lobes
  • cytoplasm with pale, lilac colored granules
  • phagocytes
  • provide protection from acute infections
  • life span 5 hours-few days
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3
Q

Basophils

  • nucleus +/-
  • role
A

lack nuclear segmentation–dots everywhere

role=similar to eosinophils

  • phagocytic
  • help fight acute infections
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4
Q

eosinophils

  • nucleus +/-
  • role?
A

two nuclear lobes

roles
-chronic immune responses–>helminth worm infections, asthma and allergies

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5
Q

Monocytes

  • nucleus +/-
  • roles
  • life span
A

kidney shaped nucleus in light blue cytoplasm

  • highly phagocytic
  • life span is long
  • keep “watch” detecting danger signals produced by infection or tissue injury
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6
Q

Lymphocytes

  • key role in?
  • structure
  • types
A

key role in adaptive immunity

  • condensed nuclei and scant cytoplasm
  • B cells
  • t cells
  • NK cells
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7
Q

where are B cells made

where are T cells made

A

B cells–>bone marrow

T cells–>thymus (transformed in thymus)

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8
Q
A

eosinophil

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9
Q
A

monocyte

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10
Q
A

lymphocyte

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11
Q
A

neutrophil

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12
Q
A

basophil

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13
Q

bone marrow produces how much:

  • rbc
  • platlets
  • neutrophils
A

RBC= 200 billion
platelets=100 billion
neutrophils=60 billion

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14
Q

define hematopoiesis

A

production of RBCs and platelets in the bone marrow

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15
Q

cytopenia

A

too few blood cells

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16
Q

cytoses

A

too many blood cells

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17
Q

what maintains hematopoeisis

A

hematopoietic stem cells (HSCs)

18
Q

what is technically transplanted

A

hematopoietic stem cells

19
Q

define hemostasis

A

stopping of blood flow

20
Q

clot formation starts with

A

platelet plug at the site of vessel injury–> PRIMARY PLAT PLUG

21
Q

steps in hemostasis

A
  1. primary platelet plug
  2. once platelets adhere to vessel wall—triggers platelet activation–>changes plat shape from circle to a spiky sea urching shape–>incrs surface area of platelet + changes platelet membrane glycoproteins—->allows it to bind to fibrinogne
  3. plat activation results in release of arachidonic acid–>converted to thromboxane A2 (protent inducer of platelets via series of enzymes Cyclooxygenase)
22
Q

what happens after platelets are activated during hemostasis

A
  1. shape changes from circle–>spiky sea urchin
  2. surface area incrs with shape change
  3. shape change also changes plats membrane glycoproteins–lets them bind to fibrinogen
  4. arachidonic acid released–>converted to Thromboxane A2–>inducer of platelets via series of enzymes including Cyclooxygenase
23
Q

cyclooxygenase

  • what is it
  • what activates it
A

enzyme that activates platelets

**thromboxane A2 activates platelets thru this enzyme

24
Q

ASA contains what

A

cyclooxygenase inhibitors

-why ASA is used to suppress platelet activation

25
Q

coagulation cascade

-three pathways and their factors invovled + lab work to test for the pathway

A
  1. INTRINSIC PATHWAY
    TEST=aPartial Thromboplastin Time (aPTT)
    *FACTORS: XII, XI, IX, VIII, X
    12, 11, 9, 8, 10
  2. EXTRINSIC
    TEST= prothrombin time (PT)
    FACTORS: VII, X
    7 and 10
  3. COMMON PATHWAY
    X from extrinsic and intrinsic
    X–> Xa–>prothrombin (II) + thrombin–>Fibrinogen (I)–> FIBRIN CLOT
26
Q

Lab assessments of the coagulation cascade

-what are the initial tests of blood coagulation cascade

A

INITIAL TESTS

  • Plat count
  • prothrombin time (PT)
  • partial thromboplastin Time (PTT) aka aPTT
27
Q

Platelet Count

  • normal?
  • below normal means? s/s?
A

> 100,000 per microliter

BELOW= takes LONGER time to clot
s/s: purpura + mucosal bleeding

28
Q

Prothrombin Time (PT)

  • normal?
  • this is testing what?
  • abnormal time?
A
  • testing of the extrinsic pathway
  • Normal 10-13 seconds— time it takes for blood to clot
  • LONGER=deficiency in one or more of the clotting factors in extrinsic pathway–>aka FACTORS VII****, X,
29
Q

INR

  • stands for
  • dervied from?
A

international normalized ratio

  • derived from PT
  • same as PT— but it is “standardized” by taking into account the potency of the tissue factor—–whifh is what is added to the plasma to perform the PT used
30
Q

aPTT

  • stands for
  • normal?
  • what is added
  • which pathway
A

Activated PARTIAL thromboplastin TIME

  • normal (time takes for blood to clot) is 25-35 secs
  • Kaolin is added to plasma–>activates factor XII–>starts INTRINSIC cascade (factors XII, XI, IX, VIII, X, prothrombin and fibrinogen)
31
Q

Thrombin TIme

  • when is this done
  • tests?
A
  • extra test— only done if there is a coagulation problem

* THROMBIN TIME (TT)–>tests functionality of fibrinogen and presence of thrombin inhibitors (heparin, etc)

32
Q

patients with inherited bleeding disorders usually have ____ deficiencies present

A

only a single

33
Q

patients with an acquired bleeding problem, they will have _____ deficiencies

A

multiple

***acquired problems like vit K deficiency or liver dz

34
Q

list the common anticoag drugs

A
  1. VIT K ANTAGONISTS–warfarin
  2. HEPARIN
  3. LOW MOLECULAR WEIGHT HEPARIN
35
Q

vitamin K anatagonist

  • what do they do
  • MC ? route?
  • what is monitored when pt on this
A

**block or slow down clotting by affecting VII, IX and X and prothrombin–>bc they all need vit K for carboxylation

MC=warfarin–PO
-pt must be monitored closely–PT/INR testing–>make sure anti-coagulation is within therapeutic range

36
Q

Heparin

  • moa
  • route
A

activates anithrombin

  • inhibits several steps in cascade
  • IV***
37
Q

low molecular weight heparin

  • route
  • moa
A

sc

*doesnt require intensive monitoring—but also doesnt work as fast

38
Q

direct inhibitor drugs

  • what are they
  • general moa
A

new oral anticoags that directly inhibit activated coagulation factors—— INDIRECTLY affects many parts of the coag cascade

39
Q

define sequestration

  • where is it done

- can cause?

A
  • spleen
  • spleen takes 1/3 of body’s platelets to store them
  • pt with splenomegaly have higher proportion of their platelets entrapped along with RBCs and WBCs
  • significant reduction in one or more of peripheral blood counts due to sequsetration is called–>HYPERSPLENISMh
40
Q

hypersplenism

  • what is it
  • what happens to plat count
A

sig reduction in one or more of the peripheral blood counts by splenic sequestration
**PTs with it generally have plat counts of 50,000-120,000 per microliter—- not really low enough to pose a serious risk of hemorrhage

Clin Med (52 decks)

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