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Pathology > Week 5: Disturbed Blood Flow > Flashcards

Week 5: Disturbed Blood Flow Flashcards

1
Q

Normal Fluid Balance

A

60% of our bodies is water!
-2/3 = intracellular
-1/3 = extracellular (15% interstitial, 5% plasma)

Depends on:

-Starling’s law

-Systemic factors (Intact circulation, overall fluid balance, salt retention)

-Physiologic ranges of intravascular pressure, osmolarity

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2
Q

What does the extracellular component of the body consist of?

A

Interstitial + blood vessels

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3
Q

What does intracellular refer to?

A

Within cells

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4
Q

Lymphatic System

A

Products are deposited in the venous side of circulation

-50% of total blood proteins leak out of capillaries into the tissue fluid and return to the blood via lymphatic vessels EVERY DAY

-Under NORMAL circumstances, only a small amount of fluid leaks from vessels to form interstitial fluid

-Fluid is removed by lymphatic vessels

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5
Q

Starling’s Law

A

Movement of fluid between vascular and interstitial spaces (at capillary level) is controlled by 4 forces:
1. Hydrostatic pressure (HP)
2. Plasma oncotic pressure (OP)
3. Interstitial/tissue fluid osmotic pressure
4. Interstitial/tissue fluid oncotic pressure (tissue tension)

**Focus on OP and HP

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6
Q

Hydrostatic Pressure

A

Force exerted by a fluid against the capillary wall (pushing force)

In vessels: Fluid contains oxygen and nutrients that move into the surrounding tissue, where they are less concentrated

In tissues: Fluid contains waste products

MOVE WITH DIFFUSION

Mean of 25mmHg between arterial and venous ends (32 arterial, 12 venous)

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7
Q

Oncotic Pressure

A

Pressure created by the presence of large molecules/particles that cannot diffuse and are prevented from moving through capillary membrane

Large molecules = plasma proteins (e.g. albumin)

Encourage osmosis, draw water towards them

Because capillary blood has a high content of plasma proteins, capillary has a HIGH oncotic pressure = 26 mmHG

Oncotic pressure does not vary from one end of capillary to another

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8
Q

Direction of Fluid Flow

A

NFP calculated: HP vs. OP in capillaries

If HP > OP, fluid will leave
If HP < OP, fluid will enter

Under normal conditions, 10% of fluid enters lymphatic capillaries. 90% re-enters the capillary.

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9
Q

Arterial End (under normal conditions)

A

HP = 32
OP =26
NFP = +6
Water moves OUT

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10
Q

Venous End (under normal conditions)

A

HP = 12
OP = 26
NFP = -14
Water moves IN

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11
Q

Edema

A

Accumulation of abnormal fluids in the interstitial/subcutaneous tissue (tissue under epithelium, the outermost layer of the skin) → swelling

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12
Q

Interstitial Pressure (Tissue Tension)

A

3-4 mmHg

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13
Q

Causes of Edema

A
  1. Congestive heart failure
  2. Deep venous thrombosis of lower legs
  3. Hypoproteinemia (liver disease, renal failure, malnutrition)
  4. Lymphatic obstruction (cancer, inflammation, blockage)
  5. Inflammation
  6. Sodium retention (heart/kidney failure)
  7. Tumours, radiation
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14
Q

Hydrostatic Edema

A

An increase in intravascular (whole system) hydrostatic pressure due to increased venous pressure (one area).

Reabsorption is decreased (fluid build-up in interstitial tissue) and lymphatics drain

Clinical Examples:
1. Congestive Heart Failure (CHF)
-Right side failure → peripheral edema and pitting edema (due to
increased HP in the venous circulation)
- Left side failure → lung edema (due to increased
HP in the arterial circulation)
2. Deep venous thrombosis of lower legs
- Obstruction of veins (blood clot - localized)
- Increased interstitial fluid buildup because the hydrostatic pressure exerted by the clot pushes all the fluid out)

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15
Q

Oncotic Edema

A

(Hypoproteinemia)
Fall in colloid osmotic pressure of plasma. Due to loss of albumin or other proteins.

