Pathology 🩺 Flashcards

1
Q

What is the definition of thrombosis?

A

Formation of a compact mass composed of the circulating blood elements inside a vessel or a heart cavity during life.

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2
Q

What are the causes and pathogenesis of thrombosis?

A

(Virchow’s triad)

  1. Roughness of the intima (Endothelial injury).
  2. Slowing of blood flow (stasis). “Bed rest”
  3. Changes in the composition of blood (hypercoagulability). “Inherited or acquired (due to cancer)”
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3
Q

What is the morphology of thrombosis?

A

Grossly and microscopically apparent laminations called lines of Zahn, which are pale platelet and fibrin deposits alternating with darker red cell-rich “RBCs and WBCs” layers.

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4
Q

What are the types of thrombosis?

A

A) According to site:
1. Venous thrombosis (phlebothrombosis): deep vein thrombosis in the lower limb

  1. Arterial thrombi: As in coronary, cerebral, & femoral arteries
  2. Heart chambers or in the aortic lumen are mural thrombi

B) Presence or absence of organism (infection): Septic “due to infection at the site of thrombosis” or Aseptic

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5
Q

What are the fate and complications of thrombosis?

A

1) Septic thrombus: fragmented by proteolytic enzymes → septic emboli → pyaemic abscesses.
2) Aseptic thrombus: fate depends upon its size
a. if small in size: Dissolution: dissolved and absorbed.

b. if large in size: (PEOC)
1. Propagation: Thrombi accumulate additional platelets and Fibrin
2. Embolization: Aseptic emboli → ischemia.
3. Organization “Replaced by fibrous tissue” & Recanalization
4. Calcification.

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6
Q

What is the definition of embolism?

A

It is the circulation of insoluble material (solid, liquid, or gaseous) in the blood and its sudden impaction in a narrow vessel.

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7
Q

What are the types of emboli?

A
1- Thrombo-embolism. 
2- Fat embolism.
3- Tumor emboli.
4- Parasitic emboli.
5- Air embolism.
6- Amniotic fluid embolism.
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8
Q

What is the origin of thromboembolism?

A

A detached thrombus may originate from:

  1. Systemic veins reach the right side of the heart, then lungs → pulmonary embolism
  2. Cardiac thrombi: Usually originate in the left side of the heart. They are carried by the systemic arterial circulation to impact any organ (spleen, kidney, brain…etc.)
  3. Portal vein or its branches passes to the liver (portal embolism).
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9
Q

What are common sites for fat embolism? “Injury in BV + Fat source”

A

Common in sites containing fat such as; Bone fractures & abdomen due to acute pancreatitis

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10
Q

What do fat globules enter through?

A

ruptured veins

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11
Q

What is the definition of tumor emboli?

A

Malignant “not just neoplastic” cells pass as emboli in the circulation and give metastases in the organs.

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12
Q

What forms parasitic emboli?

A

Bilharzial ova and worm

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13
Q

Is amniotic fluid “contains epithelium” embolism rare or common? And when does it occur?

A

Rare

Occurs during delivery→ fatal pulmonary embolism.

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14
Q

What is the definition of air embolism?

A

Sudden admission of 100 cc air in the bloodstream —->sudden death.

The air may block the right ventricle or pulmonary arteries —> acute heart failure.

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15
Q

What are the causes of air embolism?

A
  • Injury of large neck veins → gaping (because they are embedded in the fascia that prevents their collapse) → air is sucked into the vessels then the heart.
  • Faulty technique during blood transfusion.
  • Criminal abortion (air passes into uterine veins). “Using a tool that damages the BV”
  • Caisson’s disease
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16
Q

What is caisson’s disease?

A

 A type of air embolism occurs when deep divers work under high atmospheric pressure, where their nitrogen gas is dissolved in the tissues and blood.

 Sudden decompression i.e. sudden ascent produces nitrogen bubbles which act as gas emboli.

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17
Q

What is the effect of embolism?

A

emboli lodge in vessels too small to permit further passage —-> partial or complete vascular occlusion ——>ischemic necrosis (infarction) of the tissue supplied by this vessel.

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18
Q

What does the effect of embolism depend on?

A

1- Size of embolus.
2- Nature of the embolus: septic (pyemic abscess) or aseptic (infarction).
3- State of the collateral circulation in the affected organ.

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19
Q

What are the sources of pulmonary embolism?

