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Path 1 > Path 1 Quiz 4 > Flashcards

Path 1 Quiz 4 Flashcards

1
Q

What term means “the stoppage of blood loss”?

A

Hemostasis

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2
Q

What is the principle mechanism of hemostasis?

A

Blood coagulation

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3
Q

What is a blood clot?

A

A mesh of protein filaments that traps blood formed elements to form a red, gelatinous mass
*this is a major killer in the united states

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4
Q

Define Fibrin Threads

Define Fibrinogen

A

Fibrin Threads: Threads that holds the blood cells together and they seal the wound to prevent losing of blood
Fibrinogen: Creates Fibrin strands

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5
Q

Clotting factors

  • what are they, produced where?
  • when are they inactive/active
  • Vitamin most closely related?
A
  1. Are a set of PROTEINS produced in the liver
  2. Inactive in the blood circulation
  3. They are activated up injury through the extrinsic and intrinsic pathways, in the formation of a clot
  4. Vitamin K plays a key role
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6
Q

Clotting Factor I

A

Fibrinogen

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7
Q

Clotting Factor II

A

Prothrombin

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8
Q

Clotting Factor V

A

Preaccelerin

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9
Q

Clotting Factor VII

A

proconvertin

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10
Q

Clotting Factor IX

A

Christmas Factor

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11
Q

Why is clotting factor IX named what is it named?

A

Because “Christmas” was first described in a pt. with this name

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12
Q

Clotting factor X

A

Stuart Prower Factor

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13
Q

Clotting Factor XI

A

Plasma Thromboplastin antecedent

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14
Q

Clotting Factor XII

A

Hageman Factor

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15
Q

Clotting Factor XIII

A

Fibrin Stabilizing factor

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16
Q

What are the two ways blood clots are formed?

A

1) Blood Clot cascade

2) Platelet Activation

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17
Q

Which process of blood clotting involves fibrin strands?

A

Blood clot cascade

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18
Q

Fibrin Strands are made out of

A

protein fibrinogen (5 - 7% of all blood proteins)

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19
Q

In order to activate clotting factor 1 (fibrinogen), we need to activate

A

Clotting factor X (Stuart Prower Factor )

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20
Q

What are the two pathways of the Blood Clot Cascade? Where does each pathway happen?

A
  1. Extrinsic pathway: can happen in blood vessels and outside blood vessels
  2. Intrinsic Pathway: only develops within the blood vessels
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21
Q

Explain the Extrinsic pathway of the Blood Clot Cascade?.

  • AKA for “Tissue Factor”
  • Where does this occur - what cells?
  • what is “tissue factor” released from?
  • What clotting factors are involved
  • What clotting factor activates another clotting factor
A

Tissue factor AKA Tissue Thromboplastin
Released from damaged cells, both injured blood vessels cells and injured tissue cells - these activate clotting factors
Tissue factor activates proconvertin (CFVII), proconvertin then activates stuart prower factor (CF X)

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22
Q

Explain the sequence of events for the Intrinsic Pathway?

Where does this occur?

A
  • The inner layer of blood vessels are covered by endothelial cells - if there is a scratching of endothelial cells there is exposure of collagen fibers of SUBendotheial cells - they are exposed to blood flow and the clotting factor is then activated
  • This only occurs INSIDE injuries blood vessels
  • Exposure of collagen fibers to blood flow activates CF XII (HANGMAN FACTOR ) - this will activate Factor IX (Christmas) - which will then activate clotting factor X (stuart Power)
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23
Q

The clotting cascade that results in both ways is

A

Activation of clotting Factor X - Stuart Power —>
Activation of prothrombin clotting factor II —>
Leads to thrombin formation —>
Activation of fibrinogen Clotting Factor I —>
Leads to Fibrin formation

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24
Q

T/F The Intrinsic pathway and the Extrinsic pathway can occur simultaneously

A

True

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25
Q

What clotting factor needs to be activated in order to form fibrin?

A

Clotting Factor I (fibrinogen)

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26
Q

Explain the formation of fibrin strands that leads to coagulation?

