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Pathology > Chapter 5 - Fluid and Circulatory Disorders > Flashcards

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
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2
Q

Fluid intake

A

2.0 L per day

  • Ingestion: fluid and solid food
  • Cellular oxidation: Krebs cycle produces energy, CO2 and water
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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
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4
Q

Regulation of fluid balance

A
  • Thirst
  • Kidneys
  • Antidiuretic hormone ADH
  • Aldosterone
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5
Q

Thirst

A

Receptors in the hypothalamus lead to thirst sensation

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6
Q

Kidneys

A

Amount of fluid reabsorbed or secreted in urine

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7
Q

Antidiuretic hormone AHD

A
  • Produced in the hypothalamus
  • Released by posterior pituitary
  • Causes increased water reabsorption by tubules in kidney
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8
Q

Aldosterone

A
  • Produced by the adrenal cortex
  • Causes increased sodium retention by kidney tubules
  • Leading to increased water retention (like ADH)
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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%)
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10
Q

Fluid and electrolyte imbalances

A
  • Water
  • Sodium
  • Potassium
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11
Q

Water imbalance

A

“Volem”

  • Hypovolemia
  • Hypervolemia
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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
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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

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14
Q

Sodium imbalance

A

“Natrem”

  • Hyponatremia
  • Hypernatremia
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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
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16
Q

Hypernatremia

A

Increase sodium concentration in extracellular fluid

  • Causes:
    • Decreased water intake
    • Diarrhea
    • Polyuria
  • Results:
    • Thirst
    • Oliguria
    • CNS irritability
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17
Q

Potassium imbalance

A

“Kalem”

  • Hypokalemia
  • Hyperkalemia
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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
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19
Q

Hyperkalemia

A

Increase potassium concentration in extracellular fluid

  • Causes:
    • Renal failure
    • Renal insufficiency
  • Results:
    • Cardiac arrhythmias
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20
Q

Edema

A

Abnormal accumulation of fluid and intercellular spaces or body cavities

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21
Q

Anasarca

A

Severe, diffuse edema of all tissues, especially subcutaneous tissue

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22
Q

Transudate

A

Low protein filtrate of plasma: “pitting edema”

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23
Q

Exudate

A

High-protein filtrate of plasma

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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)
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25
Q

Low protein edema

A

Form from transudate causing pitting edema

  • Hydrostatic edema
  • Osmotic edema
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26
Q

Hydrostatic edema

A

Elevated capillary blood pressure

  • Increased plasma volume
  • Increased back pressure
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27
Q

Increased plasma volume

A

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
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28
Q

Increased back pressure

A
  • 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
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29
Q

Osmotic edema

A

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
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30
Q

High protein edema

A

Formed from exudate

  • Inflammatory edema
  • Lymphedema
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31
Q

Inflammatory edema

A

Increased permeability of capillary wall to exudate

  • Usually localized reaction
  • Often associated with inflammation (hives due to allergy)
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32
Q

Lymphedema

A

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)
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33
Q

Hyperemia and congestion

A

Increased blood in a particular area or tissue

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34
Q

Hyperemia

A
  • 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
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35
Q

Congestion

A
  • 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
Q

Hemorrhage

A

Abnormal escape of blood from vascular spaces

  • Clotting
  • Size
  • Hematomas of body cavities
  • Thrombus
37
Q

Clotting

A

Blood coagulation – normal response to hemorrhage that occurs extravascularly

  • Vascular factors
  • Platelets
  • Plasma coagulation
38
Q

Vascular factors

A

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
Q

Platelets

A

Release substances to promote clotting and small vessel adhesion to stop hemorrhage

40
Q

Plasma coagulation

A

Coagulation protein, mostly produced by liver

  • Fibrin: elastic, insoluble protein that becomes woven to trap blood cells and plasma
41
Q

Size

A

Smallest to largest

  • Petechiae
  • Purpura
  • Ecchymoses
  • Hematoma
42
Q

Petechiae

A

Minute hemorrhages in mucosae or serosae
• 1 mm
• Associated with platelet disorder’s, especially thrombocytopenia
• Singular = petechiae

43
Q

Purpura

A

Hemorrhages of skin, mucosae or serosae
• Widespread
• <1mm

44
Q

Ecchymoses

A

Larger hemorrhages in skin, mucosae or serosae

  • > 1mm
  • Singular = ecchymosis
45
Q

Hematoma

A

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
Q

Hematomas of body cavities

A
  • Hemothorax: blood in plural cavity
  • Hemopericardium: blood and rpericardial sac
  • Hemoperitoneum: blood and peritoneal cavity
47
Q

