Chapter 5 - Fluid and Circulatory Disorders Flashcards
1
Q
Body water distribution
A
- Total body water = 60
• Intracellular = 40
• Extracellular = 20
- Interstitial = 15
- Intravascular = 5
2
Q
Fluid intake
A
2.0 L per day
- Ingestion: fluid and solid food
- Cellular oxidation: Krebs cycle produces energy, CO2 and water
3
Q
Fluid output
A
2.0 liters per day
- Lungs = 0.3 liters
- Sweat = 0.5 liters
- Urine = 1.0 liters
- Feces = 0.2 litera
4
Q
Regulation of fluid balance
A
- Thirst
- Kidneys
- Antidiuretic hormone ADH
- Aldosterone
5
Q
Thirst
A
Receptors in the hypothalamus lead to thirst sensation
6
Q
Kidneys
A
Amount of fluid reabsorbed or secreted in urine
7
Q
Antidiuretic hormone AHD
A
- Produced in the hypothalamus
- Released by posterior pituitary
- Causes increased water reabsorption by tubules in kidney
8
Q
Aldosterone
A
- Produced by the adrenal cortex
- Causes increased sodium retention by kidney tubules
- Leading to increased water retention (like ADH)
9
Q
Flow of extracellular water
A
- Fluid delivered to capillaries by arteries in arterioles
- Fluid leaves the capillaries and enters interstitial compartment
- Delivers electrolytes and other dissolved materials to the cell
- Fluid leaves interstitial compartment via:
• Intracellular compartment: enters dehydrated cells
• Capillary call him returns directly to venous blood (85%)
• Lymphatics: answers lymphatic vessels > venous blood (15%)
10
Q
Fluid and electrolyte imbalances
A
- Water
- Sodium
- Potassium
11
Q
Water imbalance
A
“Volem”
- Hypovolemia
- Hypervolemia
12
Q
Hypovolemia
A
Depletion of extracellular fluid volume and blood causes:
• Decreased intake
• Excess loss:
- Bleeding
- Vomiting or diarrhea
- Excess sweating
- Burns: drainage of effusion
- Abnormal urine volume
13
Q
Hypervolemia
A
Excess extracellular fluid volume and blood or interstitial fluid causes:
• Chronic renal failure
• Congestive heart failure: increased BP = edema
• Excessive IV fluid
14
Q
Sodium imbalance
A
“Natrem”
- Hyponatremia
- Hypernatremia
15
Q
Hyponatremia
A
Decrease sodium concentration and extracellular fluid (blood/interstitial)
- Causes:
• Excess intake of hypotonic fluid (while running marathon)
• Diuretics – increase water loss also increases sodium and potassium loss
• Adrenal insufficiency (decreased aldosterone)
- Results: • Edema • Polyuria • Cerebral edema • CNS depression
16
Q
Hypernatremia
A
Increase sodium concentration in extracellular fluid
- Causes:
• Decreased water intake
• Diarrhea
• Polyuria - Results:
• Thirst
• Oliguria
• CNS irritability
17
Q
Potassium imbalance
A
“Kalem”
- Hypokalemia
- Hyperkalemia
18
Q
Hypokalemia
A
Decrease potassium concentration in extracellular fluid
- Causes:
• Poor intake
• Diuretics
• Hyperaldosteronism (increased aldosterone, increased sodium retention = potassium loss) - Result:
• Cardiac arrhythmias = dysrhythmias
19
Q
Hyperkalemia
A
Increase potassium concentration in extracellular fluid
- Causes:
• Renal failure
• Renal insufficiency - Results:
• Cardiac arrhythmias
20
Q
Edema
A
Abnormal accumulation of fluid and intercellular spaces or body cavities
21
Q
Anasarca
A
Severe, diffuse edema of all tissues, especially subcutaneous tissue
22
Q
Transudate
A
Low protein filtrate of plasma: “pitting edema”
23
Q
Exudate
A
High-protein filtrate of plasma
24
Q
Effusion
A
Fluid in body cavities
- Hydrothorax: fluid in plural cavity (pleural effusion)
- Hydropericardium: fluid in pericardium (pericardial effusion)
- Acites: fluid and abdominal cavity (peritoneal effusion)
25
Low protein edema
Form from transudate causing pitting edema
- Hydrostatic edema
- Osmotic edema
26
Hydrostatic edema
Elevated capillary blood pressure
- Increased plasma volume
