Term
| What are the 5 pathophysiological forms of edema? |
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Definition
1) Increased hydrostatic pressure
2) Decreased plasma osmotic pressure
3) Lymphatic obstruction (less common)
4) Sodium retention
5) inflammation |
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Term
1) How can increased hydrostatic pressure cause lower body Edema?
2) What about in the lungs? |
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Definition
1) Right heart failure
2) Left heart failure |
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Term
1) How can increased hydrostatic pressure cause lower body Edema?
2) What about in the lungs? |
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Definition
1) Right heart failure
2) Left heart failure |
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Term
| How does Pulmonary edema arise? |
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Definition
1) Most common cause is left heart failure. Major symptom is dyspnea and pulmonary rales (crackling upon inspiration).
2) Acute respiratory distress syndrome (ARDS), hypersensitivity reactions, pneumonia and renal failure are other causes. |
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Term
| how does Cerebral Edema arise? Why is it so dangerous? |
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Definition
1) Localized around tumor or generalized with encephalitis.
Can be fatal because of herniation of cerebellar tonsils into foramen magnum, compressing brain stem. |
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Term
| When might you see "nutmeg liver"? |
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Definition
Right heart failure with red centrilobular and tan peripherilobular tissue.
Congenstion. |
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Term
| What is the difference b/w Hyperemia and Congestion? |
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Definition
Hyperemia is active increase in arterial flow
Congestion is passive decrease in venous outflow
Both are common and neither are serious. Both involve blood in the pipes where they should be, but just TOO MUCH |
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Term
| What are Petechiae, Purpura and Ecchymoses? |
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Definition
Hemorrhages.
1) Petechiae- (1-2 mm) due to platelet deficiency
2) Purpura- (3-10mm) due to vasculitis, vessel fragility, ect.
3) Ecchymoses (over 1cm) subcutaneous hemorrhages that change color has Hb breaks down. |
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Term
| What are the 3 stages of shock? |
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Definition
1) Non-progressive, with reflex compensatory mechanisms that maintain perfusion of vital organs
2) Progressive, with worsening lactic acidosis
3) Irreversible, with resultant death even if shock is reversed. |
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Term
A patient presents who is clearly in shock. THeir skin is cold and clammy. What should you look for?
What if their skin had been warm and flushed? |
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Definition
1) Bleeding (hypovolemic shock)
2) Infection (Sepsis) |
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Term
| Which 3 components regulate Hemostasis? |
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Definition
1) Vascular wall (endothelium)
2) Platelets (anucluate, pieces of megakaryocyte cytoplasm in blood that initiate and propagate clotting. They contain ADP, fibrinogen, clotting factors V and VIII, calcium and epinephrine).
3) Coagulation Cascade |
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Term
| Explain the 4 stages of Hemostasis at Sites of Vascular Injury. |
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Definition
SHORT- Vasoconstriction..Platelet adhesion and thromboxane release....Coagulation cascade activating fibrin......Fibrin/Platelet plug.
1) Vasoconstriction- mediated by reflex neurogenic mechanisms that are augmented by endothelin-mediated contriction.
2) Primary Hemostasis- involving platelet adhesion to thrombogenic ECM. Activation and release of ADP and thromboxane A2 with additional platelet recruitment occurs.
3) Secondary Hemostasis- coagulation cascade is activated by membrane-bound tissue factor and platelet factors, culminating in conversion of fibrinogen to fibrin by activated thrombin.
4) Thrombus Stabilization and anti-thrombotic events-
Semi-permanent plug of aggregated platelets and polymerized fibrin is formed. |
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Term
| What are the 3 primary factors that predispose to Thrombosis? |
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Definition
MOST serious in arteries and more common in veins
1) Endothelial injury (most important-arising from cholesterol or smoking)
2) Abnormal blood flow (turbulence or stasis)
3) Hyper-coagulability (tendency to form clots/ either genetic or acquired). |
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Term
| What is the difference between Ascites and Anasarca? |
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Definition
1) Ascites is abdominal fluid build-up
2) Anasarca is generalized edema |
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Term
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Definition
| Hemorrhage enclosed within tissue |
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Term
| Why is it dangerous to rely on vital signs as indicators of shock? |
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Definition
They are the late-responders!
Look for agitation, cold/clammy (cardiogenic and hypovolemic), warm/flushed (sepsis), confusion and lethargy. |
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Term
| What is anoxic encephalopathy? |
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Definition
| Patients who are resuscitated from shock or cardiac arrest without the return of normal brain function. |
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Term
| What is a cardiac tamponade? |
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Definition
| A form of cardiac shock where bleeding into the pericardial sac prevents the heart from filling. |
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Term
| What are the two subsets of sepsis and how are they defined? |
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Definition
1) Severe Sepsis- with acute organ dysfunction
Subset of patients with severe sepsis go into Septic Shock , with refractory arterial hypotension. |
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Term
True or False
The majority of patients with Sepsis have positive blood cultures for infective agents. |
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Definition
False!
only 17%. 69% of those with septic shock (subset of severe sepsis) had (+) culture. |
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Term
| Explain, GENERALLY, what molecular events trigger sepsis? |
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Definition
1) TLRs on macrophages, neutrophils and endothelial cells bind microbial elements and activate inflammatory cells
2) Inflammatory cells produce interleukins and other pro-inflammatory cytokines (local action)
3) Cytokines cause endothelial cells to produce cell adhesion molecules to bind leukocytes and direct them to infection sites. |
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