Circulatory Pathology

Question 1

what is the difference between exudates and transudates and which of those cause non-pitting edema?

Answer 1

exudates= protein rich edema fluid
transudate= protein poor edema fluid
exudate fluid causes non-pitting edema

Question 2

what is the newspaper test?

Answer 2

to crudely determine the type of edema fluid present, you can put newspaper print behind the fluid in a test tube and if text is readable, it is transudate, if not, its exudate.

Question 3

Normally, people do not develop edema because the ________ pressure, and the _______ pressure balance one another out.

Answer 3

hydrostatic, and oncotic

Question 4

How does Hypoalbuminemia cause edema? In what types of diseases does a person develop Hypoalbuminemia?

Answer 4

Hypoalbuminemia may cause generalized edema (swelling) via a decrease in oncotic pressure. Diseases that cause hypoalbuminemia: liver disease, nephrotic syndrome, and protein deficiency (kwashiorkor)

Question 5

What is myxedema?

Answer 5

specialized form of tissue swelling due to increased extracellular glycosaminoglycans. Associated with thyroid disease (Graves disease)

Question 6

Where do effusions collect and why? (hint: potential spaces in the body)

Answer 6

collect within body cavities such as pleural and pericardial space because fluid travels the path of least resistance.

Question 7

What is the major cause of ascites, and why does this fluid typically only collect in the abdomen?

Answer 7

HTN in portal vein, fluid leaks out into the peritoneal cavity and causes abdominal distention

Question 8

What is the difference between hyperemia and congestion?

Answer 8

both are excess amount of blood in a tissue or organ secondary to a) vasodilation (active) or
b) diminished venous outflow (passive) respectively

Question 9

Be able to describe the steps of platelet adhesion and the glycoproteins involved in each

Answer 9

step 1: platelet adhesion
first, vWF adheres to subendothelial collagen. Platelet then adhere to vWF by Gp Ib

step 2: platelet activation
platelets undergo a shape change and degranulation occurs. Platelet synthesis of thromboxane A2 - for platelet aggregation

step 3: platelet aggregation
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 Gp IIb-IIIa

Question 10

Bernard-Soulier Syndrome

Answer 10

deficiency of platelet Gp Ib. Defective platelet adhesion

Question 11

Glanzmann Thrombasthenia

Answer 11

deficiency of Gp IIb-IIIa. Defective platelet aggregation

Question 12

describe which medication inhibits thromboxane production.

Answer 12

Aspirin by irreversibly acetylating cyclooxygenase, preventing platelet production of thromboxane A2

Question 13

List the major features of Imune Thrombocytopenia Purpura (ITP)

Answer 13

autoimmune mediated attack against platelets leading to decreased platelets (thrombocytopenia). Results in petechiae (broken capillaries) purpura (bruises) and bleeding diathesis (hematomas)

Question 14

Which population is affected by its acute and which by its chronic form of ITP

Answer 14

Acute: seen in children following a viral infection. self limiting
Chronic: usually seen in women in their childbearing years.

Question 15

List the pentad of characteristic signs of Thrombotic Thrombocytopenic Purpura (TTP)

Answer 15

pentad: fever, thrombocytopenia, microangiopathic hemolytic anemia (intravascular hemolysis), neurologic symptoms, and renal failure.

Question 16

describe the pathogenesis of Thrombotic Thrombocytopenic Purpura (TTP)

Answer 16

widespread formation of platelet thrombi with fibrin lead to intravascular hemolysis (thrombotic microangiopathy). Essentially there are all these little clots floating around (go into brain and cause neurological problems and infarcts in spinal cord)

Question 17

List the major features of hemolytic uremic syndrome, and what illness it typically follows?

Answer 17

a form of thrombotic microangiopathy due to endothelial cell damage. Cause: E. coli 0157. Occurs most commonly in children and follow a gastroenteritis with bloody diarrhea

Question 18

How are the extrinsic and intrinsic pathways activated (i.e. what factor initiates each)?

Answer 18

extrinsic: activated by tissue factor
intrinsic: activated by contact factors

Question 19

What test is used to monitor the extrinisic pathway?

Answer 19

Prothrombin time (PT) test factor VII, X, V, prothrombin, and fibrinogen

Question 20

What test is used to monitor the intrinsic pathways?

Answer 20

Partial thromboplastin time (PTT) tests factors XII, XI, IX, VIII, X, V, prothrombin, and fibrinogen

Question 21

What test is used to determine if platelets are functioning correctly?