A
  • Mainly arises from recent thrombi of calf veins in lower limbs (Most common).
  • Thrombi in the Rt. side of the heart e.g. in cases of Rt. sided heart failure.
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20
Q

What are the effects of pulmonary embolism?

A

Depends on the size of the embolus

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21
Q

What are the effects of pulmonary embolism in the case of large embolus?

A

Occludes the pulmonary trunk or one of its main branches produces sudden death (no time for infarction)

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22
Q

What are the effects of pulmonary embolism in the case of a medium-sized embolus?

A

If the lung is healthy, no effect will occur as the lung has a double blood supply (pulmonary and bronchial arteries).

If the lung suffers from chronic venous congestion, lung infarct occurs. “ And the patient needs observation as he has hypercoagulability”

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23
Q

What are the effects of pulmonary embolism in the case of recurrent small-sized embolus?

A

Produce pulmonary hypertension due to lung fibrosis “resists blood flow” and right-sided heart failure “higher work done to overcome resistance” (cor-pulmonale).

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24
Q

What is the definition of ischemia?

A

Decrease of blood supply to a part of tissue due to occlusion of its artery.

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25
Q

What are the types of ischemia?

A
- Sudden (acute) ischemia:
Thrombosis
Embolism
Arterial spasm
Surgical ligature
Twisting of the organ’s pedicle
  • Gradual (chronic) ischemia: Pressure on the artery by tumor or enlarged L.N.
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26
Q

What do the effects of vascular occlusion depend on?

A

The effects of vascular occlusion range from no or minimal effect to death of a tissue or person depending on:
•Nature of the vascular supply (end artery or dual blood supply).

  • Rate of vascular occlusion. “Acute or chronic”
  • Vulnerability of tissue to hypoxia: Neurons (3 to 4 minutes), Myocardial cells (20 to 30 minutes).
  • Oxygen content of the blood.
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27
Q

What is the definition of infarction?

A

It is an area of coagulative necrosis (liquefactive in the brain) due to inadequate blood supply to the affected area.

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28
Q

What is an example of ischemic necrosis?

A

Infarct

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29
Q

What are types of infarction?

A

Red (hemorrhagic) infarct

Pale (anemic) infarct:

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30
Q

Where does red hemorrhagic infarct occur?

A
  • loose tissues (allow the collection of blood in the infarcted area)
  • Vascular organs such as lung and intestine (dual blood supply)
  • Previously congested tissue. “Nutmeg liver”
  • Reperfusion of previously ischemic tissue
  • Occlusion of a vein
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31
Q

Where does pale anemic infarct occur?

A
  • Occurs in solid and less vascular organs like the kidneys, spleen, and heart
  • arterial occlusion
  • end arterial supply
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32
Q

What type of infarct could occur in the brain and spleen?

A

Infarction of the brain and spleen may be pale or red.

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33
Q

What is N/E of infarction?

A

• Size of infarct area is related to
➢size of the obstructed artery
➢susceptibility of the tissue to ischemia.

• Wedge-shaped (pyramidal) the arteries have
a fan-like distribution, The base is directed towards the surface of the organ and the apex is deep.

• Subcapsular:
raised when recent (due to edema), depressed when healed (due to fibrosis)

  • Surrounded by a red zone of hyperemia (inflammation)
  • Firm (soft in the brain)
  • Sero-fibrinous inflammation of overlying serosa.
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34
Q

What is M/E of infarction?

A

Area of coagulative necrosis (liquefactive in the brain) surrounded by a zone of acute inflammation (Hyperemia).

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35
Q

What is the fate of infarction?

A

• Small infarct:
Necrotic tissue is removed by macrophages, Granulation tissue fills the defect followed by fibrosis.

• Large infarct:

  • surrounded by a fibrous capsule
  • dystrophic calcification.

• In the brain (due to high lipid content): it leaves a cyst surrounded by glial tissue.

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36
Q

What is the definition of gangrene?

A

A type of necrosis most often affects the lower extremities or bowel and it is secondary to vascular occlusion. And it is associated with a saprophytic bacterial infection.

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37
Q

What are the types of gangrene?

A

Dry and wet

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38
Q

Where does dry gangrene start and what causes it?

A

Begins in the distal part of a limb due to ischemia.

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39
Q

What is the rate of spread of dry gangrene?

A

Slow until it reaches a point where the blood supply is adequate to keep the tissue viable.

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40
Q

In Which type of gangrene is the line of separation formed between the gangrenous part and the viable part?

