Week 6 Part 1 Flashcards

1
Q

Thrombocytopenia

A

-the same as platelets.
-there is a critical amount of platelets= 140,000 per cubic mm- if less it is associated
with bleeding.
-remember: usually results in petechial or pupoura rash only. **

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2
Q

Von willebrands disease

A

-rare genetic disease
-non production of von willebrand’s factor
-platelet activation of blood clot formation does not occur so bleeding is more common.
-one of the parents must have the same disease as well.
-manifestations:
leakage of blood in stomach and duodenal wall  development of
inflammation of mucous membrane
menorrhagia= increased amounts of blood loss during menstruation.

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3
Q

Hemophilias

A
  • rare genetic disorders where you can not produce clotting factors
  • develops only in males, but the gene is present only in females.
  • parents of the patient do not have this

Blood in joints is dangerous because it leads to degeneration of cartilage=
secondary osteoarthritis. Blood in joints should be eliminated as soon as
possible. Destruction of RBCs iron iron gets into cartilage by imbibition
death of cartilage.

  1. hemophilia A
    - defect of clotting factor 8
  2. hemophilia B
    - defect of clotting factor 9 (Christmas factor)
    - aka CHRISTMAS DISEASE
    - non production of clotting factor 8 as well
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4
Q

HEMARTHROSIS.

A

leakage of blood into the big joints, in the case of little injury

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5
Q

METRORRHAGIA

A

leakage of blood from uterus, but not during menstruation.

-this is an important and early sign of uterus cancer.

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6
Q

HEMODYNAMIC DISORDERS

A

those that arise from the interruptions of normal blood flow (BF)

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7
Q

THROMBUS

A

-sometimes the stoppage of BF occurs due to THROMBUS which is made through the process of THROMBOSIS

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8
Q

Thrombus

A

-thrombus is a result of platelet activation and platelet aggregation. Blood clots are not formed here.
Never forms outside blood vessels always formed with blood vessels.
Originate from vascular wall and always have point of attachment to vascular wall

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9
Q

FORMATION OF THROMBUS (the same as blood clot formation)

A

-exposure of collagen fibers to the BF when the endothelial cells are scratched von
willibran factor is activated which is bound to collagen fibers activated can stop themovement of first row of platelets can stop the next row of platelets and so on
formation of a platelet plug activation of clotting factors and fibrin strands.

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10
Q

DIFFERENT LOCATIONS of thrombus

A

-if thrombus occurs in the arteries where there is high speed of blood flow, there is
retraction of the thrombus because the clotting factors are washed out. There is always
point of attachment to vascular wall
-in the veins= the blood flow is slow with low pressure, there is lots of time for activation of clotting factors and the thrombus is wider and loose (instead of contracted and dense)

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11
Q

LINES OF ZAHN

A

represent special type of thrombi characterized by visible andmicroscopic lamination produced by alternating pale layers of platelets mixed with fibrin and darker layer containing red blood cells.

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12
Q

Where lines of Zahn are found

A

-develops only in low blood flow in: (only 2 regions)
 heart
-mitral stenosis: narrowing of the mitral valve for many different regions
-the blood flows through the more narrow area with less speed and less amount (the more narrow, the less BF occurs)
-there is delay of the blood in the left atrium and there is formation of a big thrombus-dark layers have RBCs and the pale layers have platelets.
 aorta

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13
Q

Factors
predisposing to
thrombosis**

A
ENDOTHELIAL DAMAGE
iatrogenic thrombosis
flow abnormalities (in arteries)
flow abnormalities ( in the veins)
flow abnormalities
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14
Q

ENDOTHELIAL DAMAGE

A

A. hemodynamic stress

B. atherosclerosis

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15
Q

hemodynamic stress

A
  • normal wear and tear of tissues.
  • the older you are the more torn your vessels are so you have higher chances of getting athrombus.
  • hypertension
  • there is increased pressure of the blood onto the walls and this increases hemodynamic stress
  • increased friction increased wear and tear.
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16
Q

atherosclerosis

A
  • this is the most common disease in the world.
  • everyone in the world has it
  • formation of atherosclerotic plaques within the arterial walls, which modify the inner surface of the BVs.
  • it can account for the exposure of collagen fibers
  • # 1 cause of hemodynamic disorders. ( stroke and myocardial infarction)
17
Q

iatrogenic thrombosis

A
  • IATROGENIC: everything associated with medical health/ medical system
  • intervention from surgeons that results in endothelial damage
  • ex. needles in veins : for sure there is damage of the endothelial cells (mechanical
    damage)  formation of many thrombites.
  • if they put a lot of needles in the cubital vein, it can result in the complete obliteration ofthe vein. They will need to look for a new vein to put the needle in
  • after IV there is no thrombus forming.
  • ex. After operation when people are immobile they can develop thrombosis.
  • This is an extremely rare situation.
18
Q

flow abnormalities (in arteries)

A
  • # 1 reduction in the rate of BF (or its complete stoppage- STASIS)
  • axial BF: there is laminar flow of the fluid, all the layers of blood flow parallel to each other without mixture. The cells flow in the center of the column and friction between the cells and the endothelium is low.
  • slowing= disruption of axial blood flow and friction occurs.
19
Q

two components associated with reduction of BF in arteries:

A

Cardiac damage: reducing the heart’s pumping ability

increased blood viscosity

20
Q

Cardiac damage: reducing the heart’s pumping ability

A

-results in swelling, there is escape of the fluid portion of the blood in all tissues. Due todamage of the heart. Blood flows slower then it is supposed to thrombosis.
myocardial infarction
-mitral stenosis-

21
Q

increased blood viscosity

A
  • if you have two tubes with the same diameter and the same length, the tube with the less viscous material will flow faster. (water flows faster then honey)
  • this is a very serious problem.
  • ex. Polycythemia or erythemia.
22
Q

Polycythemia or erythemia.

A

This is a type of leukemia associated with overproduction of RBCs
-increased RBCs increased viscosity reduction of the speed of BF thombrosis.-the capillaries will not have blood.

23
Q

flow abnormalities ( in the veins)

A

physical inactivity

varicose veins

24
Q

physical inactivity

A

-the veins have valves. They are made in a specific and smart way. They are opened only when the hydrostatic pressure below the values is greater then above. Because of this
the blood can only flow up and not down
-if we didn’t have valves our legs would be very swollen.

25
Q

varicose veins

A
  • more common in women. a factor that promotes this is pregnancy
  • normal veins: the blood flows only up because of valves
  • varicose veins: distention of the walls means that the valves no longer touch and cant prevent the back flow of blood.
26
Q

flow abnormalities

A

turbulence (disruption of laminar blood flow)

blood hyper coagulation

27
Q

turbulence (disruption of laminar blood flow)

A

-if something changes the lumen shape of the BV change in the blood flow directionleads to thrombosis. (1) axial flow is disrupted (2) close flowing of blood cells towards
the vascular wall exposure of collagen fibers to the blood thrombosis.
-factors that result in turbulent BF:
 varicose veins
 aneurysms (pouching of arterial wall) (may obstruct the adjacent blood
flow)

28
Q

blood hyper coagulation

A

-the blood can coagulate and this is normal, it keeps us from losing blood-but sometimes, the blood has increased coagulation
-change in the clotting factors of the blood
A. extensive burns
-second degree burns with fluid in the blisters.
B. some kidney diseases
C. heart failure.
D. widespread metastatic tumor growth.
E. birth control pills**

29
Q

Hemorrhagic

disorders

A
  • thrombocytopenia
  • von willebrands disease
  • hemophilias