Circulatory Pathology

Question 1

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

What is the newspaper test?

Answer 1

Transudates are edema fluid with low protein content and are clear. (Transudate–transparent)

Exudates have high protein content and cells and are opaque.

Transudates give rise to pitting edema.
(click here for explanation: http://forums.studentdoctor.net/threads/pitting-edema.809732/)

The newspaper test differentiates between the two–can you read a newspaper through the test tube?

Question 2

Normally, people do not develop edema because the _________ pressure and the ___________ pressure balance out.

Answer 2

Hydrostatic, oncotic

Question 3

How does hypoalbuminemia cause edema? In what diseases does this develop?

Answer 3

Hypoalbuminemia is low blood protein, which results in low oncotic pressure in the blood vessels.

Oncotic pressure pulls fluid in from the tissues, while hydrostatic pressure pushes fluid out. When they are out of balance in the case of hypoalbuminemia, too much fluid is pushed out into the tissues, resulting in edema.

Liver disease, nephrotic syndrome, protein deficiency (Kwashiorkor)

Question 4

What is myxedema?

Answer 4

Specialized form of tissue swelling due to increased extracellular glycosaminoglycans (pulls fluid into the extracellular space). Seen in Graves disease.

Question 5

Where do effusions collect and why?

Answer 5

They collect in potential spaces (means places where there’s a gap where fluid or gas can accumulate), especially the pericardial, pleural, and peritoneal cavities.

Question 6

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

Answer 6

Cirrhosis or other liver disease. Blood flow through the liver is not good, so patients get portal hypertension. This results in greater hydrostatic pressure (especially if the edema fluid is a transudate–low oncotic pressure) which pushes fluid out into the tissues.

Question 7

What is the difference between hyperemia and congestion?

Answer 7

Both stem from locally increased blood volumes.

Hyperemia: active process due to vascular dilation. Accompanied by erythema (redness) due to influx of oxygenated blood. May be normal or pathological (inflammation).

Congestion: passive process due to reduced outflow of blood. Accompanied by cyanosis (blueness) due to buildup of deoxy blood. Often with edema, always pathological.

Question 8

Describe the steps of platelet adhesion and the glycoproteins involved in each one.

Answer 8

1. Platelet adhesion:
   von Willebrand’s factor (vWF) sticks to collagen,
   platelets stick to vWF via glycoprotein Ib.
2. Platelet activation:
   platelets undero shape change + degranulation,
   synthesize thromboxane A2,
   express phosolipid complex on membrane
3. Platelet aggregation:
   more platelets recruited
   ADP and thomboxane A2 mediate aggregation
   platelets bind fibrinogen via glycoprotein IIb-IIIa

Question 9

What diseases are associated with deficiency of glycoprotein Ib and IIb-IIIa?

Answer 9

Ib: Bernard-Soulier Syndome (defective platelet adhesion)

IIb-IIIa: Glanzmann Thrombasthenia (defective platelet aggregation

Question 10

What medication inhibits thromboxane A2 production.

Answer 10

Aspirin irreversibly acetylates cyclooxygenase, preventing production of thromboxane A2.

Question 11

What are the major features of ITP? Which populations are affected by its acute and chronic forms?

Answer 11

Immune Thrombocytopenia Purpura:
Antiplatelet IgG destroy platelets => deficiency

Petechiae, purpura, and bleeding diathesis (propensity toward bleeding)

Acute: children post viral infection, self-limiting
Chronic: women in childbearing years, may be first signs of SLE

Question 12

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

Answer 12

Thrombotic thrombocytopenia purpura:
Widespread intravascular formation of fibrin-platelet thrombi. Due to deficient ADAMTS13 (which normally clears vWF)
Pentad: fever
thrombocytopenia
microangiopathic hemolytic anemia (=broken RBCs)
neurologic symptoms
renal failure

Question 13

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

Answer 13

Thrombotic microangiopathy due to endothelial cell damage, occuring most often in children.

Similar pentad to TTP: fever, low platelets, hemolysis, neurologic symptoms, and especially renal failure.

