ischemia and infarction

2. Def.:
Decrease blood supply to organ or tissue due to oc
clusion of it′s artery.

6. Def.:
Sudden complete arterial occlusion .
Causes:
1) Thrombus or embolus.
2) Twisting of the pedicle of a movable organ.
3) Surgical ligature of artery.
4) Extensive venous obstruction as in case of mesenteric ven
ous thrombosis ( marked venous engorgement, this imped
es the arterial blood flow leading to ischemia).

7. Effects:
a) Sudden occlusion of arteries with poor collaterals [end arteries]
→ infarction or gangrene.
b) Sudden occlusion of arteries with good collaterals → not effect
s.

9. Gradual incomplete arterial occlusion.
Cause:
(1) Atherosclerosis.
(2) Artery compression as by enlarged lymph node, tumor.
(3) Arteritis as in marked endarteritis oblitrans as in syphilis..

10. Effects:
With poor collaterals → cellular degeneration, atrophy & replac
ement by fibrosis e.g. atherosclerosis of the coronary branches cau
ses myocardial fibrosis.
With good collaterals →no effect.

12. Def.:
Is an area of ischemic necrosis caused by occlusion of bl
ood supply.
99% results from arterial occlusion caused mainly by thrombosis
or embolism.
The necrotic tissue is referred to as an infarct.

14. Causes:
1)Most common infarction caused by arterial thrombosis or emboli
2)The next most common cause obstruction of artery by vascular sp
asm or by external compression by tumor
3)Other uncommon causes of tissue infarction include torsion of a v
essel (in testicular torsion or bowel volvulus)

15. a) Red infarction "hemorrha
gic infarcts“
occur in tissues with dual circulatio
ns (lung ,liver ,small intestine)

16. B)White or pale infarction (anemic infarction )
• occur with arterial occlusio
ns in solid organs with end-
arterial circulation (heart, s
pleen and kidney)

17. Grossly
Shape:
Wedge shaped or pyramidal surrounded by a red zone of inflam
matory hyperemia. The base is directed towards the surface of th
e organ.
Consistency:
Firm or soft.
Color :
•Pale infarcts in kidney, heart and spleen.
•Red infarction in lung,liver & intestine.

18. Microscopic
•The affected area shows outlines of cells only due to Coagulativ
e necrosis while the margin of infracted area shows hemorrhage
& inflammatory cells.
•or liquefactive necrosis if infarct has caused necrosis of all the ce
lls in a portion of the brain.

21. 2) According to their age:
a)Recent or fresh.
b)Old or healed.
3) According to presence or absence of infectio
n:
a)Bland, when free of bacterial contamination.
b)occur when infected cardiac valve vegetations embolize or when
microbes seed necrotic tissue→the infarct is converted to an absces
s.

22. Fate
Small infarct:
Healing by fibrosis.
Large infarct:
Healing by fibrosis followed by dystrophic calcification.

24. Def.:
•Gangrene is massive tissue necrosis followed by putrefact
ion (coaglutive necrosis undergoes liquefaction by the action of p
utrefactive bacteria).

25. Causes:
Necrosis :
Sudden ischemia or bacterial toxins.
Putrefaction :
• Saprophytic bacteria → release collagenase and hyaluronidase → degrad
e extracellular matrix proteins → released of sulphide + hydrogen in tissue →
hydrogen sulphide [bad odor].
•sulphide +iron of hemoglobin → iron sulphide (black in color).

28. It occurs due to cut of arterial blood supply alone while th
e venous drainage and surface evaporation are normal.
Causes of arterial occlusion:
1)Atherosclerosis
2)Buerger’s disease
3)Arterial spasm in Raynaud's disease.