- Increased back pressure
27
Increased plasma volume
Due to sodium retention and excess bodyweight
- Increase sodium retention: leads to increased water retention; often due to aldosterone secretion compensating for heart failure
- Increased water volume: increases capillary BP and escape of water into interstitial spaces
28
Increased back pressure
- CHF with poor venous return: resulting in poor circulation to kidneys, also triggers hormones that increase sodium retention
- Venus thrombosis: edema localized to drainage of that area
29
Osmotic edema
Lowered colloidal osmotic pressure of the plasma
- Large molecules and cells: trapped in plasma produce osmotic pressure
• 80% of osmotic pressure is due to albumin
- Decreased albumin and blood: leads to generalized edema
• Renal disease: increased glomular permeability = loss of albumin and urine
• Cirrhosis: decreased production of albumin due to damaged hepatocytes
30
High protein edema
Formed from exudate
- Inflammatory edema
- Lymphedema
31
Inflammatory edema
Increased permeability of capillary wall to exudate
- Usually localized reaction
- Often associated with inflammation (hives due to allergy)
32
Lymphedema
Lymphatic blockage of lymph (exudate)
- Scarring: following trauma or inflammation
• Filarial elephantitis - parasitic worm causes fibrosis and lymph nodes resulting in massive edema of legs and genitals
- Cancer: Tumor replaces and obstructs lymph nodes
- Surgery: lymph node resection in cancer surgery (edema following axillary node resection for breast carcinoma)
33
Hyperemia and congestion
Increased blood in a particular area or tissue
34
Hyperemia
- Caused by: inflammation or increased metabolism due to arterial vasodilation
- Active process: engorged with bright red blood
• Sunburn – skin inflammatory response to access UV radiation
• Post exercise – skin dissipates heat by bringing blood to surface
• Blushing – neurologic response due to emotion
35
Congestion
- Caused by: impaired venous blood flow
- Passive process: engorgement with poorly oxygenated blue blood
• Acute - arm below inflated blood pressure cuff
• Chronic – pulmonary congestion (due to left-sided CHF)
- liver congestion (due to right-sided CHF)
36
Hemorrhage
Abnormal escape of blood from vascular spaces
- Clotting
- Size
- Hematomas of body cavities
- Thrombus
37
Clotting
Blood coagulation – normal response to hemorrhage that occurs extravascularly
- Vascular factors
- Platelets
- Plasma coagulation
38
Vascular factors
Normal functioning blood vessels and endothelial cells
- Trauma: disrupts normal endothelium
- Vitamin C deficiency: damages intercellular cement between endothelial cells, causing minor hemorrhages, especially bleeding gums (scurvy)
- Elderly: bruise easily because connective tissue is a week around vessels
39
Platelets
Release substances to promote clotting and small vessel adhesion to stop hemorrhage
40
Plasma coagulation
Coagulation protein, mostly produced by liver
- Fibrin: elastic, insoluble protein that becomes woven to trap blood cells and plasma
41
Size
Smallest to largest
- Petechiae
- Purpura
- Ecchymoses
- Hematoma
42
Petechiae
Minute hemorrhages in mucosae or serosae
• 1 mm
• Associated with platelet disorder's, especially thrombocytopenia
• Singular = petechiae
43
Purpura
Hemorrhages of skin, mucosae or serosae
• Widespread
• <1mm
44
Ecchymoses
Larger hemorrhages in skin, mucosae or serosae
- >1mm
- Singular = ecchymosis
45
Hematoma
Localized large accumulations of blood in deeper soft tissue
- Usually a result of trauma (bruise or black and blue)
- Usually not life-threatening (except for intracranial hematoma)
46
Hematomas of body cavities
- Hemothorax: blood in plural cavity