Thrombus

A

Pathologic blood coagulation occurring intravascularly

• Technically not clotting, but often called blood clot by clinicians (boo)

48
Q

Embolism

A

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
Q

Types of emboli

A
  • Thrombus
  • Atherosclerotic emboli
  • Fat embolism
  • Air embolism
50
Q

Thrombus

A

“Blood clot” 99% of emboli are thrombi

51
Q

Atherosclerotic emboli

A

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
Q

Fat embolism

A

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
Q

Air embolism

A

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
Q

Sites of embolism

A
  • Pulmonary

- Systematic

55
Q

Pulmonary embolism

A

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
Q

Systematic embolism

A
  • 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
Q

Infarct

A

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
Q

Arterial occlusion

A
  • 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
Q

Venus occlusion

A
  • Causes:
    • Thrombus of vein
    • External compression of vein (arteries don’t compress easily)
    • Origin of vascular pedicle
  • Deep red: blood can’t leave
60
Q

Clinically significant infarction

A
  • Myocardial
  • Cerebral
  • Ischemic infarction of extremities
61
Q

Myocardial infarction

A

30% of deaths are associated with heart disease, most of these due to myocardio infarction

62
Q

Cerebral infarction

A

Causes liquefication necrosis

63
Q

Ischemic infarction of extremities

A
  • Important complication of diabetes

- Poor peripheral circulation due to peripheral neuropath

64
Q

Shock

A

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
Q

Stages of shock

A
  • Non-progressive shock
  • Progressive shock
  • Irreversible shock
66
Q

Non-progressive shock

A

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
Q

Progressive shock

A

“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
Q

Irreversible shock

A

Organ failure has progressed and is unresponsive to therapy

  • Due to severe hypovolemic/cardiogenic/vasogenic shock
  • “Cardiovascular collapse”
69
Q

Three types of shock

A
  • Hypovolemic shock
  • Cardiogenic shock
  • Vasogenic shock
70
Q

Hypovolemic shock

A
  • Hemorrhage
  • Dehydration
  • Burns
71
Q

Hemorrhage

A 
- Causes:
   • Trauma
   • G.I. tract hemorrhage
   • Hemophilia
   • Childbirth
  • Need loss of > 10% of blood volume to reduce blood pressure and cardiac output
72
Q

Dehydration

A
  • Profuse sweating
  • Diarrhea
  • Vomiting, upper G.I. tract suctioning
  • Inadequate intake
  • Endocrine abnormalities (diabetes insipidus, Addison’s disease)
73
Q

Burn

A
  • Loss of plasma proteins through burn surface >
  • Decreased colloid osmotic pressure >
  • Fluid leaves vascular space as edema >
  • Decreased blood volume
74
Q

Cardiogenic shock

A
  • 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
Q

Vasogenic shock

A

Massive vasodilation will result in decreased peripheral resistance and thus decreased blood pressure

  • Neurogenic shock
  • Septic shock
  • Anaphylactic shock
76
Q

Neurogenic shock

A

“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
Q

Septic shock

A

Shop associated with overwhelming infection

  • Gram-negative bacteria
  • Gram-positive bacteria
78
Q

Gram-negative bacteria

A
  • Due to endotoxins that are the lipopolysaccharides in the bacterial cell wall
    • E. coli, Pseudomonas aeruginosa
79
Q

Gram-positive bacteria

A
  • Due to exotoxins that are excreted by bacteria

• Staphylococcus aureus

80
Q

Anaphylactic shock

A
  • 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
Q

Complications of shock

A
  • Lactic aciddosis
  • Adult respiratory distress syndrome RDS
  • Disseminated intravascular coagulation DIC
  • Orgon ischemia and necrosis
82
Q

Lactic acidosis

A
  • 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
Q

Too much lactic acid

A
  • Decreased myocardial contractility

- Metabolic acidosis

84
Q

Adult respiratory distress syndrome RDS

A
  • Lungs damaged by shock lead to poor air exchange and worsening hypoxia
85
Q

Disseminated intravascular coagulation DIC

A
  • 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
Q

Oregon ischemia and necrosis

A
  • Prolonged poor perfusion and ischemia eventually lead to necrosis of vital organs
    • Especially heart, brain, kidneys, lungs and liver

Pathology (6 decks)

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