Diseases and Pathology from Robbins Ch.4

Question 1

What is one of the most important causes of renal hypoperfusion?

Answer 1

CHF

• results in activation of RAAS system

Question 2

How is salt retention helpful in early stages heart failure?

Answer 2

Retention of sodium and water and other adaptations - like increased cascular tone and elevated levels of ADH - improve CO and restore normal renal perfusion

Question 3

What is the outcome of salt retention in later stages of heart failure? What does this mean clinically when you observe the obvious physical symptoms of heart failure?

Answer 3

As CO diminishes, retained fluid increases the hydrostatic pressure which leads to edema and effusions

Clinically speaking, if you evaluate someone with cankles and +4 pitting edema, they might be having problems with maintaining a normal CO

Question 4

What is filariasis?

Answer 4

Parasitic infection that causes obstructive fibrosis of lymph channels and LNs

• can result in edema of lower limbs, genitals

Question 5

What is elephantiasis?

Answer 5

Clinical condition describing your mom.

It’s actually a progression of filariasis, with massive swelling of the legs and/or genitals due to lymph vessel obstruction.

Question 6

What can complicate treatment for breast cancer?

Answer 6

Severe edema of the upper extremity can complicate surgery or radiation therapy for breast cancer, both in breasts and axillary LNs

Can occur as a result of previous treatments and biopsies for cancer

Question 7

What is subcutaneous edema a sign of? What is compromised by its presence?

Answer 7

Signals underlying cardiac or renal disease

Can compromise wound healing and infection clearance

Question 8

What is the clinical presentation of subcutaneous edema?

Answer 8

Diffuse or more conspicuous in regions with high hydrostatic pressures

Distribution often influenced by gravity

Question 9

What is dependent edema?

Answer 9

Subcutaneous edema that ‘moves’ depending on position relative to gravitational pull

• moves into legs while standing
• moves into sacrum while lying recumbent - keep this in mind with bedridden patients and pressure ulcers

Question 10

Pulmonary edema is a seen with what diseases?

Answer 10

Left ventricular failure

Renal failure

Acute Respiratory Distress Syndrome (ARDS)

pulmonary inflammation/infection

Question 11

Pulmonary edema is hazardous because it can…

Answer 11

create a favorable for bacterial infection.

Question 12

What are the gross pathological signs of pulmonary edema?

Answer 12

Lungs are heavy and full of fluid, 2-3x their original weight

Full of frothy pink fluid - a mix of air, extravasated RBCs, and edema

Question 13

What complications does ascites make patients vulnerable to?

Answer 13

Prone to seeding from bacteria, leads to life-threatening infections

Question 14

Edema from renal disfunction will end up where?

Answer 14

Areas with loose CT

Periorbital edema is a sign of severe renal disease

Question 15

Brain edema is considered life threatening. Why?

Answer 15

Brain can extrude/herniate through foramen magnum or brain stem vascular supply can be compromised

Either one can disrupt medullary respiratory centers and cause death

Question 16

What histological findings are associated with chronically congested tissues?

Answer 16

capillary rupture can produce small hemorrhagic foci, catabolism of RBCs that have extravasated leave clusters of hemosiderin-laden macrophages

Question 17

What color do congested tissues take on? Why?

Answer 17

Congested tissues take on a dusky reddish blue color due to red cell stasis and presence of de-oxygenated hemoglobin

Question 18

What microscopic findings are associated with acute pulmonary congestion?

Answer 18

Engorged alveolar capillaries

alveolar septal edema

focal intraalveolar hemorrhage

Question 19

What microscopic findings are associated with chronic pulmonary congestion?

Answer 19

thickened and fibrotic septa

alveoli contain hemosiderin-laden macrophages called heart failure cells

Question 20

What gross and cellular changes are associated with acute hepatic congestion?

Answer 20

Central vein and sinusoids are distended

Centrilobular area is at distal end of hepatic blood supply

• centrilobular hepatocytes can undergo ischemic necrosis

periportal hepatocytes can develop fatty change (better blood supply due to proximity to hepatic arterioles

Question 21

What changes are associated with chronic passive hepatic congestion?

Answer 21

Centrilobular regions are grossly red-brown and are slighly depressed

-accented against surrounding tan liver, causing nutmeg liver

Microscopically:

centrilobular hemorrhage

hemosiderin-laden macrophages

variable degrees of hepatocyte dropout and necrosis

Question 22

What is Glanzmann thrombasthenia?

Answer 22

Inherited deficiency of GIIb/IIIa results in bleeding disorder where platelet aggregation is difficult

Question 23

What does prothrombin time assay check?

Answer 23

Checks extrinsic pathway:

Factors VII, X, V, II and fibrinogen

Tissue factor, phospholipids, Ca++ are added to plasma and the time for a fibrin clot to form is checked

Question 24

What does partial prothrombin time assay check?

Answer 24

Screens intrinsic pathway function:

Factors XII, XI, IX, VIII, X, V, II, and fibrinogen

Addition of negative charge needed in order to activate XII, along with Ca++ and phospholipids

Time to fibrin clot formation assessed

Question 25

Why is heparin a clinically useful therapy?

Answer 25

Can stimulate antithrombin III activity

• antithrombin III will inhibit most of extrinsic pathway

Question 26

What are the 3 primary pathologies that lead to thrombosis?

Answer 26

1. Endothelial Injury
2. Hypercoagulability
3. Abnormal Blood Flow

Question 27

Endothelial injury can help mediate clotting in obvious ways - i.e. through direct injury/cuts - and in some not so obvious ways. How do cardiac and/or arterial plaques help create thrombi?

Answer 27

Platelet formation happens in areas with high shear stress, such as arteries

Inflammation and other noxious stimuli indice patterns of gene expression in endothelials, making them prothrombotic

• downregulates expression of thrombomodulin, protein C, Tissue Factor inhibitor
• secretes Plasminogen Activator Inhibitors (limits fibrinolysis) and downregulates expression of TPA