A 
Clotting factor X 
Activates prothrombin
Activates thrombin
Thrombin results in the activation of fibrinogen 
Fibrinogen transforms into fibrin
Fibrin turns into fibrin strands
leads to coagulation
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27
Q

What ion is essential for coagulation to occur?

- clinically what would someone with severe blood loss receive?

A

Ca++
Necessary component of coagulation - with out it it can not occur
Patients with severe blood loss are given “calcium CL” injection to help with blood clotting - INTRAvenously - if injected intravenously it would injury the tissues and cause tissue necrosis

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28
Q

Explain the sequence of Platelet activation process:

  • What is the result of an activated platelet?
  • Where does it occur?
A
  • Exposure of collagen fibers (sub endothelial cells) to blood flow
  • Von Willebrand Factor becomes activated and then attaches tot eh exposed collagen fibers (circulates in blood in inactive form until exposed to exposed collagen)
  • Von Hillebrand Factor stops the flow of blood plate movement
  • Platelets bind to Von Willebrand Factor, and form a single layer on top of the exposed collagen
  • Once there is prevention of platelet blood flow by VW, the platelets become activated and then attach a second layer of platelets, etc - they continue to build on top of each other
  • Platelet activation results in the formation of “platelet plug” - physically blocks the damaged blood vessel
  • could be potential bad when there is no danger in losing of the blood
  • Platelet activation ONLY occurs INSIDE blood vessels
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29
Q

Von Willebrand Factor

  • what is it
  • where is it located
  • How is it activated
A

This is separate from clotting factors it is in the blood circulation like blood proteins - this is its inactive form
-Inactive Von Willebrand factor is attached to the wall in the area of the exposure of the collagen fibers to the collagen fibers - this is what activates it

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30
Q

What stops the physical flow of blood?

A

Platelet activation - “Platelet plug” and Coagulation (blood clotting via CF cascade)

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31
Q

When there is platelet activation there is platelet _________.

A

degranulation (granules open)

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32
Q

What is released during platelet degranulation / activation? What is each one of their roles?

A

1) ADP: stimulates further activation of platelets, potentiates the platelet response (they become more activated)
2) Thromboxane A2 = TxA2: functions to perform VASOCONSTRICTION (narrowing of the lumen, not allowing the blood to be lost) It also promotes platelet activation (coagulation)
3) Growth Factor: attracts fibroblasts (fibroblast chemotaxis) - so when there is injury and danger of losing blood the body needs to take care of healing - wound healing

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33
Q

What are fibroblasts?

What are their function?

A
  • They are the source of components of CT
  • These are the cells that go into the area of injury and produce pro collagen and glue
  • Material for adhesions of the collagen filament to make collagen fibers and bundles
  • FB also produce ground matrix (this is the glue substance)
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34
Q

Glue Substance is made by

A

Fibroblasts

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35
Q

What is the function and what are the three components of the anticoagulation system?

A

Maintains balance within the body - prevents EXCESS or uncontrolled blood clotting

1) Hemodynamics
2) Endothelial mediation
3) Fibrinolytic System

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36
Q

Explain what hemodynamics is?

A

Speed of blood flow
The different speeds of blood flow in different blood vessel is important for movement of blood
Slow blood flow is important for blood coagulation - otherwise activated Clotting Factors get washed out and a clot can not be formed

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37
Q

What is the hemodynamics of arteries? veins?

A 
Arteries = fast
Veins = slow
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38
Q

What is the challenge in forming a clot in an artery?

A

Because the hemodynamics of the arteries are fast paced - they clotting factors are immediately washed out not allowing the blood to stop flow and form a clot
The only way to stop bleeding in artier is mechanical blood pressure

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39
Q

Explain Endothelial mediation?