- Hemopericardium: blood and rpericardial sac
- Hemoperitoneum: blood and peritoneal cavity
47
Thrombus
Pathologic blood coagulation occurring intravascularly
| • Technically not clotting, but often called blood clot by clinicians (boo)
48
Embolism
Detached intravascular mass carried by blood from its point of origin to a distant site
- Solid, liquid or gas
- Lodge in and occlude smaller blood vessels
- Results in:
• Shock – due to sudden change in localized blood flow
• Death of tissue – supplied by vessel that was occluded
49
Types of emboli
- Thrombus
- Atherosclerotic emboli
- Fat embolism
- Air embolism
50
Thrombus
"Blood clot" 99% of emboli are thrombi
51
Atherosclerotic emboli
Atherosclerotic debris break off involved vessel, usually aorta
- Usually lodge in small peripheral artery such as in the toes, G.I. tract or in brain
52
Fat embolism
Small globules a bone marrow fat in the circulation
- Seen most frequently and severe trauma with multiple fractures
- Maybe fatal if larger or numerous – most are small, without clinical symptoms
53
Air embolism
Gas embolism
- Bubbles of air enter the circulation: stupid diving – the "bends"
- Air bubbles act as masses in traveling through circulation
• Requires about 100 cc to produce disease
• Sudden death, convulsions, coma
54
Sites of embolism
- Pulmonary
| - Systematic
55
Pulmonary embolism
Most pulmonary embolism our thrombi – usually deep vein thrombus DVT of legs
- Rhombus breaks off from leg veins, goes through right side of heart to lodge and pulmonary arteries
- Consequences:
• Sudden death – especially with large emboli
• Respiratory distress and chest pain – smaller emboli
• Infarction of pulmonary parenchyma uncommon
56
Systematic embolism
- Emboli that involve the arterial system
- Lodge and small vessels causing infarction and brain, kidney, distal extremities and spleen
- Thromboemboli: from left side of heart
• Mural thrombi - following myocardial infarction
• Atrial thrombus – formed from atrial fibrillation
• Vegetation – thrombi formed on heart valve
- Atherosclerotic emboli
57
Infarct
Localized area of ischemic necrosis resulting from occlusion of either arterial supply or venous drainage
- Arterial occlusion: more common then venous obstructions
- Coagulation necrosis: most infarcts produce this type of necrosis except for brain
58
Arterial occlusion
- Causes:
• Thrombosis of artery
• Atherosclerotic narrowing of artery
• Spasm of artery: increased smooth muscle compared to veins
• Torsion of vascular pedicle (mobile tissue surrounding artery)
- Pale calling but can't get to it
- Develops a red border: inflammatory response to dead tissue
59
Venus occlusion
- Causes:
• Thrombus of vein
• External compression of vein (arteries don't compress easily)
• Origin of vascular pedicle
- Deep red: blood can't leave
60
Clinically significant infarction
- Myocardial
- Cerebral
- Ischemic infarction of extremities
61
Myocardial infarction
30% of deaths are associated with heart disease, most of these due to myocardio infarction
62
Cerebral infarction
Causes liquefication necrosis
63
Ischemic infarction of extremities
- Important complication of diabetes
| - Poor peripheral circulation due to peripheral neuropath
64
Shock
Condition in which there is an overall reduction of adequate blood flow throughout the body
- Systematic, not localized
- Includes:
• Hypotension – low blood pressure
• Tachycardia – fast heart rate
• Oliguria
• Cool, moist skin
• Restlessness and alerted levels of consciousness
65
Stages of shock
- Non-progressive shock
- Progressive shock
- Irreversible shock
66
Non-progressive shock
Initial phase
- Decreased cardiac output it and decreased peripheral resistance
- Compensation:
