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MOD > MOD 3 > Flashcards

MOD 3 Flashcards

1
Q

Where does vWF come from?

A
  1. Weibel-Palade bodies of endothelial cells

2. alpha-granules of platelets

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2
Q

What is thromboxane A2 a derivative of?

A

platelet cyclooxyrgenase

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3
Q

What is the most common symptom of primary hemostasis disorders?

A

epistaxis

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4
Q

What general type of primary hemostasis disorders get petechiae?

A

quantitative (not seen really in qualitative)

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5
Q

Tests for primary hemostasis disorders

A
  • platelet couht
  • bleeding time
  • bone marrow biospy
  • blood smear
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6
Q

ITP

A
  • AI production of IgG against platelet antigens
  • Auto Abs are produced by spleen, and spleen eats platelets that are caught by the auto Abs
  • decreased platelet count
  • normal PT/PTT
  • increased megakaryocytic in bone marrow
  • initial tx is corticosteroids
  • IVIG can raise platelet count so the spleen eats those Abs instead of the ones attached to the platelets (short lived effect)
  • splenectomy
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7
Q

What is the most common cause of thrombocytopenia in adults? children?

A

ITP in both

  • acute form arises in children though
  • chronic found in adults
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8
Q

What is a common disease associated with ITP?

A

SLE - chronic form of ITP presents typically in women of child bearing age, and often have a secondary condition like lupus

*IgG can pass placenta, and shortly affect the fetus

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9
Q

Microangiopathic Hemolytic Anemia

A
  • pathology in small BVs

- micro thrombi form, and shear RBCs –> schistocytes

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10
Q

What disorders cause Microangiopathic Hemolytic Anemia?

A
  • TTP

- HUS

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11
Q

What enzyme is decreased in TTP?

A

ADAMTS13 - used to degrade vWF –> abnormal platelet adhesion –> micro thrombi

  • decreased enzyme via auto AB
  • classic pt. is adult female
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12
Q

What causes HUS?

A
  • endothelial damage by drugs or infection (e. coli 0157:H7)
  • also leads to a problem in ADAMTS13
  • classically seen in kids exposed to undercooked beef
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13
Q

Clinical findings of TTP and HUS

A
  • skin and mucosal bleeding
  • microangipathic hemolytic anemia
  • fever
  • renal insufficiency
  • CNS abnormalities
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14
Q

What tissues are most affected in TTP and HUS?

A

kidney + CNS

  • HUS is mainly renal
  • TTP mainly CNS
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15
Q

Laboratory findings of TTP and HUS

A
  • normal PT/PTT
  • anemia with schistocytes
  • increased megarkaryocytes in bone marrow
  • thrombocytopenia with increased bleeding time

treatment:
- plasmapheresis and corticosteroids

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16
Q

Bernard - Soulier Syndrome

A
  • GP1b deficiency

- mild thrombocytopenia with enlarged platelets

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17
Q

Glanzmann Thrombasthenia

A
  • deficiency in GIIb/IIIa

- platelet aggregation is impaired

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18
Q

What does aspirin do?

A

irreversibly inactivates cyclooxyrgenase –> lack of TXA2 –> impairs aggregation

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19
Q

What can uremia cause?

A
  • adhesion and aggregation is impaired
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20
Q

Hemophilia A

A
  • factor VIII deficiency
  • X linked rec or genetic mutation
  • increased PTT, normal PT
  • normal platelet count/bleeding time
  • tx with factor 8
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21
Q

Hemophilia B

A
  • factor IX

- other than that matches hemophilia A

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22
Q

Coagulation factor inhibitor

A
  • acquired AB against coagulation factor

- most common is anti factor 8

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23
Q

How do you determine b/t hemophilia A and coagulation factor inhibitor?

A

PTT corrects with hemophilia A, and not with CFI because the donated factor 8 from the normal plasma is still inhibited in CFI

*called a mixing study

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24
Q

Von Willebrand Disease

A
  • genetic defect in vWF (MOST COMMON inherited coagulation disorder)
  • qualitative/quantitative defects
  • decreased levels of vWF
  • present with mild mucosal and skin bleeding
  • increased bleeding time + PTT
  • normal PT
  • abnormal ristocetin
  • tx with desmopressin (increased vWF from WP bodies)
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25
Q

How is vWF involved with PTT?

A

it helps stabilize factor 8

*though with disease, doesn’t cause clinical problems with secondary hemostasis

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26
Q

When do we see vitamin k deficiency?

A
  • newborns
  • long term AB therapy
  • malabsorption
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27
Q

Why can liver failure cause secondary problems?

A
  • decreased production of factors
  • decreased activation of fit K by epoxide reductase

*measured via PT

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28
Q

Heparin-induced Thrombocytopenia (HIT)

A
  • platele destruction
  • platelet fragments activate remaining platelets, which forms thrombosis
  • heparin forms a complex with platelet factor 4, and can form IgG Abs

*don’t give them caubinin

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29
Q

DIC

A
  • pathologic activation of cascade
  • micro thrombi formation
  • classically bleed form IV sites, mucosal sites…
  • almost always secondary to another disease process like sepsis or rattlesnake bite
  • decreased platelets + fibringoen
  • increased PT/PTT
  • elevated fibrin split products (D- dimer) *best
  • treated by fixing underlining cause
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30
Q

Fibrinolysis

A
  • increased PT/PTT, bleeding time, and fibringogen split products without d dimers
  • tx with aminocaproid acid

*clinically looks like DIC

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31
Q

What characterizes thrombosis from postmortem clot?

