Fluid And Hemodynamics Flashcards
(13 cards)
Q: What causes passive congestion and what are its consequences?
Q: What are “heart failure cells” and what causes them?
Q: How do heart failure cells form?
Q: What is the hallmark of chronic passive liver congestion?
Q: What causes the nutmeg appearance of the liver?
A: Venous backup → increased hydrostatic pressure → edema, chronic hypoxia, and tissue damage.
A: Hemosiderin-laden macrophages from chronic left-sided heart failure causing pulmonary congestion.
A: Pulmonary capillary pressure pushes RBCs into alveoli → macrophages engulf RBCs → hemosiderin forms.
A: Nutmeg liver with centrilobular necrosis due to right-sided heart failure.
A: Chronic congestion from right-sided heart failure → centrilobular necrosis and sinusoidal dilation.
Q: What are complications of portal hypertension?
Q: What pressures control fluid movement in capillaries?
Q: What is the difference between edema and effusion?
Q: Name 3 causes of edema.
Q: How does venous obstruction cause edema?
A: Esophageal varices, splenomegaly, ascites—all from increased hydrostatic pressure.
A: Hydrostatic pressure (out) vs plasma oncotic pressure (in).
A: Edema = interstitial fluid; Effusion = fluid in cavities (e.g., pleura).
A: Increased hydrostatic pressure, low plasma oncotic pressure, lymphatic obstruction.
A: Increases hydrostatic pressure → prevents forward flow → fluid builds up behind obstruction.
Q: What are two causes of localized increased hydrostatic pressure?
Q: What does pulmonary edema look like histologically?
Q: How does CHF cause edema?
Q: What are 3 causes of reduced plasma oncotic pressure?
Q: In nephrotic syndrome, where is protein lost?
A: Deep vein thrombosis and tumor obstruction.
A: Alveoli filled with pink-staining fluid due to transudate.
A: Backward failure increases venous pressure → capillary hydrostatic pressure → fluid leaks out.
A: Liver cirrhosis, nephrotic syndrome, protein-losing enteropathy.
A: In urine, not into the interstitial space.
Q: How does hydrostatic vs oncotic pressure affect edema distribution?
Q: What are two common causes of lymphatic obstruction?
Q: How does edema from filariasis compare to DVT?
Q: How does sodium retention contribute to edema?
Q: What’s the difference between transudate and exudate?
A: Hydrostatic = localized; Oncotic = generalized.
A: Breast cancer surgery and filariasis.
A: Filariasis causes much more severe, deforming edema.
A: Increases blood volume → raises hydrostatic pressure → fluid leaks into tissue.
A: Transudate = low protein, from pressure imbalance; Exudate = high protein, from inflammation.
Q: How do you differentiate transudate from exudate?
Q: What type of edema is associated with renal dysfunction?
Q: What is anasarca, and what causes it?
Q: Which type of edema is life-threatening and can cause herniation?
Q: What does pulmonary edema look like grossly and microscopically?
A: Transudate: low protein, SG <1.012; Exudate: high protein, SG >1.012, due to inflammation
A: Periorbital edema (eyelids).
A: Severe, generalized subcutaneous edema due to hypoalbuminemia.
A: Cerebral edema.
A: Frothy fluid + congested alveoli histologically.
Q: What are the 4 steps of hemostasis?
Q: What is the final product of both primary and secondary hemostasis?
Q: Which test monitors Warfarin therapy?
Q: What does vWF bind during platelet adhesion?
Q: What is the most important cause of arterial thrombosis?
A: Vascular constriction, platelet plug, coagulation cascade, fibrin clot.
A: Thrombus (fibrin + platelets).
A: PT (extrinsic pathway).
A: GpIb on platelet surface.
A: Atherosclerosis.
White infarct (pale)?
Red infarct?
Septic infarct?
Q: What are the 5 causes of edema?
Q: What are Lines of Zahn?
Arterial blockage (heart, kidney, spleen).