A

Dry Gangrene

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41
Q

What is the rate of development of wet gangrene and what causes it?

A

Develops rapidly due to blockage of venous and arterial blood flow (from thrombosis or embolism).

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42
Q

What are the characteristics of the affected parts with wet gangrene?

A

The affected part is stuffed with blood which favors the rapid growth of putrefactive bacteria.

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43
Q

What is the characteristic thing for wet gangrene?

A

The toxic products formed by bacteria are absorbed causing profound systemic manifestations of septicemia, and finally death.

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44
Q

What are examples of wet gangrene?

A
  • Diabetic foot: High sugar content in the necrotic tissue which favors the growth of bacteria.
  • Bedsores: Bed-ridden patient due to pressure on sites like the sacrum, buttocks, and heels
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45
Q

Compare between dry and wet gangrene according to:

Sites
Cause
Progression
Line of demarcation
Gangrenous part
Putrefaction and bad odor
Toxemia

“SCG PP LT”

A

A- Extremities e.g. lower limb

A- Internal organs e.g. intestine, lung.
Extremities in crush injury and diabetes.

B- Gradual arterial obstruction

B- Sudden arterial and venous obstruction.

C- Slowly Present

C- Rapid Absent

D- Black, Dry, and mummified

D- Swollen, edematous with ulcerated skin.

E- Minimal due to lack of fluids Mild

E- Maximal

F- Mild

F- Severe and marked

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46
Q

What is the definition of gas gangrene?

A

A special form of wet gangrene is caused by gas-forming clostridia (gram-positive anaerobic bacteria).

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47
Q

How do gas-forming Clostridia enter the tissues?

A

through open contaminated wounds, especially in the muscles, or as a complication of operation on the colon which normally contains clostridia.

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48
Q

What do Gas forming Clostridia produce?

A
  • It produces various toxins which produce necrosis and edema locally.
  • Also absorbed producing profound systemic manifestations.
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49
Q

What do both hyperemia and congestion indicate?

A

Both indicate a local increased volume of blood in a particular tissue.

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50
Q

What is the definition of hyperemia?

A

it is an active process that result from increased blood flow due to arteriolar dilation.

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51
Q

What are the causes of hyperemia?

A
  • Physiological e.g. Muscular Exercise, emotion& exposure to heat
  • Pathological e.g. Acute inflammation& fever. “VD to allow the Flow of immune cells”
  • The affected tissue is red because of engorgement with oxygenated blood.
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52
Q

What is the definition of congestion?

A

Is a passive type of hyperemia due to obstructed venous flow of the tissue.

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53
Q

What are the causes of congestion?

A

( pathologic only )

  • Acute congestion - Sudden right sided heart failure. “Leads to stopping of Venus outflow” - Shock.
  • Chronic congestion
  • Localized….pulmonary congestion in left sided heart failure.
  • Generalized….all organs (including liver) in right sided heart failure.

-Affected organ is blue red “lung congestion” in color due to increased non-oxygenated blood.

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54
Q

What is the causes of CVC of the liver? “Generalized”

A

right-sided heart failure.

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55
Q

What are the pathogenesis of CVC of the liver?

A

During the early stages:

  • The central part of hepatic lobule is affected with dilated central vein “due to blood” “from hepatic artery” and adjacent blood sinusoids “from central vein” and appear deep red in color.
  • The mid zone of the lobule suffer hypoxia “as the blood is deoxygenated” and shows fatty change and appear yellow in color.
  • The alternating red and yellow color resemble the nutmeg seed (nut meg liver).

“Periphery isn’t affected”

During late stages of the disease,

  • The central cells become necrotic with destruction of the reticular framework. This area of necrosis will be replaced by fibrosis.
  • This is called cardiac cirrhosis.
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56
Q

What are the causes of CVC of the lung? “Localized”

A

1- Left sided heart failure..

2- Mitral stenosis

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57
Q

What is the pathogenesis of CVC of the lung?

A

In early stage:
- Congestion and distention “increased hydrostatic pressure” of alveolar capillaries leads to transudation of fluid into alveolar spaces

  • Rupture of capillaries leads to passage of RBCs into the alveoli.
  • Phagocytosis and degradation of red cells result in intra-alveolar hemosidrin-laden macrophages “due to HB” called Heart failure cells.
  • At this stage the lungs are “EHBO”
  • Enlarged
  • Heavy “Due to transudate and blood”
  • Bluish-red in color “deoxygenated”
  • C/S oozes bloody froth. “Bubbles of air”

In late stage:
-Fibrosis of interstitium & hemosidrin deposition results in Brown induration “fibrosis” of the lung.

