Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Kaplan: Pathophysiology 1-5 > Circulatory Pathology > Flashcards

Circulatory Pathology Flashcards

1
Q

What is anasarca?

A

severe generalized edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is effusion?

A

fluid within the body cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is transudate?

A

edema fluid with low protein content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is normal platelet count?

A

(150,000 - 400,000 mm3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

mucocutaneous bleeding in childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the defect in Bernard-Soulier Syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the inheritance pattern of Bernard-Soulier syndrome?

A

AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What factors does PT test for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What factors does PTT test for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does thrombin time (TT) test for?

A

adequate fibrinogen levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why may we measure FDP fibrin degradation products?

A

this tests the fibrinolytic system (increased with DIC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of ITP?

A

petechiae, purpura (bruises) and bleeding diathesis

chronic ITP ecchymoses, menorrhagia, nosebleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of HSR is ITP?

A

Type II HSR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the different type of ITP?

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?

A

dec. plt count; and hence prolonged BT

PT and PTT normal

24
Q

Treatment for ITP?

A
  • corticosteroids which decrease ab production
  • Immunoglobulin therapy which floods Fc receptors on splenic macrophages
  • splenectomy
25
Q

Pathology of TTP?

A

deficiency of the enzyme ADAMTS13 which is responsible for breaking down vWF.

Therefore there is widespread intravascular formation of fibrin-platelet thrombi

26
Q

What are the clinical signs of TTP

A

fever
thrombocytopenia
MAHA
neurologic symptoms
renal failure

27
Q

Describe lab studies of those with TTP?

Important lab values and what you may see on a smear

A

dec. plt count and prolong BT

normal PT and PTT

peripheral blood smear will show thrombocytopenia, schistocytes, and reticulocytes

28
Q

What is HUS?

A

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
Q

What is the typical presentation of HUS?

A

abdominal pain
diarrhea
MAHA
thrombocytopenia
renal failure (more common than in TTP)

30
Q

Treatment for HUS?

A

supportive with fluid management, dialysis, erythrocyte transfusions

plasma exchange is only used for atypical cases.

31
Q

What is Glanzmann Thrombasthenia?

A

Disorder caused by defective GpIIb/IIIa receptor leading to defective platelet aggregation

32
Q

What is the inheritance pattern of Glanzmann thrombasthenia?

A

AR

33
Q

Which is classic hemophilia? A or B?

A

hemophilia A

34
Q

What is the inheritance pattern of hemophilia A? Why does it occur?

A

X- linked recessive condition resulting from a deficiency of factor VIII. Clinically Hemophilia A predominantly affects males

35
Q

What are some major clinical signs of Hemophilia A ?

A

hemarthrosis hemorrhage into joints
bleeding (prolonged)
bruising

36
Q

Describe lab values for hemophilia A?

A

normal BT; normal platelet count

Increased PTT
normal PT

37
Q

Treatment for hemophilia A?

A

VIII concentrate

38
Q

Another name for Hemophilia B?

A

Christmas disease

39
Q

Hemophilia B results from a deficency in which clotting factor?

A

defiency in factor IX that is clinically identical to hemophilia A

40
Q

Clinical features of vWF disease?

A

prolonged bleeding from wounds and menorrhagia in young females

41
Q

What are the lab values you must remember for vWD?

A

prolonged BT
normal PT and prolonged PTT because vWF because factor 8 binds to vWF.
abnormal response to ristocetin

42
Q

What is the treatment for vWF disease?

A

mild classic cases (type 1) you can give desmopressin (an ADH analog) which release vWF from the Weibel- Palade bodies of endothelial cells

43
Q

Lab studies of those with DIC?

A

show decreased platelet count, prolonged PT/PTT, decreased fibrinogen and elevated fibrin split products (D dimers)

44
Q

What are the factors in Virchow’s Triad?

A

endothelial injury
alterations in laminar BF
Hypercoaguability

45
Q

What is the classic presentation of those with pulmonary embolism?

A

hemoptysis, dyspnea, and chest pain

46
Q

What is the difference between anemic infarcts (white infarcts) and hemorrhagic infarcts (red infarcts)?

A

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
Q

What is the general sequence of tissue changes after infarction?

A

ischemia > coagulative necrosis > inflammation > granulation tissue > fibrous scar

48
Q

What is shock?

A

characterized by vascular collapse and widespread hypo perfusion of cells and tissue due to reduced BV, CO, or vascular tone.

49
Q

Cardiogenic shock.

A

(pump failure) can be due to MI, cardiac arrhythmias, PE, and cardiac tamponade

50
Q

Hypovolemic shock.

A

(reduced blood volume) can be due to hemorrhage, fluid loss secondary to severe burns, and severe dehydration

51
Q

Septic shock.

A

(viral or bacterial infection) causes cytokines to trigger vasodilatation and hypotension, acute respiratory distress syndrome (ARDS) DIC, and multiple organ dysfunction syndrome

52
Q

What is neurogenic shock.

A

(generalized vasodilation) caused by decreased sympathetic tone; seen with anesthesia and brain or spinal cord injury

53
Q

What is anaphylactic shock?

A

Generalized vasodilation; type I hypersensitivity reaction

Kaplan: Pathophysiology 1-5 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions