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Kaplan: Pathophysiology 1-5 > Circulatory Pathology > Flashcards

Circulatory Pathology Flashcards

(53 cards)

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1
Q

What is anasarca?

A

severe generalized edema

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2
Q

What is effusion?

A

fluid within the body cavities

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3
Q

What is transudate?

A

edema fluid with low protein content

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4
Q

What is exudate? What are some types of exudate?

A

edema fluid with high protein content and cells.

Types of exudates include purulent (pus), fibrinous, eosinophilic, and hemorrhagic

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5
Q

Difference between transudate and exudate?

A

Transudate usually involved high hydrostatic pressure pushing fluid into a space while exudate typically involves increased permeability and leakage of fluid because of inflammation

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6
Q

What is the difference between passive and active hyperemia?

A
  • Active hyperemia happens when there’s an increase in the blood supply to an organ. This is usually in response to a greater demand for blood — for example, if you’re exercising.
  • Passive hyperemia is when blood can’t properly exit an organ, so it builds up in the blood vessels.
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7
Q

What occurs during the first step of platelet adhesion?

A

when vWF adheres to sub endothelial collagen and then platelets adhere to vWF by gp 1B

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8
Q

What occurs during platelet activation (Step 2)?

A

Occurs when platelets undergo a shape change and degranulation occurs.

Platelets synthesize thromboxane A2.

Platelets also show membrane expression of the phospholipid complex, which is an important substrate for the coagulation cascade

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9
Q

Describe what happens during platelet aggregation?

A

occurs when additional platelets are recruited from the bloodstream. ADP and thromboxane A2 are potent mediators of aggregation

Platelets bind to each other by binding to fibrinogen using GPIIb - IIIa

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10
Q

What is normal platelet count?

A

(150,000 - 400,000 mm3)

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11
Q

What is a common presentation that both Bernard- Soulier syndrome and Glanzmann thrombasthenia have in common?

A

mucocutaneous bleeding in childhood

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12
Q

What is the defect in Bernard-Soulier Syndrome?

A

defects of the GPIb-IX-V
leading to defective platelet adhesion

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13
Q

What is the inheritance pattern of Bernard-Soulier syndrome?

A

AR

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14
Q

What factors does PT test for?

A

the factors of the extrinsic pathway II (prothrombin) , VII, IX, X, fibrinogen

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15
Q

What factors does PTT test for?

A

the factors of the intrinsic pathway IIa, Xa, VIIIa, IXa, XIa, XIIa and fibrinogen

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16
Q

What does thrombin time (TT) test for?

A

adequate fibrinogen levels

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17
Q

Why may we measure FDP fibrin degradation products?

A

this tests the fibrinolytic system (increased with DIC)

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18
Q

What are some bleeding disorders caused by platelet abnormalities involving platelet destruction?

A

ITP immune thrombocytopenia
TTP thrombotic thrombocytopenia purpura
DIC disseminated intravascular coagulation
HUS hemolytic uremic syndrome
Hypersplenism

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19
Q

What is ITP?

A

immune thrombocytopenia
an immune mediated attack (usu. IgG antiplatelet ab) against platelets leading to decrease platelet (thrombocytopenia).

involves antiplatelet ab against plt antigens like GPIIb/IIIa and GP1b-IX

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20
Q

What are the symptoms of ITP?

A

petechiae, purpura (bruises) and bleeding diathesis

chronic ITP ecchymoses, menorrhagia, nosebleeds

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21
Q

What type of HSR is ITP?

A

Type II HSR

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22
Q

What are the different type of ITP?

Study These Flashcards
A

acute ITP seen in children following viral infection

Chronic ITP: usu. seen in women in childbearing years

23
Q

Why are important labs to remember of a person with ITP?

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A

dec. plt count; and hence prolonged BT

PT and PTT normal

24
Q

Treatment for ITP?

