Haemodynamic Disorders

Flashcards covering fluid dynamics, edema, hyperemia, congestion, hemorrhage, hemostasis, thrombosis, embolism, infarction, and shock based on Dr. Okezie Ugwa's lecture on Haemodynamic Disorders.

What terms designate fluid collections in the pleural, pericardial, and peritoneal cavities?

Fluid collections in the pleural cavity are designated as hydrothorax, in the pericardial cavity as hydropericardium, and in the peritoneal cavity as hydroperitoneum (more commonly called ascites).

What is anasarca?

Anasarca is a severe and generalized edema characterized by widespread subcutaneous tissue swelling.

What opposing vascular forces primarily control the movement of water and low molecular weight solutes between intravascular and interstitial spaces?

The movement is controlled primarily by the opposing effects of vascular hydrostatic pressure and plasma colloid osmotic pressure.

What are the key protein, cellular, and clinical differences between transudates and exudates?

Transudates are protein-poor ($<3\,g/dL$) and cell-poor fluids that produce dependent pitting edema; exudates are protein-rich ($>3\,g/dL$) and cell-rich fluids (e.g., neutrophils) that produce tissue swelling and non-pitting edema.

What clinical conditions lead to decreased vascular plasma oncotic pressure (hypoalbuminemia) resulting in edema?

Malnutrition/malabsorption (decreased protein intake), cirrhosis (decreased albumin synthesis), and nephrotic syndrome (increased loss of protein in urine).

What causes lymphedema, and what parasite is an example cause of lymphatic obstruction?

Lymphedema is caused by lymphatic obstruction (producing protein-rich non-pitting edema). An example is filariasis caused by Wuchereria bancrofti.

How do hyperemia and congestion differ in terms of pathophysiology and tissue appearance?

Hyperemia is an active process caused by arteriolar dilation leading to increased oxygenated blood flow (causing erythema). Congestion is a passive process caused by reduced blood outflow leading to accumulation of deoxygenated hemoglobin (causing cyanosis).

What histological features distinguish acute pulmonary congestion from chronic pulmonary congestion?

Acute pulmonary congestion exhibits engorged alveolar capillaries with septal edema and focal hemorrhage. Chronic pulmonary congestion shows thickened, fibrotic septa with congested capillaries and intra-alveolar heart failure cells (hemosiderin-laden macrophages).

What gross liver appearance is shown in this specimen, and what underlying mechanism produces it?

Nutmeg liver (chronic passive hepatic congestion), where red-brown depressed centrilobular regions accentuate against surrounding zones of uncongested tan liver due to central hemorrhage and hepatocyte necrosis.

How are petechiae, purpura, and ecchymoses categorized by lesion size?

Petechiae are minute $1\text{ to }2\,mm$ hemorrhages; purpura are $\ge 3\,mm$ to $<10\,mm$ hemorrhages; and ecchymoses are $>1\text{ to }2\,cm$ subcutaneous hematomas.

What enzymatic breakdown sequence accounts for the characteristic color changes in a bruise (ecchymosis)?

Hemoglobin (red-blue color) is enzymatically converted into bilirubin (blue-green color) and eventually into hemosiderin (gold-brown color).

What processes define primary hemostasis versus secondary hemostasis?

Primary hemostasis involves platelet adherence and activation to form an initial primary hemostatic plug. Secondary hemostasis involves tissue factor exposure and factor VII interaction culminating in thrombin generation, which cleaves fibrinogen into insoluble fibrin.

What three primary factors constitute Virchow's triad in thrombus formation?

1. Endothelial cell dysfunction, 2. Stasis of blood flow, and 3. Hypercoagulability.

What are lines of Zahn and what diagnostic importance do they hold?

Lines of Zahn are gross and microscopic laminations of pale platelet and fibrin deposits alternating with darker red cell-rich layers. Their presence signifies that a clot formed in flowing blood, distinguishing antemortem thrombosis from postmortem clots.

How do postmortem blood clots differ morphologically from antemortem red thrombi?

Postmortem clots are gelatinous, unattached to the vessel wall, with a dark red dependent portion and yellow 'chicken fat' upper portion. Antemortem red thrombi are firmer, focally attached, and typically show lines of Zahn on sectioning.

Where do the majority of pulmonary emboli originate, and what can cause sudden death in pulmonary embolism?

The majority originate from the femoral vein (extension of deep vein thrombosis). Sudden death is caused by a large saddle embolus occluding major pulmonary artery branches.

What clinical triad characterizes fat embolism syndrome following long bone fractures?

Symptoms appear $24\text{ to }72\,hours$ after trauma and include neurological changes (restlessness, delirium, coma), respiratory distress (dyspnea, tachypnea, hypoxemia), and a petechial rash over the chest and upper extremities.

What causes 'the bends' and 'the chokes' in decompression sickness?

Rapid ascent causes dissolved nitrogen gas to form bubbles; gas expansion in muscles, joints, and bones causes pain ('the bends'), while gas bubbles in the pulmonary vasculature cause edema, hemorrhage, and respiratory distress ('the chokes').

What type of organ infarct is shown in this gross lung image, and in what pathological settings does it occur?

A red (hemorrhagic) infarct. It occurs in venous occlusions, loose tissue (e.g., lung), tissues with dual circulations, previously congested tissues, or when blood flow is re-established following arterial occlusion.

What type of infarct is shown in this spleen specimen, and where do such infarcts typically form?

A white (pale/anaemic) infarct. It occurs with arterial occlusions in solid organs with end-arterial circulations (e.g., heart, spleen, kidney) where tissue density limits blood seepage from adjacent beds.

How long after vascular occlusion does it take for frank tissue necrosis to become demonstrable, and what type of necrosis predominates in non-CNS vs CNS infarcts?

It takes $4\text{ to }12\,hours$ for tissue to show frank necrosis. Non-CNS organ infarcts show dominant ischemic coagulative necrosis, whereas central nervous system infarction results in liquefactive necrosis.

How is shock defined?

Shock is defined as reduced tissue perfusion resulting in impaired tissue oxygenation (cellular hypoxia), characterized by systemic hypotension due to reduced cardiac output or reduced effective circulating blood volume.

What are the hemodynamic parameter changes in cardiogenic shock, and why are IV fluids contraindicated?

Cardiogenic shock is characterized by decreased cardiac output (CO), increased peripheral vascular resistance (PVR), and increased left ventricular end-diastolic pressure (LVEDP). Rapid IV fluid infusion is contraindicated because fluid overload worsens existing pulmonary congestion.

What volume of blood loss causes hypovolemic shock, and what are its hemodynamic parameters?

Loss of greater than $20\%$ of blood volume ($1000\,mL$) results in shock. Hemodynamic changes include decreased CO, decreased LVEDP, and increased PVR.

What hemodynamic parameters and clinical findings distinguish septic shock from cardiogenic and hypovolemic shock?

Septic shock exhibits increased CO, decreased PVR, and decreased LVEDP. Key clinical findings include warm skin (due to peripheral vasodilation), a bounding pulse, acute respiratory distress syndrome, and DIC.

What are the three sequential stages of shock?

1. An initial non-progressive phase (compensatory mechanisms maintain vital organ perfusion), 2. A progressive stage (tissue hypoperfusion and circulatory/metabolic imbalances like acidosis), and 3. An irreversible stage (severe cellular injury where survival is impossible).

What renal complication and metabolic derangement commonly arise secondary to tissue hypoxia in shock?

Ischemic acute tubular necrosis (coagulation necrosis of proximal tubule cells and thick ascending limb cells) and lactic acidosis.