  • At this stage the lung appears *dark brown
  • firm consistency (indurated) due to associated fibrosis.
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58
Q

What is the definition of edema?

A
  • Pathological accumulation of excess fluids in the interstitial tissue spaces or body cavities “pleura, peritonitis and pericardium”
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59
Q

where does fluid accumulates in case of edema?

A

Fluid is outside cells and outside vascular structures

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60
Q

What is the pathogenesis of edema? “Inc filtration or dec Absorbtion or problem in lymphatics”

A
  1. Increased intravascular hydrostatic pressure: due to venous obstruction “congestion”
  2. Decreased plasma oncotic pressure:
    A)Decrease protein synthesis as in liver disease
    b) Protein loss as in renal disease
  3. Lymphatic obstruction: due “to SC 4I”
    a) Congenital absence of the lymphatics.
    b) Surgical removal of LNs. “Edema at that place”
    c) Infection: Filariasis.
    d) Tumor infiltration. “Obstruction”
    e) Irradiation.
    f) Inflammation (lymphangitis)
  4. Increased vascular permeability as in acute inflammation
  5. Sodium retention as in impaired renal function.
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61
Q

What is edema classified according to?

A

1- According to the site of edema
2- According to consistency of edema
3- According to edema fluid

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62
Q

What are the types of edema according to the site?

A

1- Localized edema

2- Generalized edema (anasarca) “central affection”

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63
Q

What are types of local edema?

A

Inflammatory “exudate”

obstructive (Venous “transudate” or lymphatic “lymph” ) (lymphedema)

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64
Q

What are the types of generalized edema?

A

Cardiac, renal, hepatic and nutritional (hypoproteinemia) “low protein which decreases oncotic pressure”

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65
Q

What are the types of edema according to consistency?

A

1- Pitting edema: When pressure is applied to an area of edema a depression or dent results as excessive interstitial fluid is forced to adjacent areas.

2- Non-Pitting edema .

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66
Q

What are the causes of non-pitting edema?

A

1) Inflammatory edema (exudate)
2) Lymphatic edema (Lymph)

“Contain fibers”

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67
Q

What are pitting edemas?

A

Generalized and venous localized

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68
Q

What are the types of edema according to edema fluid?

A

1- Transudate: In generalized edema and localized venous obstructive edema.

2- Exudate: In inflammatory edema.

3- Lymph: In lymphatic obstruction edema (lymphoedema)

  • So Edema fluid is a transudate except [inflammatory edema (exudate) and lymphatic edema (lymph).
69
Q

What is anasarca?

A

Extensive generalized edema involving serous sacs, lung and brain

70
Q

What is the definition of each of the following?

Hydrothorax:
Hydropericardium:
hydroperitoneum:
hydrocele:
hydrarthrosis:
A
  • Hydrothorax (pleural effusion): Fluid in the pleural cavity
  • Hydropericardium (pericardial effusion): Fluid in the pericardium
  • Hydroperitonium (Ascites): Fluid in the peritoneal cavity
  • Hydrocele: Fluid in tunica vaginalis around testis.
  • Hydroarthrosis: Fluid in joint cavity.
71
Q

What is a fluid in the pleural cavity?

A

Hydrothorax (pleural effusion)

72
Q

What is fluid in the pericardium?

A

Hydropericardium (pericardial effusion)

73
Q

What is fluid in the peritoneal cavity?

A

Hydroperitonium (Ascites)

74
Q

What is fluid in tunica vaginalis around the testis?

A

Hydrocele

75
Q

What is fluid in joint cavity?

A

Hydroarthrosis

76
Q

What is the definition of hemorrhage?

A

Escape of blood outside the cardio- vascular system.

77
Q

What are the causes of hemorrhage?

A
  1. Trauma
  2. Spontaneous due to:
    ➢ Destruction of vascular wall “due to weak BV” (TB, malignancy “infiltration of BV wall” ,…)

➢ Diseases of vascular wall (atherosclerosis “weak BV” , aneurysm, vasculitis “inflammation of BV” , varicosities “Enlarged veins filled with blood” …)

➢ Systemic diseases (hemorrhagic diathesis “Problem in coagulation system” , Vit.C and K deficiency “Gums bleeding” , hypertension,….)