Oncotic pressure decreases and fluid goes to tissues. We can decrease the fluid amount but this is not enough.

Clinical Examples:
1. Liver disease as cirrhosis (liver failure): decrease synthesis of albumin
-Hepatic ascites (Because increased HP in portal veins increases the fluid in the abdominal cavity)
If you have fewer proteins occupying/IMF bonding to the fluid/water molecules, more water molecules will be free to exert pressure on the vasculature
- Decreases fluid in circulation after it leaves for the insterstitium; increases oncotic
pressure
2. Renal failure: loss of albumin in urine
3. Malnutrition: if you don’t eat enough protein in meals

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16
Q

Lymphatic Obstruction

A

Increases interstitial oncotic pressure (with normal OP and HP).

Accumulation of interstitial fluid because of insufficient reabsorption and deficient removal of proteins → increasing the oncotic pressure of the fluid in the interstitial space

Proteins cannot go back into the circulation through lymphatics

Clinical examples:
1. Cancer (tumour on lymphatics)
2. Inflammation
3. Postsurgical lymphedema
4. Postradiation

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17
Q

Inflammatory and Traumatic Edema

A

Local or systemic
Vascular bed becomes leaky following injury to the endothelium (cells lining blood vessels)

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18
Q

Sodium Retention (Edema)

A

Causes both increase in hydrostatic pressure and reduced vascular osmotic pressure

Sodium is a MAJOR cation that determines the osmolarity of the extracellular fluid volume

Increased total body sodium must be balanced by more extracellular water to maintain constant osmolarity

Clinical examples:
1. Kidney diseases
2. Heart diseases
-CHF → decreased blood perfusion to kidney →
triggers renin-angiotensin-aldosterone complex
3. Increase intake of sodium
- Increases water retention
- Increases plasma volume: Hypervolemia
(increases HP or expansion of intravascular fluid
volume, decreases OP or dilution of protein)

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19
Q

Localized Edema

A

Due to:
-Increased hydrostatic pressure due to vascular/venous obstruction (local)
-Inflammation (epithelial injury)
-Lymphatic obstruction (lymphedema): compression by tumour or inflammation (local)
-Tumour
-Inflammation
-Postsurgical
-Postradiation
-Burns (edema by disrupting local permeability of local vasculature)

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20
Q

Generalized Edema (Anasarca – swelling of the whole body)

A

Affects the visceral/internal organs (think visceral fat) and skin of trunk and lower extremities.

Due to:
-Increased hydrostatic pressure: i.e. heart failure.
-Decreased oncotic pressure (colloid osmotic pressure) due to:
-Loss of albumin in renal failure (nephrotic
syndrome)
-Decreased synthesis of albumin in liver failure
(Ascites)
-Malnutrition
-Sodium retention → Kidney disease (can start around the eye)

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21
Q

Hydrothorax (Pleural Effusion)

A

Fluid in chest cavity

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22
Q

Hydropericardium

A

Fluid in the pericardium

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23
Q

Hydroperitoneum (Ascites)

A

Fluid in the abdominal cavity (e.g. due to liver failure)

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24
Q

Transudate

A

Results from disturbances in Starling Forces

Protein < 3 g/dl
Specific gravity < 1.012

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25
Q

Exudate

A

Results from damage to capillary wall

Protein > 3 g/dl
Specific gravity > 1.012

26
Q

Hyperemia (Active Process)

A

The tissue appears red because of engorgement with oxygenated blood.

Dilatation of arteries/arterioles results in increased blood flow (perfusion) of a tissue or organ (increased inflow)

Examples:
1. Acute inflammation (e.g. when you have an infection)
2. Skeletal muscle during exercise (more blood needed to exercise)

27
Q

Congestion (Passive Process)

A

Impaired venous drainage (venous blood being unable to get to the heart) results in stasis and the accumulation of deoxygenated blood. This condition is due to increased hydrostatic pressure. Think of it like a plugged drain.