A

The wall of the blood vessel is covered by endothelial cells
Injury occurs to the endothelial tissues and platelet plug is formed BUT
Uninjured endothelial cells release PG12 (prostacyclin) which prevents extra or excess platelet aggregation
- this could potential prevent blood clot

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40
Q

PG12

  • common name?
  • Place of production
  • Function
  • Where is it released from?
A
  • Prostacyclin
  • Endothelial Cells
  • Prevents the formation of the blood clot - prevents excess/extra platelet aggregation - stops wide spread coagulation in the body
  • Only released from the ENDS of the damaged areas (where the damaged area ends and becomes undamaged area)
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41
Q

Explain the Fibrinolytic System

A

Tissue plasminogen activator is released from damaged tissue of the same endothelial cells

  • This activates inactive plasminogen - Clotting factor 12
  • Plasminogen FACTOR, converts plasminogen into PLASMIN
  • Plasmin causes degradation of clotting factors and stops the formation of too much coagulated blood
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42
Q

What is Tissue Plasminogen Factor

-What is its main function?

A

Enzyme that degrades plasma proteins (fibrin)

  • To stop the formation of too much coagulated blood
  • It is an important fighter of thrombus which is the major cause of cardiovascular deaths
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43
Q

What strengthens fibrinolytic activity?

A

Physical activity

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44
Q

What are the different types of hemorrhages? (types of bruises)

A
  1. Petechiae Rash
  2. Purpura
  3. Ecchymosis
  4. Hematoma
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45
Q

Which hemorrhage is 2 cm in diameter (larger than a pinpoint) and occurs in Henoich-Schonen Disease?

A

Purpura Rash

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46
Q

Which hemorrhage is pin point bleeding and often occurs in scurvy? What vitamin are they deficient in?

A

Petechiae Rash

Vitamin C

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47
Q

Which hemorrhage is AKA bruise - is more than 2 cm in diameter - can occur in periorbital hemorrhage?
Examples

A

Ecchymosis

  • Raccoon sign
  • Battle sign
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48
Q

Ecchymosis can easily occur in what autoimmune disease?

-Why does this occur in this syndrome?

A

Cushing’s Syndrome

  • over production of corticosteroids (cortisol) from the adrenal cortex
  • leads to extremes brittleness of blood vessels - even small impacts can result in bruises
  • if you have pt.s with cushing’s syndrome you must explain to them that if they have bruises after an adjustment that you are not hurting them
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49
Q

What is Cushing’s Syndrome?

- What causes it?

A

Overproduction of corticosteroids by the adrenal cortex (hyperplasia)
- the amount of cortisol is equal to the amount of corticosteroids produced
Can be caused by adenoma of the adrenal cortex or carcinoma of adrenal cortex

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50
Q

List the characteristics of Cushing Syndrome

A 
Brittle blood vessels 
Systemic or severe osteoporosis
Diabetes
High Blood Pressure
Moon face
buffalo hump
thin skin
red striae 
Red cheeks
Very high brusiability
poor wound healing 
redistribution of fat is very obvious (moves from butt and back to the face (moon face) stomach (pendulous abdomen) and upper back (buffalo hump)
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51
Q

What bone disease(s) and other autoimmune diseases are related to Cushing’s syndrome?

A 
Osteoporosis 
- Causes fish VT in spine
- contraindicates high force techniques
Dermatomyositis 
-Autoimmune process of the necrosis of skeletal mm.  (pt has had 50 - 60 mg of corticosteroids per day) 
Diabetes mellitus and hypertension
52
Q

What hemorrhage leaks into large cavities or into tissues or any part of the body.
Explain one specific one
(what blood vessel has been ruptured?)

A

Hematoma

Epidural hematoma = rupture of MIDDLE meningeal artery and bleeding into the space between the dura mater and the skull

53
Q

List the hemorrhagic disorders

A

Thrombocytopenia
Von Willebrand’s Disease
Hemophilia’s

54
Q

Thrombocytopenia

  • Etiology
  • What occurs
  • what type of hemorrhage
  • how many platelets do they typically have?
A
  • Has multiple etiologies - most common is decreased amount of thrombocytes in the circulation
  • Results in leakage of blood from everywhere
  • Typical in petechia and puppura type hemorrhages are typical - needs to be less than 2 cm
  • Less than 140,000 = prone to hemorrhage
55
Q