A
  1. lines of Zahn
  2. attachment to vessel wall

*seen in thrombus and NOT postmortem clot

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32
Q

What are the risk factors for thrombosis?

A
  1. disruption in blood flow
  2. endothelial cell damage
  3. hyper coag ulable state
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33
Q

Why is turbulence bad?

A
  • clotting factors get mixed up with blood, which activates them
  • endothelium gets shredded
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34
Q

What is the role of PGI2?

A
  • blocks platelet aggregation
  • made by endothelial cells*

*also make NO + heparin like molecules (activate anti thrombin 3 –> inactivates thrombin) + tPA + thrombomodulin

35
Q

What causes high levels of homocysteine? what can this cause?

A
  1. vitamin B12 deficiency + cystathionine beta synthase deficiency
  2. endothelial damage
36
Q

Protein C/S deficiency

A
  • they should inactivate factors 5 + 8 to shut down cascade
  • without them, pt.s are hyper coagulable
  • increased risk of warfarin skin necrosis
37
Q

Facto V Leiden

A
  • mutated factor V that can’t be cleaved by protein C/S
  • excessive coagulation

*most common inherited cause of a hyper coagulative state

38
Q

Prothrombin 20210A

A
  • point mutation in prothrombin gene
  • results in increased GE
  • promotes thrombus formation
39
Q

What happens to the PTT in pt.s with ATIII deficiency when given heparin?

A
  • does NOT rise because the ATIII isn’t around for the heparin to activate
40
Q

Why are OCT involved in hyper coagulable states?

A

estrogen increases production of coagulation factors

41
Q

What happens to the d dimer in a DVT?

A

it is elevated

42
Q

What is the difference b/t edema and effusion?

A

edema - interstitial space
effusion - pleural, peritoneal, pericardial, and joint spaces

*both are abnormal accumulations of fluid

43
Q

What causes edema?

A
  1. decreased oncotic pressure
  2. increased intravascular hydrostatic pressure
    a. Na/H2O retention
    b. congestion
  3. increased vascular permeability
  4. Lymphatic obstruction
44
Q

What is the difference b/t hyperemia and congestion?

A

hyperemia - too much blood arriving (physiological; blood goes to site in need like active muscle; regulated by precapillary sphincter)

congestion - not enough blood leaving (pathological; blood pools)

45
Q

How does HF cause edema? effusion?

A
  1. less blood to the kidneys–> they activate RAAS (renal failure) –> more water/Na retained –> increased blood volume/decreases oncotic pressure –> edema
  2. HF –> increased capillary hydrostatic pressure –> edema
  3. decreased pump acitivty –> back up pulmonary enough circulation (congestion) –> effusion
46
Q

What can cause lower albumin levels? what does this lead to?

A
  1. malnutrition, decreased hepatic synthesis, nephrotic syndrome
  2. edema due to decreased osmotic pressure
47
Q

What is commonly associated with HF?

A

pleural effusion/pulmonary edema because of the close anatomical relationship

48
Q

What is involved with liver failure?

A

less production of albumin/portal HTN –> decreased oncotic pressure –> ascites/edema

*portal HTN leads to congestion –> the ascites (abdomen is where the blood goes)

49
Q

How can kidney failure cause edema?

A
  1. water/Na retention (like as is seen with HF)

2. Nephrotic syndrome (protein is lost in the urine at high rates; due to abnormally permeable glomerular capillaries)

50
Q

Malnourished children may suffer fro what condition that leads to edema?

A

Kwashiorkor - protein is insufficient from diet

51
Q

Pt. presents with one LE that is 4x the size of the other. What is the dx?

A

Lymphedema* caused by…

  • infection
  • inflammation
  • trauma
  • tumor
  • surgery
  • malformations
  • cause of localized edema
  • elephantiasis
52
Q

What is Filariasis?

A
  • helminth infection (wuchereria) that causes extreme lymphedema
53
Q

Transudate vs. Exudate

A

fluid leakage vs. protein and fluid leakage

increased Pc vs. increased inter endothelial space

54
Q

Causes of Increases Hydrostatic Pressure

A

Decreased Venous Return:

  • congestive HF
  • constrictive pericarditis
  • ascites
  • venous obstruction/compression (ex. thrombosis, external pressure like a mass, LE inactivity)

Arteriolar Dilation:

  • heat
  • neurohumoral dysregulation
55
Q

Causes reduced plasma osmotic pressure

A
  • protein losing glomerulopathies
  • liver cirrhosis
  • malnutrition
  • portion losing gastroenteropathy
56
Q

Causes of Lympahtic obstruction

A
  • inflammatory
  • post surgical
  • post irradiation
  • neoplastic
57
Q

Causes of Sodium retention

A
  • excessive salt intake with renal insufficiency
  • increases tubular reabsorption of sodium
    • renal hypo perfusion
    • increases RAAS secretion
58
Q

Causes of Inflammation

A
  • acute, chronic

- angiogenesis

59
Q

What conditions does chronic congestion lead to?