So deoxygenated blood just builds up across your body
If the first bit of blood can’t get oxygen, then everything after it can’t.

Due to an increase in venous hydrostatic pressure

Tissue has a bluish tinge due to the accumulation of deoxygenated hemoglobin

Examples (no physiologic conditions):
1. Cardiac failure
2. Isolated venous obstruction (thrombophlebitis)
-Thrombophlebitis (vein inflammation) results in
stasis of blood
3. Nutmeg liver (due to chronic passive congestion of liver secondary to right heart failure)
-Chronic dilated congested central veins →
necrosis (dark spots) with unaffected
surrounding liver tissue (pale spots)

28
Q

Thrombosis

A

Formation of mass (clotted blood) in the heart or blood vessels. The mass is called “thrombus” and it consists of:
-Red blood cells
-White blood cells
-Platelets
-Fibrin

Plug formation (platelets → fibrin network → WBC, RBC)

Thrombus appearance:
-Alternating layers of platelets and fibrin with dark erythrocyte-rich layers
-Adherent to the luminal surface of the vessel

Venous is darker, takes shape of the vein

29
Q

Causes of Thrombosis

A
  1. Vessel wall damage/alteration/endothelial injury:
    -Injury/trauma → tear
    -Inflammation
  2. Changes in blood flow:
    -Stasis (slow circulation)
    -Lack of activity, prolonged bed rest
    -Decreased cardiac output
    -Increased blood viscosity (dehydration -
    sweating, vomiting)
  3. Changes in blood composition:
    ↑ in platelets (increases chances of blood clots)
30
Q

Prognoses of Thrombosis

A
  1. Lysis (dissolution)
  2. Propagation
    -Enlargement and extension of the thrombus
  3. Organization
    -Fibrosis of the thrombus
  4. Recanalization
    -During organization, new channels may form within
    the thrombus
  5. Breakdown → emboli (e.g. lung embolism)
31
Q

Complications of Thrombosis

A

Fragments of thrombus break off and result in thromboembolization/emboli.

Reduced blood flow to a tissue/organ resulting in ischemic injury or infarction (necrosis)

32
Q

Embolism

A

Occlusion of a blood vessel by a mass (embolus) transported to the site through the bloodstream.

Process = embolization

Embolus: particle/mass which is carried in the bloodstream as far as its size will allow

Becomes lodged at that point and obstructs the vessel

33
Q

Types of Emboli

A
  1. Thrombi (Thromboembolus)
    -The most common type of emboli
    -Thromboemboli arise from thrombi and range in
    size from microscopic to those which are large
    enough to occlude major arteries
    -Thromboemboli may occur in either arteries or
    veins
  2. Gas (air) = divers
  3. Fat = often fracture of large bones
  4. Tumour
  5. Others = foreign body (e.g. in drug addicts who inject themselves with substances).
34
Q

Venous Thromboembolus

A

Most commonly from a thrombus in the deep leg veins

Mostly produced in patients with varicose veins and/or prolonged bed rest (e.g. post-surgery)

Fragments of thrombi travel to the lung where they occlude the pulmonary artery

May result in infarction in the lung

Pulmonary embolism results in death

35
Q

Arterial Thromboemboli

A

Systemic arterial thromboemboli usually arise from mural thrombi in the heart (blood clots from the heart)

Ruptured thrombi travel via the systemic arterial system to organs such as the brain, kidneys, spleen, and extremities (not lungs)

Usually result in infarctions in those sites

36
Q

Paradoxical Emboli

A

Emboli which travel from venous to arterial circulation via a communication between arterial and venous circulation
-Right side blood clots can move to the left side
through an opening
20% of population

37
Q

Air/Gas Emboli

A

Air in the circulation; moves with the circulation until it reaches the heart (and stops it)