Von Willebrand’s Disease

  • Etiology
  • What occurs
A
  • Genetic / autosomal disease - associated with NON - production of von willebrnad factor (it’s completely absent usually the parents have this too)
    No platelet activation - they have no platelet plug
    Results in the development:
    1) hemorrhage of the stomach/abdominal wall
    - gastric and duodenal hemorrhages - pain in this area
    2) menorrhagia
    - menstruation blood becomes a very significant blood loss amount during normal period
    3) Metrorrhagia
    • characteristics to VW disease - this is blood leakage from uterus - term used for leakage of uterus blood in times other than mostly menstruation bleeding - indicator of uterus cancer - blood loss in-between periods
56
Q

What is an indicator of uterus cancer?

A

Metrorrhagia

57
Q

Hemophilia

  • what is it?
  • Etiology
  • Explain each type of hemophilia
  • what is a big problem with this?
A
  • Hemophilia is non production of certain protein clotting factors
  • genetic diseases, victims do not have sick parents usually typical for boys and is associated with the sexual chromosomes - Chromosome X - mom passes this on (skips a generation)
    1) Hemophilia A (non production of clotting factor VIII)
    2) Hemophilia B (Non production of clotting factor IX = christmas disease)

Small trumps may lead to severe blood loss

58
Q

In the case of hemophilia - trauma results in hemorrhage of the big joints (blood in joint) called _____. Why does this occur?
Most common place?

A

Hemoarthrosis

  • IRON from heme ends up in the cartilage of the joint - this is not a normal metabolite of the chondrocytes and results in their death (Iron destroys the joint cartilage) - this cause SECONDARY OA (degeneration of the joint) - THIS IS NOT INFLAMMATORY (no fusion/ankylosing is occurring)
  • Knee joint is the most common place
59
Q

What are hemodynamic disorders?

A

Those that arise from interruptions of normal blood flow

60
Q

Common known hemodynamic disorders

A

strokes and lacunar infarct

61
Q

Thrombosis (thrombus formation = platelet plug)

-Explain the sequence of events

A

*when platelet activation and platelet aggregation has occurred with out the threat of blood loss or vascular damage; platelet plug WITHOUT BLOOD CLOT

  • When there is an interruption in the endothelial continuity is interrupted by trauma, or atherosclerosis - the sub epithelial collagen is exposed to blood and stimulates adhesion of platelets to vessel walls (activation of V.W.)
  • Platelets then discharge thromboxane A2 which causes aggregation of adjacent platelets
  • The more platelets aggregate fibrin network develops and stabilizes the mass into “white thrombus” which then retracts into vascular wall. In some cases, endothelium may later heal over with or without narrowing of lumen - if the thrombus develops further - RBCs become enmeshed in platelet - fibrin aggregate to form “red thrombus” which may grow and block vessel lumen
  • either platelet - fibrin aggregates a more fully formed clots may break off and create an embolization into the distal arterial branches
62
Q

Where are thrombosis always located?

Where do they always orientate at?

A

Always with in Blood vessels

Always originates from the vascular wall and Always has point of an attachment on the vascular wall

63
Q

Thrombus that do form in arteries are often small and firm, and dense and strong —why?

A

Because they have a fast hemodynamic - blood travels through quickly

64
Q

Thrombus that forms in veins are large and not as condensed, weak and loose, and could potentially break off pieces of it…why?

A

Because of the slow hemodynamic in veins - blood travels slowly

65
Q

What are “Lines of Zahn”

A

A special type of thrombi characterized by visible and microscopic laminations produced by alternating Pale layers of Platelets mixed with fibrin and darker layers containing RBCs

66
Q

Where do Lines of Zahn form?

Specific example would be

A

Heart
Aorta - usually in the arch area
(NO VEINS)
Example: Mitral Stenosis: narrowing of the valve between the left atrium and left ventricle. (left atrioventricular opening) - so blood flow is slower, thrombi are formed with “lines of zahn”

67
Q

List the factors predisposing to thrombosis

A

Endothelial damage and hypertension

68
Q

A factor related to predisposition of thrombosis includes normal wear and tear of blood vessels.