Answer 21

Thrombin time (TT) tests for adequate fibrinogen levels and Fibrin Degradation products (FDP) tests the fibrinolytic system

Question 22

List the major features of Disseminated Intravascular Coagulation (DIC)

Answer 22

Causes: obstetric complications (placental tissue factor activates clotting), gram-negative sepsis (TNF) activates clotting, microorganisms, AML M3, adenocarcinomas
Path: widespread microthrombi, consumption of platelets and clotting factors causes hemorrhages
Lab: platelet count is decreased, prolonged PT/PTT, decreased fibrinogen, elevated fibrin splot products (D-dimers). ALWAYS SECONDARY TO ANOTHER DISORDER

Question 23

What factors are missing in hemophilia A and B? Do these diseases produce petechiae or ecchymoses?

Answer 23

Hemophilia A: deficiency of factor VIII. No petechiae or ecchymoses
Hemophilia B: deficiency of factor IX. No petechiae or ecchymoses

Question 24

What are the vitamin K dependent clotting factors?

Answer 24

vit. K deficiency leading to decreased synthesis of factors II, VII, IX, X and protein C & S. Caused by liver disease and the resulting decreased synthesis of virtually all clotting factors.

Question 25

Describe the major features of Von Willebrand disease

Answer 25

Inherited bleeding disorder characterized by either a deficiency or a qualitative defect in von Willebrand factor. Clinical features: spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, menorrhagia in young females, hemarthrosis is uncommon

Question 26

What is Virchow’s triad, and what are examples of the diseases/conditions contributing to stasis, vascular injury, and hypercoagulability?

Answer 26

Virchow’s triad are the factors involved in thrombus formation (stasis, wall injury, hypercoagulability)
stasis (immobilization), vascular wall (atherosclerosis), hypercoagulability (clotting disorders)

Question 27

What is the difference between an embolism and a thrombus?

Answer 27

thrombus is a blood clot and an embolus is any intravascular mass that has been carried down the bloodstream from its site of origin resulting in the occlusion of the blood vessel (most often a clot carried- thromboemboli)

Question 28

What are the features of pulmonary emboli?

Answer 28

PE most often is a complication of a condition called deep vein thrombosis (DVT-95% of the time). In DVT, blood clots form in the deep veins of the body—most often in the legs. These clots can break free, travel through the bloodstream to the lungs, and block an artery (right side of heart).

Deep vein clots are not like clots in veins close to the skin’s surface. Those clots remain in place and do not cause PE.

It is the most commonly missed diagnosis, often clinically silent, found in almost half of all hospital autopsiesj

Question 29

What is the most common potential outcome of PE?

Answer 29

1. no sequelae (75%)
2. infarctions (15%)
3. sudden death (5%)
4. chronic secondary pulmonary HTN (3%)

Question 30

What is a paradoxical emboli?

Answer 30

any venous embolus that gains access to the systemic circulation by crossing over from the right to the left side of the heart through a septal defect

Question 31

Where do anemic and hemorrhagic infarcts occur, and how do they differ on gross pathology?

Answer 31

anemic infarcts occur in solid organs with a single blood supply (spleen, kidney, heart) and has a pale/white color
hemorrhagic infarcts occur in organs with a dual blood supply or collateral circulation (lung and intestines), they also occur with venous occlusion

Question 32

What are the 4 major causes of shock?

Answer 32

cardiogenic (pump failure), hypovolemic shock (reduced blood volume), septic shock (bacterial infection), neurogenic shock (generalized vasodilation)

Question 33

How is hypovolemic shock classified (i.e. classes I-IV)?

Answer 33

Class 1 hemorrhage (0-15% loss)
-little tachycardia
-usually no significant change in BP, pulse pressure, respiratory rate
Class II hemorrhage (15-30% loss)
-HR >100 b/m, tachypnea, decreased pulse pressure
Class III hemorrhage (30-40%)
-marked tachycardia and tachypnea, decreased systolic BP, oliguria
Class IV hemorrhage (>40%)
-marked tachycardia and decreased systolic BP, narrowed pulse pressure, markedly decreased (or no) urinary output
-immediately life threatening

Question 34

What are the 3 stages of shock?

Answer 34

stage 1: compensation, in which perfusion to vital organs is maintained by reflex mechanisms (incr. sympathetic tone, release of catecholamine, activation of the renin-angiotensin system)
stage 2: decompensation (progressive decrease in tissue perfusion, potentially reversible tissue injury, development of metabolic (lactic) acidosis, electrolyte imbalances, and renal insufficiency)
stage 3: irreversible (irreversible tissue injury and organ failure, ultimately resulting in death)