May occur during delivery/abortion (endometrial blood vessels), chest wall/lung trauma

May occur as the result of a rapid change in atmospheric pressure (e.g. scuba divers)
-While diving, increased ambient pressure allows
increased gas to dissolve in the blood
-With too rapid decompression coming to the
surface, gas comes out of solution and forms
bubbles (emboli) in the blood - especially nitrogen

38
Q

Fat Emboli

A

Severe bone fractures

Fat/fragments from bone marrow suctions into injured blood vessels due to fracture; moves into circulation

First stop is the lung → respiratory failure

Fat embolism syndrome: we will also have emboli to the BRAIN
-Death within 48 hours

39
Q

Prognosis of Embolism

A

Like thrombi they may undergo:
1. Lysis
2. Propagation
3. Organization and/or recanalization
4. Can result in ischemic injury and infarction (decreased blood supply)

40
Q

Ischemia

A

Due to: Inadequate blood supply to an area of tissue.
The result is infarction → area of necrosis (death) produced by ischemia

41
Q

Causes of Ischemia

A
  1. Decreased blood supply
  2. Inadequate cardiac output
  3. Obstruction of blood vessel (artery) by:
    a. Thrombus
    b. Embolus
    c. Outside pressure (tumours, cast for a fracture)
    d. Damage of the vessel wall (e.g. during surgery) →
    inflammation
42
Q

Effects of Ischemia

A

Depends on degree of ischemia.

No effects → if there is alternate blood supply
-Lungs have 2 different blood supplies

Complete obstruction → tissue death (infarction)
-Irreversible

43
Q

Infarction

A

An area of necrosis which typically produced by ischemia

Infarct area is wedge-shaped

Infarction is an irreversible process and healing occurs by fibrosis

44
Q

Types of Infarct

A

-Depends on the vessel that is occluded
-Brain infarction can be either white or red

White infarct
-Arterial occlusion
-Solid organs as Heart, spleen, kidney, brain
-Leg gangrene

Red infarct
-Venous or arterial occlusion
-Loose tissue as lung
-Dual blood supply (e.g. lung)
-Brain, intestine

45
Q

Hemorrhage

A

A discharge or escape of blood from the blood vessels into the surrounding tissues or to the exterior of the body or into a body cavity (bleeding)

Presented clinically as
-Petechiae (dots)
-1-2mm
-Rupture of a capillary/arteriole
-Skin, mucous membranes, serosal surfaces
-Purpura (splotchy)
-3-5mm, up to 1cm
-Diffuse
-Superficial hemorrhages in skin

46
Q

Causes of Hemorrhage

A
  1. Trauma to large blood vessels
    -Surgery
    -fracture
  2. Weakened artery
    -Atherosclerosis, which can become aneurysms
    -Atherosclerosis → hemorrhage in
    retroperitoneal space/stomach cavity
    (abdominal aortic aneurysm)
    -Congenital weakness (berry aneurysm in Willis
    circulation - brain circulation); subarachnoid
    hemorrhage (type of stroke)
  3. Infections (e.g. pulmonary tuberculosis; blood vessels can rupture here)
  4. Invasive tumours (erosion of blood vessel wall by the tumour, leading to rupture of vessels)
  5. Hypertension (increase intraluminal blood pressure; results in ruptured blood vessels)
    -Common cause of stroke in older age group
  6. Hemorrhagic diathesis (spontaneous hemorrhage)
    -Ruptures spontaneously due to lack of platelets
    -Affecting capillaries (small blood vessels)
    including:
    a. Thrombocytopenia (Severe decrease
    in number of platelets
    b. Deficiency of coagulation/clotting
    factors
47
Q

Hematoma

A

Bleeding into soft tissues
Small: bruise
Large: cavity, organs

48
Q

Ecchymosis/Bruise/Subcutaneous Hematoma

A

A large superficial hemorrhage (black eye)

Skin discoloration reflects products of heme degradation from hemoglobin in the RBCs

Black → yellow → disappear
Causes: Trauma (e.g. black eye)

49
Q

Petechia

A

A pinpoint hemorrhage (1-2 mm), usually in the skin; represent rupture of capillaries or arterioles and mainly involving skin, mucous membranes and serosal surfaces.

