Intro to Hemodynamic Disorders Flashcards
- Define edema.
an increased amount of fluid in the tissue interstitial spaces and potential spaces
- Define effusion.
accumulation of fluid in a particular body cavity such as pleural effusion or a pericardial effusion
- Define ascites.
a fluid accumulation in the abdominal cavity
- Define anasarca.
severe and generalized edema with diffuse involvement of all interstitial tissues with grossly evident diffuse subcutaneous swelling
- Define exudate.
loss of fluid with proteins from vessel
- Define transudate.
loss of fluid (without protein and cells) from the vessel
- Define chronic passive congestion.
generally results from impaired outflow of blood, generally appears darker blue-red due to accumulation of deoxygenation
- Define heart failure cells.
hemosiderin-laden macrophages in the alveoli and pulmonary interstitial spaces are termed heart failure cells
- Define nutmeg liver.
a result of passive congestion, noted by discoloration of the liver; back up of capillary beds cause pressure necrosis around hepatic veins
- Define cardiac cirrhosis.
cirrhosis that is caused by right heart failure causing cetrilobular necrosis due to hypoxic/ischemic injury due to back of blood from the right side of the heart
- Define hematoma.
blood accumulation in a space or tissue; causes a displacement of tissue, creating pressure
- Define contusion, ecchymosis.
extraversion of blood into the tissue, often cutaneous or subcutaneous tissue, due to vascular rupture in which is the skin is not broken
- Define petechiae.
small (1-2mm) punctate hemorrhages usually due to thrombocytopenia and seen on skin or mucosal/serosal surfaces
- Define purpura.
larger punctate hemorrhages, common with vasculitis, or with low platelets
- Define saddle embolus.
really large pulmonary thromboembolism which occludes right and left pulmonary arteries
- Define paradoxical embolus.
a venous thromboembolus passing through an atrial or ventricular heart defect to lodge in the systemic arterial system
- List 5 major pathophysiologic categories of edema.
- increased hydrostatic pressure/impaired venous return
- reduced plasma oncotic pressure
- lymphatic obstruction
- sodium retention
- inflammation
(6) Compare and contrast hyperemia and congestion
both describe local increase in blood volume, hyperemia as in active arteriolar dilation occurs naturally in exercise (appears more red) while congestion is a result of the outflow of capillary beds getting is obstructed (appear more cyanotic)
- What is hemorrhage?
extravasation of blood due to vessel rupture as in vascular injury or injury coupled with disease or neoplasia
- Hemostasis requires three components…
vascular wall
platelets
coagulation proteins
- Name the major steps of hemostasis. (~3)
- arteriolar vasoconstriction
- platelet adherence, activation and aggregation (primary hemostasis)
- generation of thrombin and fibrin with polymerization of fibrin and platelet aggregates (secondary hemostasis)
- Describe the molecules that are involved in primary hemostasis.
- collagen is exposed to blood von Wilebrand F and bind together
- platelets bind to vWF factor via a Gp1b
binding of platelets causes flattening and release of granules
- Describe the molecules of secondary hemostasis.
- endothelial cells release tissue factor, which initiates the clotting cascade- activation of thrombin
- thrombin cleaves fibrinogen to fibrin which can polymerize
- What is thrombosis?
pathologic activation of hemostatic mechanism (clot occurs inside blood vessel without disruption)
- What are the three parts of the Virchow triad.
- endothelial injury (interruption of endothelium)
- abnormal blood flow (due to stasis or turbulence)
- hyper-coagulability
- Differentiate between abnormal blood flow patterns that usually contribute to venous v. arterial thrombosis.
arterial- turbulent flow
venous- stasis
- Differentiate between primary and secondary hyper coagulable state and I’ve examples of each.
primary/genetic: factor V Leiden, prothrombin mutation
secondary/acquired: visceral malignancy, hyperestrogenic states (pregnancy, oral contraceptive)
- Describe the four possible outcomes of thrombosis.
- propagation of thrombus
- repair and wound healing causes organized reanalyzed
- clots organized and incorporated into a cell wall
- complete resolution of the clot
- clot can cause embolus to travel to the lung
- Differentiate between thrombus, embolus and thromboembolus.
thrombus is a clot that stays where it occurs, where an embolus can be a solid, liquid or gaseous mass that travel to a distant site; a thromboembolus is an embolus made of thromboses blood
- Describe pulmonary thromboembolism with respect to pathogenesis, risk factors and clinical outcome.
95% of these originate in the deep venous system of the lower limbs called DVT, it is the most common type of embolism, consider also a air embolism caused by trauma or complicated births
- Contrast venous and arterial thromboembolism.
venous embolism usually lodges in the lung while an arterial embolism is more likely to cause infarction
- Give two mechanisms for infarction and distinguish between red and white infarcts.
mechanisms: arterial thrombosis or thromboembolism, red infarcts are caused when blood flow is restored after tissue death, white infarcts is tissue death without resumption of blood flow
- Describe four major factors influencing the development of an infarct.
nature of vascular supply (dual v. end-arterial)
rate of occlusion of vascular supply
susceptibility of tissue to infarction
oxygen of content of blood
- Describe the three major types of shock.
cardiogenic: failure of pump (cardiac infarction, cardiac tamponade)
hypovolemic: substantial loss of intravascular volume (burns, diarrhea, vomiting, dehydration)
septic: wide spread connotation of widespread infection with severe systemic inflammation (most popular gram-positive bacteria)
- How do gram negative bacteria trigger septic shock?
lipopolysaccharides= LPS= endotoxin released when inflammatory response lyses bacteria
- Describe the events that lead up to the profound hypotension due to sepsis.
microbial produces cause reaction of neutrophils and macrophages
release of cytokines and mediators cause endothelial cells to cause as systemic vasodilation and profound dilation
- List 3 major complication so septic shock.
acute reparatory distress
diffuse alveolar disease
disseminated intravascular coagulation
- Describe acute respiratory distress.
(ARDS) is a clinical syndrome of pulmonary dysfunction caused by a diffuse alveolar capillary damage;
- Describe diffuse alveolar disease.
(DAD) describes the histology of the lung pathoneumonic fixing of hyaline membranes caused by fluid and fibrin leaking into the pulmonary interstitial and alveoli (associated with ARDS)
- What is disseminated intravascular coagulation.
widespread activation of coagulation within blood vessels and is characterized by consumption of coagulation factors as well as widespread activation of fibrinolytic system which leads to excessive bleeding
- List two specific independent mechanisms by which hepatic cirrhosis and liver failure can generate edema
lack of production of plasma proteins and chronic passive congestion
Platelet aggregation is mediated by platelet receptor _______.
GpIIb-IIIa.
Name two non-thromboembolic infarcts.
twisting of a loop of the intestine (volvulus) or similarly testicular or ovarian torsion
How long a period of hypoxia before neurons and cardiomyocytes show damage?
3-5 min for neurons and 30min for myocytes
What are the signs of multi system organ failure?
hypoxemia/ acidosis (2ary to necrosis and ARDS) oliguria/anuria (tubular necrosis) and confusion (hypoxia to brain)
considered a terminal complication in fatal cases of septic shock