• Increased heart rate
• Vasoconstriction
• Activation ofrenin-angiotensin-aldosterone system that result in:
- Increased blood volume and vasoconstriction
• Release of ADH from posterior pituitary results in:
- Increased blood volume and vasoconstriction
67
Progressive shock
"Uncompensated shock"
- Compensatory mechanisms above have failed: continued poor perfusion results in ischemia of vital organs
- Organ failure: especially heart, kidneys, lungs, G.I. tract and liver
68
Irreversible shock
Organ failure has progressed and is unresponsive to therapy
- Due to severe hypovolemic/cardiogenic/vasogenic shock
- "Cardiovascular collapse"
69
Three types of shock
- Hypovolemic shock
- Cardiogenic shock
- Vasogenic shock
70
Hypovolemic shock
- Hemorrhage
- Dehydration
- Burns
71
Hemorrhage
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- Causes:
• Trauma
• G.I. tract hemorrhage
• Hemophilia
• Childbirth
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- Need loss of > 10% of blood volume to reduce blood pressure and cardiac output
72
Dehydration
- Profuse sweating
- Diarrhea
- Vomiting, upper G.I. tract suctioning
- Inadequate intake
- Endocrine abnormalities (diabetes insipidus, Addison's disease)
73
Burn
- Loss of plasma proteins through burn surface >
- Decreased colloid osmotic pressure >
- Fluid leaves vascular space as edema >
- Decreased blood volume
74
Cardiogenic shock
- Pump failure: failure of heart to pump will result in decreased perfusion
- Decreased venous return: anything that prevents venous blood from entering heart
• Cardiac tamponade, pericardial effusions will fill a pericardial space and press on heart not allowing to expand and fill with blood
75
Vasogenic shock
Massive vasodilation will result in decreased peripheral resistance and thus decreased blood pressure
- Neurogenic shock
- Septic shock
- Anaphylactic shock
76
Neurogenic shock
"Spinal shock"
- Muscle tone of blood vessels is maintained by neural stimulation, controlled in medulla
• Interference with the function of the medulla or nerves may result in vasodilation
- Causes:
• Head or spine trauma
• Deep general anesthesia
• Drug overdose
77
Septic shock
Shop associated with overwhelming infection
- Gram-negative bacteria
- Gram-positive bacteria
78
Gram-negative bacteria
- Due to endotoxins that are the lipopolysaccharides in the bacterial cell wall
• E. coli, Pseudomonas aeruginosa
79
Gram-positive bacteria
- Due to exotoxins that are excreted by bacteria
| • Staphylococcus aureus
80
Anaphylactic shock
- Due to type I hypersensitivity (allergy) reaction
- An IgE binds to mast cells
- Stimulated by its specific antigen, IgE causes mast cells to release it's granules
- Granular substances mediate shock (histamine, bradykinin, prostaglandins)
81
Complications of shock
- Lactic aciddosis
- Adult respiratory distress syndrome RDS
- Disseminated intravascular coagulation DIC
- Orgon ischemia and necrosis
82
Lactic acidosis
- In shock cells are hypoxic because of poor perfusion
| - When cells must produce energy without oxygen they use an alternate pathway that makes lactic acid a byproduct
83
Too much lactic acid
- Decreased myocardial contractility
| - Metabolic acidosis
84
Adult respiratory distress syndrome RDS
- Lungs damaged by shock lead to poor air exchange and worsening hypoxia
85
Disseminated intravascular coagulation DIC
- Shock leads to increased activation of coagulation factors and platelets aggregate
- This abnormal coagulation of the blood uses up coagulation factors and leads to increased bleeding
86
Oregon ischemia and necrosis
- Prolonged poor perfusion and ischemia eventually lead to necrosis of vital organs
• Especially heart, brain, kidneys, lungs and liver