30. Pathogenesis:
Arterial occlusion →ischemia in distal to the occlusion → massive necrosis
→the affected part is pale and cold due to ischemia → Later the dead part beco
mes dryness, shrunken and mummified → rapidly invaded by saprophytic bact
eria.
The necrotic tissues then undergo putrefaction and become gangrenous.
The gangrenous process spreads proximally until it reaches an area of good b
lood supply, where the tissues respond to irritation by inflammation.
Now the gangrenous process stops and a red line of acute inflammation kno
wn as line of demarcation ( appears separating the healthy skin above from the
gangrenous skin below) → groove formed by granulation tissue

32.  This groove separates the healthy ti
ssues above from the gangrenous ti
ssues below) known as line of sepa
ration → change to fibrosis which
gradually deepens until it separates
the gangrenous part called (natural
amputation) leaving a conical stum
p (conical shape of the stump is due
to variation of blood supply in bone
, muscles ,skin).

33. Gross:
The necrotic part appears
pale and cold at first
Gangrene develops it app
ears dry, shrunken and dark
black, resembling the foot o
f a mummy.

35. Def.
•Moist gangrene caused by occlusion of both arterial and venous
blood supply .
•Usually affects :
1)Moist internal organs (mouth, lung, cervix)
2)Bowl (strangulation hernia - twisting - intussusception)
3)Uncontrolled diabetic
4)Bed sores.

36. Moist gangrene of the intestine
Pathogenesis:
First venous obstruction occurs →the affected loop shows
congestion + edema→ appears dark red and swollen.
Next arterial occlusion occurs →necrotic loop →invaded by pu
trefactive bacteria from the intestinal lumen and putrefaction occu
rs rapidly→ the loop stains black (iron sulphid ) & bad odors (hy
drogen sulphid).

37. Gross:
•The affected part is soft, swo
llen, putrid, rotten and dark.

38. Diabetic gangrene
 Uncontrolled diabetes results in hyperlipidemia →to atheroscl
erosis at an earlier age.
 It begins in the tip of the big toe or in the sole of the foot.
Pathogenesis:
 The gangrene starts dry but rapidly becomes moist because excess sugars in
the tissues help multiplication of the bacteria followed by inflammatory &
thrombosis of blood vessels.
 It is characterized by rapid putrefaction, rapid spread, excess toxins, severe
toxemia, poorly developed line of demarcation, no line of separation and no
natural amputation.

40. Bed sores
• Skin ulcer over bony promin
ence (sacrum and greater trochanter)
due to prolonged recumbence as i
n paralysis or bone fracture.
Pathogenesis:
•The ulcers are due to blood stagnation
and thrombosis of the vessels followed
by tissue necrosis. Bacterial infection ca
uses putrefaction in the ulcers.

43. It is gangrene rich by gas caused by gas-forming clostridi
a (clostridium perfringens) highly infected of soft tissue as musc
les .
Causes and pathogenesis:
Out side body as in →deep ischemic wounds contaminated by soil
containing anaerobic spores (contaminated by animal fecal material
) as in agricultural accidents.
Inside body as in colon surgery

44.  The most common cause of gas gangrene is saccharolytic grou
p ( Cl. perfringens) produces →
 a) Powerful exotoxin and b) Hyaluronidase → dissolved the tissue cement
substance → rapid spread of infection resulting in progressive muscle necr
osis.+ putrefaction → gangrene
 c) Fermentation of muscle carbohydrates resulting in production of carbon
dioxide and hydrogen gases →formation of gas bubbles crepitus sensation i
n palpation.
• Gas gangrene is highly fatal due to the severe toxemia

46. Dry Gangrene Wet gangrene
1) Caused by occlusion arterial blood
supply alone.
2) Usually affects exposed limbs.
3) Putrefaction is slow.
4) Spread is slow.
5) Toxemia is mild (not fatal).
6) Line of demarcation is well
developed.
7) Line of separation is well developed .
8) Natural amputation can occur.
9) Affected part is shrunken & black
1) Caused by occlusion of both
arterial and venous blood supply.
2) Usually affects internal organs.
3) Putrefaction is rapid.
4) Spread is rapid.
5) Toxemia is Severe (fatal).
6) no Line of demarcation
developed.
7) no Line of separation.
8) Natural amputation cannot occur.
9) Affected part is swollen & black.