Circulatory Pathology

Question 1

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

Answer 1

Transudate: edema fluid with low protein content

Exudate: Edema fluid with high protein content and cells

Exudate fluid causes non-pitting edema

Question 2

What is the newspaper test?

Answer 2

Whether or not you are able to read a newspaper through the test tube tells you what kind of fluid it is. Clear = transudate Cloudy = exudate

Question 3

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

Answer 3

hydrostatic

oncotic

Question 4

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

Answer 4

a decrease in oncotic pressure (of the blood) allows fluid to seep out into extracellular space = edema

Liver disease, nephrotic syndrome, protein deficiency (kwashiorkor)

Question 5

What is myxedema?

Answer 5

a specialized form of tissue swelling due to increased extracellular glycosaminoglycans. seen with Graves disease

Question 6

Where do effusions collect and why?

Answer 6

potential spaces: exists between two adjacent structures that are not tightly adjoined but usually does not open up during normal functioning. Path of least resistance

ex. pericardium, subdural space, pleura, peritoneum

Question 7

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

Answer 7

cirrhosis and other liver disease

Increased portal hypertension, due to a poorly functioning liver, leads to an increase in hydrostatic pressure and fluid to be forced out into the peritoneum.

Question 8

What is the difference between hyperemia and congestion?

Answer 8

hyperemia is an ACTIVE increase in the volume of blood in the tissues. It is caused by arteriolar dilation and can be pathological or physiological

congestion is a PASSIVE increase in the volume of blood in tissues; usually also accompanies by edema. It is caused by impaired venous flow from tissues and is always pathological

Question 9

What is the first step of platelet adhesion and what glycoprotein is involved?

Answer 9

platelet adhesion

vWF adheres to subendothelial collagen and platelets stick to vWF with GLYCOPROTEIN 1b

Question 10

What is the second step of platelet adhesion?

Answer 10

platelet activation

platelets shape change and degranulate. THOMBOXANE A2 is formed by platelets

Question 11

What is the third stem of platelet adhesion and what glycoprotein is involved?

Answer 11

platelet aggregation

More platelets arrive and bind to each other by binding to fibrinogen using GLYCOPROTEIN IIb-IIIa

Question 12

What two things are potent mediators of platelet aggregation?

Answer 12

ADP and Thromboxane A2

Question 13

What disease occurs with the deficiency of platelet GP Ib and results in defective platelet adhesion?

Answer 13

Bernard-Soulier Syndrome

Question 14

What GP is deficient and what step of platelet adhesion is affected with Glanzmann Thrombosthenia?

Answer 14

GP IIB-IIIa

platelet aggregation

Question 15

How does aspirin affect platelet aggregation?

Answer 15

irreversibly acetylates cyclooxygenase, preventing platelet production of thromboxane A2

Question 16

List the major features of ITP, and which population is affected by its acute and which by its chronic form.

Answer 16

Immune Thrombocytopenia Purpura
Autoimmune mediated attack (IgG) against platelets/GP
sx: petechiae, purpura (bruises) and bleeding diathesis
Acute: children after viral infection
Chronic: women in childbearing years

Question 17

List the pentad of characteristic signs of TTP, and describe its pathogenesis

Answer 17

Fever
Thrombocytopenia
Microangiopathic hemolytic anemia
Neurologic symptoms
Renal failure

Widespread formation of platelet thrombi with fibrin leading to intravascular hemolysis (deficiency of enzyme ADAMTS13, which is responsible for cleaving vWF)

Question 18

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

Answer 18

Viremia causes cell damage, which leads to clots that damage small blood vessels
Occurs in children
Follows: gastroenteritis with bloody diarrhea

Question 19

How are the extrinsic and intrinsic pathways activated?

Answer 19

Extrinsic: the release of tissue factor
Intrinsic: contact factors (contact with subendothelial collagen or HMWK)

Question 20

What tests are used to monitor the extrinisic and intrinsic pathways?

Answer 20

PT: prothrombin time EXTRINSIC (VII, X, V, prothrombin, fibringogen)
PTT: partial thromboplastin time INTRINSIC (XII, XI, IX, VIII, X, V, prothrombin, fibrinogen)

Question 21

List the major features of DIC? (3)

Answer 21

Always second to another disorder (infection, adenocarcinomas, obstetric complications…)
Widespread microthrombi
Consumption of platelets and clotting factors cause hemorrhages

Question 22

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

Answer 22

A: factor VIII
B: factor IX

Neither produce petechiae or ecchymoses

Question 23

What is the pathogenesis for ITP, TTP and DIC?

Answer 23

ITP: antiplatelet antibodies
TTP: endothelial defect
DIC: thrombin excess

Question 24

What are the vitamin K dependent clotting factors?

Answer 24

Factors II, VII, IX, X and protein C & S

Question 25

Describe the major features of Von Willebrand disease.

Answer 25

Inherited bleeding disorder characterized by either a deficiency or qualitative defect in von Willebrand factor

spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, menorrhagia in young females, hemarthrosis in uncommon

normal platelet count, prolonged bleeding time
normal PT, prolonged PTT
abnormal platelet response to ristocetin

Question 26

What is Virchow’s triad and what might contribute to its presence (LOTS to choose from)?

Answer 26

Virchow’s Triad: stasis, vascular injury, hypercoagulation

endothelial injury, atherosclerosis, vasculitits, immobilization, turbulence, hyperviscosity of blood, clotting disorders, neoplasia, advanced age, pregnancy, oral contraceptives

Question 27

What is the difference between an embolism and a thrombus?

Answer 27

thrombus: blood clot
embolism: any intravascular mass that has been carried down the bloodstream from its site of origin, resulting in the occlusion of a vessel (98% thromboemboli but could be gas, amniotic fluid, tumor/metastasis)

Question 28

Know the features of pulmonary emboli?

Answer 28

clinically silent, often misdiagnosed

95% from DVTs
Pelvic venous plexuses of the prostate and uterus
Right side of the heart

Classic presentation: ICU, postoperative, or bedridden pt. who gets out of bed and collapses

Question 29

What is the most common potential outcome of PE?

Answer 29

No sequelae (75%)
asymptomatic or transient dyspnea/tachypnea
no infarction
complete resolution

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: solid organs with single blood supply (spleen, kidney, heart)
PALE/WHITE

hemorrhagic: organs with a dual blood supply or collateral circulation (lungs and intestines)
RED

Question 32

What are the 4 major causes of shock?

Answer 32

Cardiogenic (pump failure)
Hypovolemic shock (reduced blood volume)
Neurogenic (generalized vasodilation)
Septic (bacterial infection)

Question 33

How is hypovolemic shock classified

Answer 33

Class I hemorrhage (loss of 0-15%)
Class II hemorrhage (loss of 15-30%)
Class III hemorrhage (loss of 30-40%)
Class IV hemorrhage (loss of >40%)

Question 34

What is the first stage of shock?

Answer 34

Stage 1: compensation
reflex mechanisms maintain organ perfusion
increased sympathetic tone
release catechomalines
activation of renin-angiotensin system

Question 35

What is the second stage of shock?

Answer 35

Stage 2: decompensation
progressive decrease in tissue perfusion
potentially reversible tissue injury occurs
development of a metabolic acidosis, electrolyte imbalances and renal insufficiency

Question 36

What is the third stage of shock?

Answer 36

Irreversible
irreversible tissue injury and organ failure
ultimately resulting in death