Fluid and Hemodynamic Disorders Flashcards
Normal distribution of water in the body
60% total body weight
2/3 intracellular
1/3 extracellular (interstitial or circulating)
Normal in/output 2.5 litres/day
Edema
Excess fluid in interstitial spaces and/or body cavities
Results from imbalance between hydrostatic and oncotic pressures
Anasarca
Generalized (non-local) edema
Ascites
Ash-eye-teez
Edema within the peritoneal cavities
Exudate
Edematous fluid rich in protein, larger molecules, cells.
Typical of inflammation
Transudate
Edematous fluid which contains less protein than exudate, and low in cells and other large molecules
What may cause the accumulation of transudate?
Increased hydrostatic pressure
Decreased oncotic pressure
Lymphatic obstruction
Sodium retention
Hydrostatic pressure
Promotes passage of fluids from blood vessel into interstitial fluid
Arterial end of capillary
Oncotic pressure
aka Colloid Oncotic Pressure
Promotes passage of fluid from interstitial fluid to blood vessel
Due to relatively high concentration of colloids (large molecules) in blood vessel
Venue end of capillary
Inflammatory edema
Fluid leaks through increasingly permeable vessel wall
Acute inflammation
Hydrostatic edema
Intravascular pressure promotes transmembranous passage of fluids. Increased venous back pressure
Hypertension, heart failure
Oncotic edema
Decreased concentration of plasma proteins (specifically albumin) in blood vessel/ decrease in colloid osmotic pressure
Liver disease, malnutrition, nephrotic syndrome
Obstructive edema
Rare. Can be caused by parasites or tumours
Hypervolemic edema
Kidney dysfunction leading to the retention of sodium and water
Clinical Forms of Edema
Cerebral Pulmonary Pitting (of lower extremities) Periorbital Hydrothorax Hydroperitoneum
Hyperemia
Increase of blood flow due to the presence of metabolites and/or a change in general conditions
Three forms: active, reactive, passive
Active hyperemia
AKA functional hyperemia
Increased blood flow that occurs when tissue is active and requires more metabolites
Blushing, exercise, acute inflammation
Reactive hyperemia
Occurs in response to a profound increase in blood flow to an organ after being occluded
Passive hyperemia
AKA congestion
Caused by venous backpressure, typically due to heart failure
Often occurs in chronic form; can lead to cyanosis
How much blood loss can be endured without clinical consequence?
10-15% (up to 500ml).
1000-1500 ml: shock
1500+ ml: death
How to tell the difference between arterial and venous blood
Arterial: bright right and under pressure, often pulsing
Venous: dark red or bluish, not pulsating
Hemothorax
blood in thoracic cavity
Hemoperitoneum
blood in peritoneal cavity
Hemopericardium
blood in pericardial cavity
Hematomas
blood filled swelling
Petechiae
small haemorrhages of skin and mucosa
Purpura
medium hemorrhages of skin a mucosa
Ecchymoses
large blotchy bruises
Hemoptysis
blood in respiratory tract (cough)
Hematemesis
vomiting blood
may be due to esophogeal cancer
Melena
Black, discoloured blood in stool.
May be due to stomach cancer
Hematochezia
Anorectal bleeding
May be due to hemmorrhoids
Metrorrhagia
uterovaginal bleeding
cervical or uterine cancer
Menorrhagia
heavy menstrual bleeding
endometriosis
Hematuria
blood in urine
kidney infection
Vomiting blood
Hematemesis
Coughing blood
Hemoptysis
Anorectal bleeding
Hematochezia
Black discoloured blood in stool
Melena
Blood in urine
Hematuria
Uterovaginal bleeding
Metrorrhagia
Thrombosis
Transformation of fluid into solid
Clotting of whole blood into blood cells and fibrin
Fibrin
Polymerized fibrinogen.
Forms a network of think filaments that bind together the cellular elements of blood, forming a thrombus.
Thrombus
Hemostatic plug
Only forms in living creatures.
What promotes thrombosis?
Clotting factors
Platelets
What inhibit/counteract thrombosis?
Endothelial cells
Plasmin.