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A
  • corticosteroids which decrease ab production
  • Immunoglobulin therapy which floods Fc receptors on splenic macrophages
  • splenectomy
25
Pathology of TTP?
deficiency of the enzyme ADAMTS13 which is responsible for breaking down vWF. Therefore there is widespread intravascular formation of fibrin-platelet thrombi
26
What are the clinical signs of TTP
fever thrombocytopenia MAHA neurologic symptoms renal failure
27
Describe lab studies of those with TTP? | Important lab values and what you may see on a smear
dec. plt count and prolong BT normal PT and PTT peripheral blood smear will show thrombocytopenia, schistocytes, and reticulocytes
28
What is HUS?
Hemolytic uremic syndrome is a form of thrombotic microangiopathy due to endothelial cell damage. It occurs mostly in children typically after gastroenteritis (typically due to Shiga toxin-producing E. coli E 0157: H7)
29
What is the typical presentation of HUS?
abdominal pain diarrhea MAHA thrombocytopenia renal failure (more common than in TTP)
30
Treatment for HUS?
supportive with fluid management, dialysis, erythrocyte transfusions plasma exchange is only used for atypical cases.
31
What is Glanzmann Thrombasthenia?
Disorder caused by defective GpIIb/IIIa receptor leading to defective platelet aggregation
32
What is the inheritance pattern of Glanzmann thrombasthenia?
AR
33
Which is classic hemophilia? A or B?
hemophilia A
34
What is the inheritance pattern of hemophilia A? Why does it occur?
X- linked recessive condition resulting from a deficiency of factor VIII. Clinically Hemophilia A predominantly affects males
35
What are some major clinical signs of Hemophilia A ?
hemarthrosis hemorrhage into joints bleeding (prolonged) bruising
36
Describe lab values for hemophilia A?
normal BT; normal platelet count Increased PTT normal PT
37
Treatment for hemophilia A?
VIII concentrate
38
Another name for Hemophilia B?
Christmas disease
39
Hemophilia B results from a deficency in which clotting factor?
defiency in factor IX that is clinically identical to hemophilia A
40
Clinical features of vWF disease?
prolonged bleeding from wounds and menorrhagia in young females
41
What are the lab values you must remember for vWD?
prolonged BT normal PT and prolonged PTT because vWF because factor 8 binds to vWF. abnormal response to ristocetin
42
What is the treatment for vWF disease?
mild classic cases (type 1) you can give desmopressin (an ADH analog) which release vWF from the Weibel- Palade bodies of endothelial cells
43
Lab studies of those with DIC?
show decreased platelet count, prolonged PT/PTT, decreased fibrinogen and elevated fibrin split products (D dimers)
44
What are the factors in Virchow's Triad?
endothelial injury alterations in laminar BF Hypercoaguability
45
What is the classic presentation of those with pulmonary embolism?
hemoptysis, dyspnea, and chest pain
46
What is the difference between anemic infarcts (white infarcts) and hemorrhagic infarcts (red infarcts)?
anemia (pale or white color) occur in solid organs with a single blood supply such as the spleen, kidney and heart while; hemorrhagic infarcts (red color) occur in organs with a dual blood supply or collateral circulation, such as the lung an intestines, and occur with venous occlusion (e.g testicular torsion)
47
What is the general sequence of tissue changes after infarction?
ischemia > coagulative necrosis > inflammation > granulation tissue > fibrous scar
48
What is shock?
characterized by vascular collapse and widespread hypo perfusion of cells and tissue due to reduced BV, CO, or vascular tone.
49
Cardiogenic shock.
(pump failure) can be due to MI, cardiac arrhythmias, PE, and cardiac tamponade
50
Hypovolemic shock.
(reduced blood volume) can be due to hemorrhage, fluid loss secondary to severe burns, and severe dehydration
51
Septic shock.
(viral or bacterial infection) causes cytokines to trigger vasodilatation and hypotension, acute respiratory distress syndrome (ARDS) DIC, and multiple organ dysfunction syndrome
52
What is neurogenic shock.
(generalized vasodilation) caused by decreased sympathetic tone; seen with anesthesia and brain or spinal cord injury
53
What is anaphylactic shock?
Generalized vasodilation; type I hypersensitivity reaction

Kaplan: Pathophysiology 1-5 (6 decks)

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