Venous congestion (lung, bowel).
Septic infarct: Infected emboli (endocarditis).
A: 1. ↑ Hydrostatic pressure, 2. ↓ Oncotic pressure, 3. Lymphatic obstruction, 4. Sodium retention, 5. Inflammation.
A: Alternating layers of platelets/fibrin—seen in pre-mortem thrombi.
Q: What triad leads to thrombosis?
Q: What is the most common site for DVT?
Q: What are symptoms of DVT?
Q: What is the danger of mural thrombi?
Q: Which cancers are most associated with hypercoagulability?
A: Virchow’s triad: endothelial injury, stasis/turbulence, hypercoagulability.
A: Deep veins of the legs (>90%).
A: Warmth, erythema, swelling, +Homan’s sign, elevated D-dimer.
A: They can embolize to brain, kidney, spleen, lungs.
A: Mucinous adenocarcinomas (pancreas, ovary).
Q: What distinguishes white vs. red infarcts?
Q: What causes edema in CHF?
Q: What is the hallmark of nephrotic syndrome leading to edema?
Q: What type of fluid is seen in inflammation-related edema?
Q: How do you differentiate transudate vs exudate on labs?
A: White = arterial, solid organs; Red = venous/congested, spongy tissues.
A: Increased hydrostatic pressure from poor venous return.
A: Proteinuria > 3.5 g/day → ↓ oncotic pressure.
A: Exudate (high protein, specific gravity >1.02).
A: Transudate: low protein, low SG; Exudate: high protein, high SG, contains inflammatory cells.
Q: What lab monitors warfarin therapy?
Q: What factor is deficient in hemophilia A?
Q: What protein is deficient in von Willebrand disease?
Q: What are the 3 components of Virchow’s triad?
Q: What is Homan’s sign?
A: PT (extrinsic pathway).
A: Factor VIII.
A: von Willebrand factor.
A: Endothelial injury, stasis, hypercoagulability.
A: Pain on dorsiflexion of foot in DVT.
Q: Where do red infarcts typically occur?
Q: What is the primary lab finding in DIC?
Q: What is the #1 cause of death in ICUs?
Q: What is the warm vs cold phase in septic shock?
Q: What are the 5 P’s of acute arterial occlusion?
A: Lungs, intestines – dual blood supply.
A: Elevated D-dimer, prolonged PT/PTT.
A: Septic shock.
A: Warm = hyperdynamic (↑ CO), Cold = hypodynamic (↓ perfusion, hypotension).
A: Pain, Pallor, Pulselessness, Paresthesia, Paralysis.
Q: What makes a thrombus resistant to lysis?
Q1: What is the most common source of arterial thromboembolism?
Q2: What is the most common site of systemic embolism?
Q4: What causes most pulmonary embolisms?
Q5: What is a saddle embolus?
A: Extensive fibrin deposition.
A1: Mural thrombi from the heart (post-MI, atrial fibrillation).
A2: Lower extremities (75%), followed by the brain (10%).
A4: Deep vein thromboses (DVTs), especially from the legs.
A5: A large embolus that blocks the pulmonary artery bifurcation, often fatal.
Q6: What is paradoxical embolism?
Q7: When does fat embolism typically occur after trauma?
Q8: What is the triad of fat embolism syndrome?
Q: What is the pathogenesis of decompression sickness?
Q: What is a classic histologic finding in amniotic fluid embolism?
Q: What complication is commonly associated with amniotic fluid embolism?
A6: Venous embolus enters systemic circulation via an atrial/ventricular septal defect.
A7: 1–3 days post long bone fracture (e.g., femur).
A8: Respiratory distress (ARDS), petechial rash, neurologic symptoms (confusion, coma).
A: Rapid drop in pressure → nitrogen forms gas bubbles → vascular obstruction, joint pain, and ischemic necrosis (bones).
A: Fetal squamous epithelial cells in maternal pulmonary vessels.
A: Disseminated intravascular coagulation (DIC).