50
Q

Purpura

A

Diffuse, superficial hemorrhages in the skin, as large as 1 cm

51
Q

Hemothorax/Hemopericardium

A

Collection of blood in the pleural cavities due to trauma or rupture of aorta (hemothorax)

Collection of blood in pericardial cavity around heart due to rupture of heart or the aorta (hemopericardium)

Pericardial tamponade (large accumulation of blood in pericardium sac compresses the heart)

52
Q

Hemoperitoneum

A

Collection of blood in the abdominal cavity due to rupture of an aortic aneurysm or trauma to liver, spleen, or aorta

53
Q

Hemoarthrosis

A

Collection of blood in joint due to trauma

54
Q

Shock

A

Characterized by failure of the circulatory system to maintain an appropriate blood supply to the microcirculation with resultant inadequate perfusion of vital organs.

Generalized inadequate perfusion of all cells and tissue of vital organs.

Due to:
1. Decreased blood volume
2. Decreased cardiac output
3. Redistribution of blood

4 Types of Shock
1. Hemorrhagic/hypovolemic
2. Cardiogenic
3. Septic
4. Anaphylactic/Neurogenic

55
Q

Perfusion

A

Passage of fluid through circulatory or lymphatic system to organs/tissues

56
Q

Hemorrhagic/Hypovolemic

A

Due to loss of fluid from the vascular compartment (decreased blood volume) as a result of:
1. Loss of blood
-Hemorrhage (external)
-Massive internal hemorrhage
2. Decrease plasma volume
-Burns
3. Fluid loss
-Diarrhea
-Excessive urine formation
-Sweating or vomiting
4. Decreased blood volume

57
Q

Cardiogenic Shock

A
  1. Inability of the heart to pump blood (decreased cardiac output)
    -Myocardial infarction
    -Pericardial tamponade (fluid accumulate in the
    pericardium around the heart)
  2. Extensive impairment of cardiac output
    -Pulmonary embolism (blood clot; lung does not
    receive/return blood)
  3. Normal blood volume
58
Q

Septic Shock

A
  1. Redistribution of blood
    -Peripheral vasodilation/increased permeability of
    vessels
  2. Bacteremia - bacteria in the blood
  3. Cytokines, bacterial endotoxins → irreversible situation of systemic vasodilation, endothelial damage, and direct injury to cells
    -Total body response to inflammation
  4. Normal blood volume
59
Q

Anaphylactic/Neurogenic Shock

A

Redistribution of blood
-Peripheral vasodilation/increased permeability of
vessels

Anaphylaxis: Allergic condition (edema obstructs airways)

Neurogenic: anaesthesia, injury of spinal cord
-Peripheral vasodilation - associated with
anaphylaxis, neurogenic and septic shock (due to
release of factors (cytokines, bacterial endotoxins,
etc.) that cause dilation and increased permeability
of the vessels).
-Blood vessels are dilated, no longer contract,
accumulate more blood in the peripheral
circulation

60
Q

Mechanism of Shock

A

Decreased tissue perfusion –> hypoxic/anoxic cell injury –> Reversible or irreversible changes

Give blood to patients quickly

Effect of shock: The result of decreased tissue perfusion is hypoxic or anoxic cell injury which may lead to further decline in cardiac output (for example as a result of renal failure, heart failure, further endothelial cell damage).

Irreversible damage → further failure of organs, heart, kidney, liver → more decline in cardiac output → more endothelial cell damage → no recovery, compensation fails

Last organ failure = brain → death

61
Q

Hypoxia

A

A part of the body does not receive enough oxygen

62
Q

Anoxia

A

Extreme form of hypoxia; body does not receive ANY oxygen

Pathology (7 decks)

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