  • What is an AKA for this?
  • What is a cause of this?
  • Explain the mechanism of normal wear and tear
A

Normal Wear and Tear AKA Hemodynamic stress
Caused by hypertension
Mechanism: stretching of endothelial cells from the inner surfaces of blood vessel –> collagen fibers are exposed –> thrombus formed

69
Q

What is hypertension’s effects on hemodynamic stress?

A

Hypertension STRENGTHENS hemodynamic stress because it increases resistance in the blood flow

70
Q

What is atherosclerosis?

How does it effect hemodynamic stress?

A

Atherosclerosis are specific changes, formation of plaque in the vascular wall - changes the rate of the blood flow “atherosclerotic plugs” - this Strengthens hemodynamic stress

71
Q

What is Iatrogenic thrombus?

A

Multiple injections into veins can cause thrombosis in the veins because there has been epithelial damage
Ex) IVs and injections into veins
Rare for this to happen but intravenous injections are common
Veins are protected from thrombosis

72
Q

Explain flow abnormalities in the arteries?

A

Reduction in the rate of blood flow (or its complete stoppage - stasis) - results in a disruption of axial blood flow —> platelets flow closer to the vessel wall

73
Q

What can cause abnormalities (decrease) in blood flow?

A

Cardiac damage, Increased Blood Viscosity, Physical Inactivity, Varicose Veins, Turbulence, Aneurisms

74
Q

Cardiac Damage/Arterial System

  • AKA
  • What does this mean?
A
  • Cardiac Damage aka Heart failure aka Congestive heart failure
  • Reduction of the hearts pumping ability
75
Q

Why does heart mm die?

A

Because of an O2 deficiency

76
Q

IF there is an O2 deficiency in the heart what is this clinically called?
Explain the mechanism and what follows after this damage.
What is its effect on the mechanics of the heart?

A

O2 deficiency in the heart is known as a Myocardial Infarction
The heart mm can not contract because it is dead tissue - no longer contractile - it can be replaced with CT - CT still can not contract cause it is not mm - This means that part of the heart can not help with pushing blood so blood flow is slower here then the rest of the body.
A thrombus begins to form here - it can break off and floats throughout the body and cause a blockage some where else

77
Q

When there is a reduction in the speed of blood flow there is a serious risk for thrombosis - 90% of thrombus end up….

A

in the deep veins of legs - which would result in sudden death of the individual

78
Q

Explain a thrombosis formation in Mitral stenosis/rheumatic heart disease.
Age range this commonly occurs in?

A

Formation of thrombus within the left atrium - leads to a thrombus embolism - this a disease of YOUNG people

79
Q

An increased blood viscosity disease is Polycythemia.
AKA?
Explain this disease

A

Polycythemia aka cancer of blood
Rare disease *type of leukemia
Characterized by a great production of RBCs
People with this disease are Extra HEALTHY looking because the RBCs transport nutrition to the tissues
However; they can die from thrombosis at any moment
Blood is too thick

80
Q

Why does physical activity HELP with avoid thrombosis?

*Valves in the legs and veins move blood up/down?

A

Inactivity predisposes to thrombus especially in the LOWER LEGS
When “mm. contraction” it squeezes the veins helping to push the blood up (required for return of blood)- preventing back flow - provides endothelial pressure that is needed - pressure is low in veins though
Black flow occurs when you are inactive and this can lead to thrombosis
Valves in the legs and veins move blood up

81
Q

Explain Varicose Veins

A

Distention of the veins (twists and turns) - usually in the legs - valves move away from each other so the blood ends up back flowing - valves are not accomplishing their function.
Blood flow is flowing much slower which may result in thrombosis and become dangers
*Recommendation - we need to keep veins less dilated so people should wear compression socks - keep legs above hip and don’t be obese - once this begins it does not stop

82
Q

Explain Turbulence

A

Disruption of laminar blood flow
- blood flow is normally parallel to each other
When there is a change in the lumen - there is a disruption in the laminar blood flow - the blood will start traveling in different ways - such as backwards
With this they can move platelets back bringing more plaque into the vessel wall and then there is a formation of thrombus

83
Q

Explain Aneurisms

A

Abnormality of blood vessels, develops in 1 % of the population - expanding lumen

84
Q

What is Blood Hypercoagulation

A

Increase ability of the blood to coagulated to certain events of the body
Bleeding stops too fast

85
Q

Factors that lead to blood hyper coagulation?

