Hemodynamic Disorder Flashcards
In order to maintain fluid homeostasis what 3 things must be in check?
- Vascular wall integrity: trauma causes focal defect in vessel wall
- Intravascular hydrostatic pressure: congestive heart failure causes alveolar capillary congestion and eventuall pulmonary edema
- osmolarity: liver failure (cirrhosis) cause low intravascular protein leading to edema
Blood is maintained as a _______ state until injury requires_______
List 2 failures of this
Blood is maintained as a liquid state until injury requires clot formation
*hypercoagulability state due to mutation in Factor V gene results in blood clotting when it shoudln’t
*hypocoagulability state due to platelet defect results in blood not clotting when it should
What is edema and where does it occur?
accumulation of interstitial fluid in tissues
occurs in subcutaneous tissues and body cavities (pleural cavity, peritoneal cavity, pericardial cavity)
What is Anasarca?
very severe generalized edema
Describe th normal fluid balance/distribution in the body
2/3 intracellular
1/3 extracellular (mostly interstitial) with 5% of extracellular fluid in blood plasma
what are 3 factors tha affect fluid balance
- vascular hydrostatic pressure
- plasma colloid osmotic pressure ( due to plasma proteins-abumin, globulin)
- normally balanced so no net loss or gain of fluid
- **lymph vessels pick up any residual fluid)**
When does edemea result?
when increased hydrostatic pressure or decreased osmotic pressure leads to net accumulation of fluid (in interstitium)
WHat 2 things cause increased hydrostatic pressure and what are some examples?
- Venous Obstruction/ Impaired Venous return
- DVT, Mass lesion, lower extremity inactivity, cirrhosis (ascites)
- CHF-increased hydrostatic pressure in alveolar capillaries due to left ventricular heart failure pulmonary edema and eventually peripheral edema
- hypoperfusion of kidneys causes secondary hyperalodsteronism
- Arteriolar dilartion
- heat, neurohumoral dysfunction
Why does CHF cause edema?
It leads to increased capillary pressure
increased hydrostatic pressure in alveolar capillaries due to left ventricular failure pulmonary edema and eventually peripheral edema
How does reduced plasma osmotic pressure occur and how does it lead to edema?
- occurs due to excessive loss of albumin
- nephrotic syndrome (protein losing)
- protein losing enteropathy (IBS)
- malnutrition
- Liver disease (reduced synthesis, cirrhosis)
- Excessive loss of albumin leads to edema bc it:
- leads to decreased intravascular volume, and secondary hyperaldosteronism
- albumin is serum protein most reposible for maintaining colloid osmotic pressure
Lymphatic obstruction can lead to edema. How does lympathic obstruction occur?
- usually localized
- inflmmatory (ex: parasitic infection causing lymphatic fibrosis)
- neoplastic (ex: infiltration and obstruction of lymphatic by neoplastic cells)
- post-surgical/ post-radiation (ex: after mastectomy w/ lymph node dissection, scarring and removal of lymph channels leads to edema)
Sodium (and water) retention can lead to edema. How does this occur?
sodium and water retention increasd hydrostatic pressure (expanded intravascular volume) and decreased colloid osmotic pressure
causes: excessive salt intake w/ renal insufficiency
acute reduction of renal function (ex: glomerulonephritis)
Describe the morphology of edema:
When do we normally see:
- subcutaneous edema
- pulmonary edema
- edema of the brain
edema is more easily recognized grossly. microscopically subtle cell swelling and separation of extracellular matrix elements
subcutaneous edema: CHF and Renal failure
Pulmonary edema: left ventricle failure
What is this image showing?
Pulmonary edema
WHat is hyperemia and what makes it occur?
hyperemia is increase in blood colume within a tissue
- due to increased bloow flow and arteriolar dilation. It is an Active process
- occuras at sites of inflammation (ex: conjuctivitis) or in exercising skeletal muscles
WHat is congetsion and why does it happen?
congestion: increase in blood volume within a tissue (passive)
due to decreased/impaired outflow of venous blood (Passive)
may occur systemically (liver and lung congestion due to heart failure) or locally (obstruction of superior sagittal sinus of dura)
WHat is the mechanism of the change in the liver and lungs during heart failure?
