Diseases and Pathology from Robbins Ch.4 Flashcards
What is one of the most important causes of renal hypoperfusion?
CHF
- results in activation of RAAS system
How is salt retention helpful in early stages heart failure?
Retention of sodium and water and other adaptations - like increased cascular tone and elevated levels of ADH - improve CO and restore normal renal perfusion
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?
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
What is filariasis?
Parasitic infection that causes obstructive fibrosis of lymph channels and LNs
- can result in edema of lower limbs, genitals
What is elephantiasis?
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.
What can complicate treatment for breast cancer?
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
What is subcutaneous edema a sign of? What is compromised by its presence?
Signals underlying cardiac or renal disease
Can compromise wound healing and infection clearance
What is the clinical presentation of subcutaneous edema?
Diffuse or more conspicuous in regions with high hydrostatic pressures
Distribution often influenced by gravity
What is dependent edema?
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
Pulmonary edema is a seen with what diseases?
Left ventricular failure
Renal failure
Acute Respiratory Distress Syndrome (ARDS)
pulmonary inflammation/infection
Pulmonary edema is hazardous because it can…
create a favorable for bacterial infection.
What are the gross pathological signs of pulmonary edema?
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
What complications does ascites make patients vulnerable to?
Prone to seeding from bacteria, leads to life-threatening infections
Edema from renal disfunction will end up where?
Areas with loose CT
Periorbital edema is a sign of severe renal disease
Brain edema is considered life threatening. Why?
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
What histological findings are associated with chronically congested tissues?
capillary rupture can produce small hemorrhagic foci, catabolism of RBCs that have extravasated leave clusters of hemosiderin-laden macrophages
What color do congested tissues take on? Why?
Congested tissues take on a dusky reddish blue color due to red cell stasis and presence of de-oxygenated hemoglobin
What microscopic findings are associated with acute pulmonary congestion?
Engorged alveolar capillaries
alveolar septal edema
focal intraalveolar hemorrhage
What microscopic findings are associated with chronic pulmonary congestion?
thickened and fibrotic septa
alveoli contain hemosiderin-laden macrophages called heart failure cells
What gross and cellular changes are associated with acute hepatic congestion?
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
What changes are associated with chronic passive hepatic congestion?
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
What is Glanzmann thrombasthenia?
Inherited deficiency of GIIb/IIIa results in bleeding disorder where platelet aggregation is difficult
What does prothrombin time assay check?
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
What does partial prothrombin time assay check?
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
Why is heparin a clinically useful therapy?
Can stimulate antithrombin III activity
- antithrombin III will inhibit most of extrinsic pathway
What are the 3 primary pathologies that lead to thrombosis?
- Endothelial Injury
- Hypercoagulability
- Abnormal Blood Flow
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?
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