Follows gastrogenteritis with bloody diarrhea due to E. coli 0157:H7 infection.

Question 14

How are the extrinsic and intrinsic hemostatic pathways activated?

Answer 14

Intrinsic: contact factors interacting with collagen
Extrinsic: release of tissue factor following trauma

Question 15

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

Answer 15

Intrinsic: PTT–Partial thromboplastin time (I II V VIII IX X XI XII)
Extrinsic: PT–Prothrombin time (I II V VII X)

Question 16

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

Answer 16

Bleeding time

Question 17

What are the major features of DIC?

Answer 17

Disseminated intravascular coagulation

Widespread microthrombi. Hypercoagulation due to excess thrombin outpaces patient’s ability to produce platelets and coag factors, results in hemorrhages.

Always a secondary condition. Look for it in meningococcal infections.

Question 18

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

Answer 18

A: Factor XIII
B: Factor IX
Disease does not result in petechiae or ecchymoses.

Question 19

What are the vitamin K-dependent clotting factors?

Answer 19

II, VII, IX, X, proteins C & S

Question 20

Describe the major features of von Willebrand disease.

Answer 20

Inherited, due to deficiency/defect in vWF

Spontaneous bleeding from mucous membranes
Prolonged bleeding from wounds
Menorrhagia in young women

Question 21

What is Virchow’s triad? Give examples of conditions contributing to each factor.

Answer 21

1. venous stasis (atrial fib, left ventricle dysfunction, immobility, varicose veins, venous obstruction)
2. vascular injury (trauma, venipuncture, chemical irritation, heart valve dz, atherosclerosis, catheters)
3. hypercoagulability (clotting disorders, pregnancy, oral contraceptives, nephrotic syndrome, age, IBD, malignancy)

Question 22

What is the difference between an embolus and a thrombus?

Answer 22

Thrombus: a blood clot in a vein
Embolus: A mass that travels in the blood vessels until it blocks one (may be a broken off piece of a thrombus)

Question 23

What are the features of pulmonary embolism?

Answer 23

Often clinically silent, arising from DVTs.
Classic presentation is postop patient who gets out of bed and collapses.
Dyspnea, tachypnea, pleural chest pain, cough + hemoptysis (coughing up blood)

Question 24

What is the most common potential outcome of PE?

Answer 24

No sequelae and complete resolution in 75% of cases.

Question 25

What is a paradoxical embolus?

Answer 25

Generally, arterial and atrial clots go to the brain (stroke) and DVTs go to the lungs (PE).
A paradoxical embolus is when a DVT skips the pulmonary circuit by passing from the right heart to the left heart through a septal defect, gaining access to the systemic circulation.

Question 26

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

Answer 26

Anemic: occur in solid organs with a single blood supply (kidney, spleen, heart), appear white

Hemorrhagic: Occur in organs with dual blood supply or collateral circulation (liver, intestines), appear red.

Question 27

What are the four major causes of shock?

Answer 27

Cardiogenic (pump failure): incl. MI, arrhythmia, PE

Hypovolemic (fluid loss): incl. hemorrhage, burns, dehydration

Septic (bacterial infection): due to Gram-neg endotoxin resulting in cytokine release

Neurogenic (generalized vasodilation): due to anesthesia or CNS injury (lose vascular tone)

Question 28

How is hypovolemic shock classified?

Answer 28

I: loss of 10%. Little tachycardia, no significant change in bp, pulse pressure, rr

II: 20%. HR >100bpm, tachypnea, decreased pulse pressure

III: 30%. Marked tachycardia and tachypnea, decreased systolic bp, oliguria

IV: 40%. Market tachycardia, decreased systolic bp, narrow pulse pressure, little urine output. Immediately life threatening.

Question 29

what are the three stages of shock?

Answer 29

I: Compensation
(perfusion to vital organs maintained by reflex mechanisms)
II: Decompensation
(progressive decrease in tissue perfusion, potentially reversible tissue damage, kidney problems)
III: Irreversible
(irreversible tissue injury and organ failure ultimately leading to death)