A
  1. edema
  2. hemosiderosis (iron overload disorder resulting in the accumulation of hemosiderin)
  3. tissue damage
60
Q

Why do cells closest to the central hepatic vein die off first?

A

because they are furthest from the oxygenated blood, and the blood can’t get to them because the vein is blocked and won’t let more in

61
Q

What is the first step in hemostasis?

A

vasoconstriction - neurogenic factors + endothelin

*goal is to decrease BF (less blood loss), and SA (easier to repair)

62
Q

What are the steps in primary hemostasis?

A
  1. platelet adeshion
  2. shape change
  3. granular release
  4. recruitment
  5. Aggregation (plug is formed)
63
Q

How do platelets attach to the endothelium?

A

the exposed collagen binds to vWF, which then binds to GpIb on the platelet

64
Q

How/why do platelets change shape?

A
  • increases SA
  • GpIIb-IIIa change shape to allow fibrinogen links (allows for aggregation)
  • thrombin initiates release of ADP (more activation) and thromboxane A2 (more aggregation)
65
Q

How does aspirin work?

A

inhibits thromboxane A2

66
Q

Glanzmann Thrombasthenia

A

deficiency of GpIIb-IIIa - can’t get enough platelets to aggregate

67
Q

What do we worry about if a pt. presents with a platelet count of under 10,000?

A

spontaneous intracranial bleeds

68
Q

Thrombocytopenia

  1. Mxn
  2. Platelet count
  3. Platele adhesion
  4. Platele aggregation
A
  1. loss or impaired production of paltelets
  2. low
  3. yes
  4. yes
69
Q

Von Willebrand Disease

  1. Mxn
  2. Platelet count
  3. Platele adhesion
  4. Platele aggregation
A
  1. deficiency in vWF
  2. Normal
  3. No
  4. Yes
70
Q

Bernard-Soulier Disease

  1. Mxn
  2. Platelet count
  3. Platele adhesion
  4. Platele aggregation
A
  1. deficiency in GpIb
  2. Normal - low
  3. No
  4. Yes
71
Q

Glanzmann’s Thromboasthenia

  1. Mxn
  2. Platelet count
  3. Platele adhesion
  4. Platele aggregation
A
  1. deficiency of GpIIb-IIIa
  2. Normal
  3. Yes
  4. No
72
Q

What is a second name for factor I? II? VIII?

A
  1. Fibrinogen
  2. Prothrombin
  3. Antihemophilic A factor (AHF)
73
Q

What factors are vitamin K dependent?

A

2, 7, 9. 10, Protein C/S

*Ca2+ required to activate vit K and to get factor 10 –> 5 (?)

74
Q

What is the purpose of Coumadin?

A
  • blocks formation of active vitamin K

- helpful in clot formation prevention

75
Q

What is the difference b/t petechiae? purpura? ecchymosis?

A

a. small
b. larger
c. palpable

*common in platelet dysfunction

76
Q

What is Hemoarthrosis?

A
  • bleeding within the joint

- seen with factor deficiencies like hemophilia A

77
Q

How do we break up a clot?

A
  • blood flow washes away the activated clotting factors

- plasmin is activated by TPA, and breaks apart the fibrin

78
Q

What do we see in thrombosis formation triad 1: endothelium activation?

A
  • down regulation of thrombomodulin and activated protein C

- elaboration of plasminogen activator inhibitors

79
Q

When do we see turbulent blood flow?

A
  • normal bifurcation
  • dilated vessels (aneurysm, hemorrhoids)
  • internal obstruction
  • external compression
  • inadequate heart chamber function
80
Q

When do we see hyper coagulability?

A
  • antithrombin (III) deficiency
  • protein C/S deficiency
  • factor Va increase
  • prothrombin increase
81
Q

What are high risk factors for thrombosis?

A
  • bed rest
  • MI
  • atrial fibrillation
  • tissue injury
  • cancer
  • prosthetic cardiac valves
  • disseminated intravascular coagulation
  • heparin induced thrombocytopenia
  • antiphropholipid ab syndrome
82
Q

What are some lower risk factors for thrombosis?

A
  • cardiomyopathy
  • nephrotic syndrome
  • hyperestrogenic states
  • OTCs
  • sickle cell anemia
  • smoking
83
Q

What happens with a large saddle emboli? smaller emboli? extremely small emboli?

A
  1. instantly fatal - right sided HF
  2. dyspnea
  3. typically asymptomatic; resolves on its own
84
Q

Heparin-induced thrombocytopenia

A
  • prothromotic state caused by Abs to PF4-heparin
    • exposure to unfracrtionated heparin
    • formation of platelet factor 4-heparin complexes
    • IgG cross-linking of platelet Fc receptors and PF4- heparin complexes
    • platelet activation and aggregation

*leads to necrosis of fingers and toes

MOD (10 decks)

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