Diseases and Pathology from Robbins Ch.4 Flashcards

(27 cards)

1
Q

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

A

CHF

  • results in activation of RAAS system
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2
Q

How is salt retention helpful in early stages heart failure?

A

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

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3
Q

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?

A

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

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4
Q

What is filariasis?

A

Parasitic infection that causes obstructive fibrosis of lymph channels and LNs

  • can result in edema of lower limbs, genitals
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5
Q

What is elephantiasis?

A

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.

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6
Q

What can complicate treatment for breast cancer?

A

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

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7
Q

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

A

Signals underlying cardiac or renal disease

Can compromise wound healing and infection clearance

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8
Q

What is the clinical presentation of subcutaneous edema?

A

Diffuse or more conspicuous in regions with high hydrostatic pressures

Distribution often influenced by gravity

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9
Q

What is dependent edema?

A

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
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10
Q

Pulmonary edema is a seen with what diseases?

A

Left ventricular failure

Renal failure

Acute Respiratory Distress Syndrome (ARDS)

pulmonary inflammation/infection

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11
Q

Pulmonary edema is hazardous because it can…

A

create a favorable for bacterial infection.

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12
Q

What are the gross pathological signs of pulmonary edema?

A

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

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13
Q

What complications does ascites make patients vulnerable to?

A

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

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14
Q

Edema from renal disfunction will end up where?

A

Areas with loose CT

Periorbital edema is a sign of severe renal disease

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15
Q

Brain edema is considered life threatening. Why?

A

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

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16
Q

What histological findings are associated with chronically congested tissues?

A

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

17
Q

What color do congested tissues take on? Why?

A

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

18
Q

What microscopic findings are associated with acute pulmonary congestion?

A

Engorged alveolar capillaries

alveolar septal edema

focal intraalveolar hemorrhage

19
Q

What microscopic findings are associated with chronic pulmonary congestion?

A

thickened and fibrotic septa

alveoli contain hemosiderin-laden macrophages called heart failure cells

20
Q

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

A

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

21
Q

What changes are associated with chronic passive hepatic congestion?

A

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

22
Q

What is Glanzmann thrombasthenia?

A

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

23
Q

What does prothrombin time assay check?

A

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

24
Q

What does partial prothrombin time assay check?

A

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

25
Why is heparin a clinically useful therapy?
Can stimulate antithrombin III activity - antithrombin III will inhibit most of extrinsic pathway
26
What are the 3 primary pathologies that lead to thrombosis?
1. Endothelial Injury 2. Hypercoagulability 3. Abnormal Blood Flow
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?
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