- Which one is the MOST common

A 
Extensive burns: loss of blood because of formation of exudate
Kidney Disease
Heart Failure
Widespread Metastatic tumor growth
Birth Control Pills***** most common
86
Q

Define Sequela

A

Of some even is the pathological consequence of this event (the cascade of events following one event)

87
Q

Sequela of Thrombosis - List

A 
Resolution
Organization
Recanalization
Propagation
Infarction
88
Q

In the sequela of thrombosis which event is the least dangerous? Explain it

A

Resolution: thrombus disappears due to high fibrinolytic function in the blood - this is the least dangerous but they have a a high chance of developing another thrombus.

89
Q

Explain Resolution phase of thrombosis

A

If a patient has good fibrin in the blood there will be a full resolution of the thrombus

90
Q

Example of a resolution of thrombosis

A

Temporary Ischemic Attack/stroke (TIA)
Sudden episode of focal weakness or numbness, aphasia, unilateral loss of vision (amaurosis fagax), homonymous hemianopsia or symptoms from vertebrobasialr artery
-Could progress to severe focal neurologic deficit and eventually

91
Q

List the progression of stroke from TIA

A

TIA -> RIND (days) –> Storke (months)

92
Q

Explain the Organization phase of sequela of thrombosis

A

Phagocytic digestion of the thrombus two or three days after it forms, and replacement by CT

93
Q

Explain Propagation

-where is this most commonly seen?

A

Enlargement of the thrombus

*Most common in veins - can not occur in arteries because the blood flow in arteries is too fast

94
Q

Explain Infarction

A

The PROCESS in which an infarct is formed

95
Q

Define Infacrt

A

a region of necrosis caused by oxygen deficiency *coagulation

96
Q

Characteristics of Myocardialinfarction

A

red/brown tissue - zone of necrosis in the cardiac mm due to O2 deficiency

97
Q

Characteristics of Ischemic stroke

A

infarction of the brain tissue - due to obstruction of vessel - lack of O2 to brain tissue - very sensitive to O2 deficiency

98
Q

Damaged brain tissue best filled with __________.

A

Neuroglia

99
Q

What is the process called when neuroglia is put down to replace damaged tissue in the brain?

A

Gliosis

100
Q

White Infarction

A

develops in the tissue from an organ from one blood supply

ex) infarct in the myocardial tissue - looks white

101
Q

Red Infarction

A

develops in the tissue in an organ that receives more than one blood supply
ex) lung infacrtion

102
Q

Causes of Infarction

A

Major cause = arterial thrombosis

Vasculitis = inflammation of blood vessel wall = swelling of vascular wall —-> narrowing of the good vessel

103
Q

Arterial thrombosis is caused mainly by

A

arterlerosclerosis

104
Q

Thrombosis of the basal artery would lead to an ischemic stroke - this infarction could be caused by

A

arterial thrombosis

105
Q

Superficial temporal artery

  • AKAs?
  • This is the most common type of ______ for causes of infarction.
  • what is this commonly due to?
  • Characteristics?
A

AKA: temporal arteritis, Giant Cell Arteries, Horton’s disease

  • most common vasculitis
  • Due to Granulomatous inflammation
  • Characterized: acute inflammation of large to small size arteries, autoimmune disease, idiopathic - 50 years old and older - very rare - manifested for any type of inflammatory process - weakness, fever, fatigue
106
Q

Predominately where is arteritis commonly seen?

A

Predominantly: superficial/temporal, vertebral artery, ophthalmic artery, aorta* sometimes

107
Q

Retina Infarct

A

Loss of vision - usually temporary at first then it comes back but if not treated it can go away permanently

108
Q

Polymyalgia Rheumatic

A 
Pain in the mm
Women over 50
Severe mm. pain in the proximal areas of extremities (commonly hip joint and shoulder joint)
Temporal cephalglia = scalp tenderness
visual disturbances 
blind may develop rapidly
low grade fever malaise
symmetric pain and stiffness
109
Q

What are two types of venous infarctions?