Intervascular coagulation is the result of interaction between:
- Coagulation proteins
- Endothelial cells
- Platelets.
Role of coagulation proteins in thrombosis
Involved in intrinsic and extrinsic pathways of blood clotting.
Leads to creation of thrombin, which catalyzes transformation go fibrinogen into fibrin.
Fibrin is framework for clot.
Role of endothelial cells in hemostasis
Normally secrete antithrombic substances.
When injured (activated by injury or trauma) become procoagulant
Activated by cytokines (IL-1 or TNF)
Role of platelets in thrombosis
Neutralize heparin and other anticoagulant factors
secretes thromboxane
Stimulates coagulation.
Heparin
Blood thinner
Thromboxane
In platelet plug formation, a prostaglandin “liberated” by platelets
Activates nearby platelets
Cause vasoconstriction
Directly stimulates coagulation process
Plasmin
Thrombolytic chemical.
Degrades small thrombi
Virchow’s Triad
Predisposing conditions for pathological thrombi
- Endothelial cell injury
2 Hemodynamics changes - Hypercoagulability of whole blood
Endothelial cell injury
Part of Vichow’s triad
Under influence of SMIs endothelium go from anticoagulant to thrombogenic
Hemodynamics changes
Part of Vichow’s triad
Two kinds:
1 Disturbance of blood flow (Turbulence and margination)
2 Slowing of blood flow (Sedimentation and blood eddies)
Hypercoagulability of blood
Part of Vichow’s triad
Often due to changes in fluid balance/hemoconcentration (burns, Cancer, cardiac failure, bun in oven).
Thrombi classified by location
Intramural
Valvular (debilitated persons; sterile thrombotic endocarditis)
Arterial (contributes to atherosclerosis/aneurysms)
Venous (common in varicose veins; DVTs)
Microvascular (typical of DIC/shock)
Red (conglutination) thrombi
Thrombi in small vessels are red composed of tightly intermixed RBCs and fibrin.
Layered (sedimentation) thrombi
Distinct layers of cellular elements and fibrin
In large arteries, vein, mural thrombi
Lines of Zahn
In layered thrombi, the white lines. Made up of fibrin and platelets.
Fate of thrombi
- Lysis and resolution
- Organization. Granulation replaced by collagenous fibrous tissue
- Recanalization
- Can break off an embolize (which can lead to infarction).
Most common cause of myocardial infarction
Sudden thrombotic occlusion
Clinical correlations of thombosis
Myocardial infarction Chronic heart failure Embolus Infarct Stroke (cerebral infarct) Septic emboli
Embolus
freely moveable, intravascular mass that is carried from one anatomical site to another via the blood
(emboli – plural)
Embolism
infarct caused by embolus
Thromboemboli
thrombi carried by venous or arterial blood
*only clinically significant emboli
Liquid emboli
more squishy than liquid
fat emboli following bone fracture
amniotic fluid emboli in veins
Venous emboli
typically lodge in pulmonary artery and cause pulmonary embolism
smaller emboli can cause pulmonary infarcts (–> sub pleural pain)
Arterial emboli
Common cause of ischemia in spleen, kidney and intestines
Usually originates from cardiac mural or valvular thrombi
Mechanically fragmented because of fast arterial blood flow –> tend to lodge in small and medium sized arteries (esp middle cerebral artery –> basal ganglia infarcts)
Gaseous embolism
air injected into veins, or air liberated under decreased pressure (caisson disease or decompression sickness)
Solid particle emboli
cholesterol, tumour cells, bone marrow
Infarction
Sudden insufficiency of blood supply leading to local necrosis
Usually caused by thrombi or thromboemboli
Arterial vs venous
Red vs white
Renal infarct
associated with hematuria
Intestinal infarct
Can cause gangrene – medical emergency
White infarct
Typical of solid organs (heart, kidneys, spleen)
Ischemic necrosis paler than surrounding tissues
Red infarct
Typical of venous infarction, particularly of intestines or testes
Fate of infarcts
Ischemic necrosis irreversible
Liquifactive necrotic tissue can be resorbed and leave clear fluid-filled cyst
