Week 5 Part 2 Flashcards

1
Q

-REPITELIALIZATION

A

healing of epithelial cells.

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2
Q

Granulation tissue

A

tissue which develops on 2nd post injury day in the wound.
Represents formation of new BVs within the media (exudate)
Damage of tissue inflammatory response acute inflammation results inexudate which is the media where healing occurs

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3
Q

Myofibroblast

A

Causes wound contraction because they have contractile properties** CT gets stronger then thread.

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4
Q

Contracture

A

when a newly formed collagen demonstrates an exaggerated contraction as it matures.

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5
Q

sclerodactyly

A

claw hand due to shrinking of soft tissue.

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6
Q

Rheumatoid arthritis

A

when there is chronic inflammation of the joints ends with healing due to development of CT contractures. There is very limited range of m

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7
Q

Structure

A

narrowing of the lumen of the organ
contracture of empty organs
-due to healing by repair (development of CT)

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8
Q

Healing of peptic ulcer of the stomach

A

Any healing results in inflammation,development of CT, and it pulls the walls of the stomach towards the center= deformity of the stomach

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9
Q

Adhesions

A

joining of serous membranes

  • a result of operations in abdomen.
  • development of CT between peritoneum and the intestines. Can lead to compressionof the colon and narrowing of the colon
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10
Q

Dehiscence

A

breaking open of a healing wound.

  • after operation on appendix is can break open.
  • the wound is not properly healed and can pull apart
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11
Q

Herniation

A

the displacement of an organ from its normal body cavity

Complication of dehiscence

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12
Q

Hiatal hernia

A

stomach moves out into thoracic cavity from abdominal cavity

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13
Q

Para esophageal herniation

A

occurs around the esophagus. There is development ofvenous infarction and gangrene which requires immediate operation.

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14
Q

Umbilical herniation

A

check this by placing the pinky in belly button, if pinky goesinside they may get one in the future.

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15
Q

Herniation of linea alba

A

an aponeuroses between two rectus abdominals muscles. inelderly, it becomes too elastic and it bulges.

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16
Q

Inguinal herniation

A

typical for males. There is pulling of the intestines into theinguinal canal*** aka 3 BALL DISEASE.

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17
Q

Femoral herniation

A

more common in women. The intestines move into the anterior medial portion of the thigh. Women so not have wide inguinal canals

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18
Q

Keloids

A

irregular masses of scar tissue that protrude from the surface ofthe skin.

  • some people are more prone to this.
  • if you remove it you create new scars and the keloids develop.
  • common in black people
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19
Q

promoted by TGF- beta (transforming growth factor beta)

A

too much development of CT

20
Q

Proud flesh

A

EXUBERANT GRANULATIONS- the overproduction ofgranulation tissue.

  • tissue that looks like tissue with pink granules.
  • media (exudate) which becomes more firm.
  • these are new formed BVs
21
Q

Hemostasis

A

The process of stopping blood loss

22
Q

Blood coagulation

A

The principal mechanism of hemostasis

23
Q

Blood clot

A

A mash of protein filaments traps blood’s form elements to form a red, gelatinous mass.

24
Q

Clotting factors

A

Special proteins made by the liver

* influenced by vitamin K

25
Q

Calcium ion

A

If there is no calcium ions there is no coagulation
When you are bleeding, they inject you with calcium ions to prevent blood loss
Its dangerous, it should go into veins if it goes into soft tissue it causes necrosisof tissue

26
Q

The role of the platelet

A

Aka thrombocytes

Their major function is participation in hemostasis.

27
Q

exposure of collagen fibers to blood flow

A

(1) exposure of collagen fibers to the blood flow
-there is (2) activation of proteins in blood circulation which is known as VON
WILLEBRANCH FACTOR – which is normally in the blood and inactive.
-(3)the factor attaches to the collagen fibers to the vascular wall
-(4)causes the first row of platelets to become active and move towards the wall and
attach to the factor. They stop the flow. The next row of platelets is stopped= activated
which stops the next row of platelets= activated etc etc. platelet activation results inthe development of PLATELET PLUG

28
Q

Platelet degranulation

A
platelets release things into the surrounding which causes more platelet activation
platelet activation releases:
ADP
TxA2
Growth factor
29
Q

ADP

A

more platelet activation platelet plug,strengthening the plug

30
Q

TxA2

A

vasoconstriction less blood will be lost, also promotes platelet**aggregation

31
Q

Growth factors

A

attracts fibroblasts to the area of injury release components of the CT (procollagen and mucopolysccharides) healing

32
Q

Anticoagulation system

A
  • fibrinogen in the blood is so numerous is might result in coagulation of the entireblood in the human body.
  • it need a counter action.
  • required for balance, protects us from too much coagulation.
33
Q

Hemodynamics

A

different speed of blood flow

-important because blood coagulation is a time consuming process

34
Q

Endothelial mediation

A

injury injury of endothelial cells produced PGI2 function inhibits aggregationof platelets** which prevents activation of platelets

35
Q

Finbrinolitic system

A

this is the system which directly dissolves the blood clot or destroys the platelet plug.- tissue plasminogen activator (can be activated by clotting factor 12)
plasminogen (in the blood circulation) plasmin DEGRADATION OF
CLOTTING FACTORS.

36
Q

Bleeding disorders

A

Petechia
Pupoura
Ecchymosis (bruising)
Hematoma

37
Q

Petechia

A
  • pin point bleeding
  • very thin bleeding on the body
  • can be seen scurvy (vit C deficiency) on the skin
  • can be seen in the brain as a result of fat embolism.
38
Q

Pupoura

A

subcutaneous leakage of the blood

  • size of the hemorrhage is less then 2cm
  • there is presence of a rash on the thighs
39
Q

Ecchymosis (bruising)

A

the size of the leakage is more then 2cm in diameter.

40
Q

Cushing’s syndrome

A

too much hormones from the adrenal cortex
(cortical steroids) may be associated with adrenal cortex/ pituitary tumors. Rarely caused by tumors today but it is common due to steroid hormone pills.

41
Q

Side effects with corticosteroid therapy:

A

Redistribution of fat ( in abs, in buffalo hump) (disappearance from thighs,
buttox)
Striae on abdomen. – they are red (during pregnancy they are white)
Moon face.
Formation of bruises because the BVs become brittle= ECCHYMOSES- even
touching the skin may result in bruises (you might not be able to adjust them)
Hypertension
diabetes mellitus- degeneration of beta cells of pancreas
tuberculosis – long term case of corticosteroid= suppression of immune
response. (they are used when the immune system is hyperactive)
always leads to osteoporosis. (fracture o ribs puncture of lungs
pneumothorax)

42
Q

Hematoma

A

tumor made of blood

-blood leakage into the spaces or soft tissue masses

43
Q

Epidural hematoma

A

blood leaks into the brain

-big crash of musculature might also cause this. (leakage of blood into blood cavities)

44
Q

Extrinsic pathway

A
Tissue thromboplastin (tissue factor)-> when tissue is injure, this is released into surroundings-> activates clotting factor VII-> clotting factor X
* tissue injury both inside and outside BVs
45
Q

Intrinsic pathway

A

Exposure of collagen fibers to blood -> activation of Hagemann factor (clotting factor XII) -> clotting factor X I -> clotting factor I X -> clotting factor X
* happens inside the BVs

46
Q

REVASCULARIZATION (angiogenesis)

A

healing of the BVs

formation of new BVs