A

Para-esophageal hernia

Sheehan’s syndrome AKA postpartum syndrome

110
Q

Explain para-esophageal hernia

A

Rare
Pulling esophagus and stomach up into the thoracic area through a hole in the diaphragm
There can be strangulation of the stomach resulting in compression of the blood vessel
This is strong enough to compress veins but NOT arteries
Pressure on the veins in the stomach makes the vessels so large that the blood pressure becomes the same as the arteries - this is not good because now there is no difference in hydrostatic pressure - This means there is now NO flow of blood - STASIS - this will result in necrosis of the stomach wall (gangrene)

111
Q

Sheehan’s syndrome

  • AKA?
  • When does this occur?
  • What happens
A

Sheehan’s syndrome AKA postpartum syndrome
Occurs DURING delivery
Hypertrophy of the pituitary gland - this occurs to help make more hormones for pregnancy and birth - it will then go to atrophy after baby is born normally
Pituitary gland is supplied by the venous veins
If the pituitary gland is getting bigger it can lead to full obstruction of the veins and develop in a pituitary gland infarction

112
Q

Symptoms and signs of sheehan’s syndrome?

A 
Failure of lactation
Adrenal cortical insufficiency (Acute initial shock, loss of pubic and body hair, asthenia, hypoglycemia)
Gonadal Insufficiency (Amenorrhea)
Hypothyroidism
Pallor out of proportion to anemia
113
Q

Factors that can lead to infarction

A

tissues innate vulnerability to hypoxia
pattern of vascular supply
Anastomosis (the union of branches of two or more arteries supplying the sam body region)
O2 delivery capacity of the blood = how many blood cells are able to carry O2
The rate of development of the occlusion

114
Q

O2 capacity of the blood:
Deep hemoglobin is carried in the ____.
____. Determines if the O2 capacity is good or not
Normal =
How much would a pt. have if they were anemic?

A
  • deep hemoglobin is carried in the RBC - determined if the O2 capacity is good or not
  • Normal is 3 - 5 million or 12 grams of hemoglobin
  • If pt. has anemia they mauve 1.5 - 2 million RBC = the O2 delivery of the blood is decreased - instead of the 12 grams they would have 6 grams of hemoglobin
115
Q

Rate of development of occlusion:
_____ of occlusions leads to sign of the disease.
People at only ____ will have no symptoms

A

75%

70%

116
Q

Embolism is…

Most common type is..

A

the sudden occlusion of a blood vessel by an embolus, an abnormal mass moving with the blood stream.
Most common type is thromboembolism

117
Q

Subacute Bacteiral endocarditis is

A

moral stenosis with Ball - value thrombus

118
Q

AKA for air embolism

A

Air Lock

119
Q

Caisson Disease AKA

A

Bends disease

Driver’s disease

120
Q

T/FClotting factors are present in the blood at ALL times in their “Inactive” form.

A

True

121
Q

What is the inactive form? What does it get activated by and what clotting factor?

A

Fibrinogen, thrombi, clotting factor X (stuart power)

122
Q

AKA for platelets

A

Thrombocytes

123
Q

“Blood clots” can be formed

A

Inside AND outside blood vessels

124
Q

“Platelet plugs” can be formed

A

Only INSIDE blood vessels

125
Q

How is metrorrhagia different from menorrhagia?

A

Metrorrhagia is a serious disorder manifested usually from uterian cancer, which results in loss of blood between metnruation periods

Menorrhagia: is increase in blood loss udrin menstrual periods

126
Q

A change in blood viscosity means there has been a change in ________ - resulting in a ______ blood flow

A

A change in blood viscosity means there has been a change in PROPERTIES - resulting in a DECREASED blood flow.

127
Q

Reason for Varicose Veins

A 
congenital 
women more common
pregnancy due to increased pressure
tumor
tight socks all the way up to knees

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