- passive increase in blood flow (decreased venous return)
- extravasation of blood out ot eh sinusoids (liver) and alveoli wall capillaries (lungs)
- hydrostatic pressure has resulted in increased fluid in the interstitium
- lack of oxygen has resulted in necrosis of central regions of the liver ( secondarily to the long-standing congetsion resulting in stadid and lack of oxygen)
What is involved in primary hemostasis and what dominates it
what is involved in secondary hemostasis and what dominates it
Primary (dominated by the platelet)
- vasculature
- blood flow
- platelet count and function
- extracellular matrix proteins
Secondary (clotting factors build upon the platelet plug)
- platelet plug
- coagulation factors
What are the 5 steps of primary hemostasis?
- platelet adhesion
- shape change
- granule release (ADP, TXA2)
- Recruitment (other platelets and factors)
- Aggregation (hemostatic pug)
WHat are the steps involved in secondary hemostasis?
- tissue factor
- phospholipid complex expression
- thrombin activation
- fibrin polymerization
**fibrin strengthens the plug. generating thrombin is the goal which will turn fibrin into fibrinogen which forms the mesh network
What are the laboratory screenings for primary hemostasis?
- platelet count
- platelet function
- PFA-100
- platelet aggregation studies
- vWillebrand studies
- vW antigen
- vW activity
What are the laboartaory screenings for secondary hemostasis?
Prothrombin time (PT) (extrinsic and common pathway)
activated partial thromboplastin time (aPTT) (intrinsic and common pathway)
fibrinogen activity
Bleeding disorders are defects in:
- vascular integrity
- platelet count and/or function
- Von Wilebrand factor deficiency or dysfunction
- Clotting factor deficiency/inhibition
- Hemophilia (Factor VIII)
- Liver Disease (CF’s are made in the liver so liver dysfunction you dont make all of the necessary CFs)
- anticoagulants
What is a hemorrhage and what are some common causes of hemorrhages?
- extravasion of blood from vessels
- accumulation of blood within a space
- hemopericarium, hemothorax, hemoperitoneum, hemoarthosis
- causes:
- ruptured vessel; trauma, weakening of vessel wall (ahterosclerosis, inflammation vasculitis, aneurysm)
- peptic ulcer
- chronic congestion: liver, lungs
- predisposition to hemorrhage with minimal trauma (homorrhagic diathesis) seen with decreased ability to clot
What is a hematoma
an accumulation of blood within a tissue
ex: epidural, subdural, intracerebral, subcutaneous (bruise)
What are Petechial hemorrhages?
hemorrhages into skin, mucous membranes or serosal surfaces. Associted with low platelt counts (thrombocytopenia) platelet dysfunction, loss of vascuular wall support, or local pressure
What is purpura?
>3mm hemorrhages associated with same disorders as petechiae w/trauma, vasculitis, and vascular fragility
What is Ecchymoses?
>1-2 cm subcutaneous hematomas (bruises). associated with trauma, exacerbate by above conditions
WHat is an ulcerated atherosclerotic plaque and what is it an example of?
Thrombis!
- rupture in endothelial surface of plaque caused thrombis
- turbulent blood flow dur to atherosclerosis likely contributed to rupture in plaque surface
- clinical significance: myocardial infarction
What is an abdominal aortic aneurysm and what is it often secondary to?
abdominal aortic anerysm secondary to atherosclerosis
- abnormal blood flow:
- atheroscleosis causes weakening of the wall of the aorta resulting in aneurysm
- anerysm leads to turbulent blood flow and stasis
- stasis slows washout of clotting factors and impedes inflow of clottin gfactor inhibitors
- Endothelial injury and activation
- also occurs with atherosclerosis, stasis, and turbulent flow
- Clinical significance: possible rupture of aorta, possible embolism of thrombis to legs
What is the difference between a Red infarct or a White infarct?
- Red Infarct: hemorrhagic, classic example is lung infarct secondary to embolus
- “Loose” tissues allow blood to collect
- dual circulation tissues (Lung: bronchial arteries and pulmonary arteries)
- when flow is re-establised (repurfusion due to break up of embolus
- veous occlusions)
- White Infarct: anemic (no blood0
- occurs in solid organs wih end arterial circulation (spleen or kidney)