78
Q

What are the types of hemorrhage?

A

According to its site it may be
I- External Hemorrhage……Outside the body.

II- Internal Hemorrhage…….In serous sacs. “Pleura, peritoneum and pericardium)

III- Interstitial Hemorrhage….In tissue spaces.

79
Q

What is the definition of external hemorrhage?

A

It is hemorrhage through body orifices.

80
Q

What are the systems from which the body bleeds?

A

Respiratory system, GIT system, unitary system and a female genital system

81
Q

What are types of Hemorrhage from the respiratory system?

A
  • Epistaxis: bleeding form the nose.

* Hemoptysis: coughing of blood.

82
Q

What are types of Hemorrhage from GIT system?

A
  • Hematemesis: vomiting of blood.
  • Melena: passage of black digested blood with stool. “By the stomach” “Due to parasites”
  • Bleeding per rectum: passage of fresh blood with stool. “بواسير - sigmoid”
83
Q

What are types of Hemorrhage from the urinary system?

A

• Hematuria: passage of blood with urine.

84
Q

What are types of hemorrhage from the female genital system?

A
  • Menorrhagia: excessive or prolonged menstruation.

* Metrorrhagia: bleeding form female genital system in time rather than the cycle.

85
Q

What is the definition of internal hemorrhage?

A

It is hemorrhage inside body cavities.

86
Q

What is the definition of each of the following?

  • Hemothorax
  • Hemopericardium
  • Hemoperitonium
  • Hemoartherosis
  • Hematocele
A
  • Hemothorax → hemorrhage into the pleura.
  • Hemopericardium → hemorrhage into the pericardium.
  • Hemoperitonium → hemorrhage into the peritoneal sac.
  • Hemoartherosis → hemorrhage into a joint cavity.
  • Hematocele → hemorrhage into the tunica vaginalis of the testis.
87
Q

What is the definition of interstitial hemorrhage?

A

Accumulation of blood within the interstitial tissues space.

88
Q

What are the types of interstitial hemorrhage and what are they classified according to?

A

According to the size it is called:-
Petechiae (1-2 mm)
Purpura (3-5 mm)
Ecchymosis (1-2 cm) “‏كدمة” = hematoma (bruise) “ if high”

89
Q

What do the effects of hemorrhage depend on?

A

Depends upon amount, rate and site of hemorrhage.

90
Q

What happens in case of chronic external blood loss?

A

Iron deficiency anemia

91
Q

What happens in case of acute or chronic loss of 20% of total blood volume?

A

Doesn’t affect healthy individuals “those with no heart failure or lung diseases”

92
Q

What happens in case of acute loss of more than 25% of blood volume?

A

Produce hypovolemic shock “ ‏ ‏إغماء”

93
Q

What are the diseases of lymphatic vessels?

A
1- Acute lymphangitis
2- Erysipelas
3- Chronic lymphangitis
4- Hamartomas
5- tumours
94
Q

What is the definition of acute lymphangitis?

A
  • acute inflammation of lymphatic vessels and the peri lymphatic blood vessels.
95
Q

What causes acute lymphangitis?

A

streptococcus pyogenes infection

96
Q

What are the complications of acute lymphaginitis?

A

Chronic lymphangitis

97
Q

What is the definition of erysipelas?

A
  • Spreading acute lymphangitis of dermis usually of the face due streptococcus pyogenes infection
98
Q

What is the Pathology of erysipelas?

A

 The area is raised, painful, red with well-defined and indurated margin and Spreads rapidly

 Cervical lymphadenitis

99
Q

What is the course of erysipelas?

A

Disease lasts 1-3 weeks and heals with no disfigurement.

100
Q

What are the types of chronic lymphaginitis?

A

Non specific: Following acute lymphangitis

Specific: T.B, Syphilis, Filariasis.

101
Q

What are the types of hamartomas?

A
  • Capillary lymphangioma

- Cavernous lymphangioma

102
Q

What are tumors of lymphatic vessels?

A

Malignant: Lymphangiosarcoma

103
Q

What are the diseases of lymph nodes?

A

Acute and chronic lymphadenitis

104
Q

What are types of acute lymphadenitis?

A

Bacterial and viral

105
Q

What is the source of bacterial acute lymphadenitis?

A
  • Acute inflammation of regional lymph nodes draining an acute bacterial infection (usually pyogenic mainly face and hand)
106
Q

What is the N/E of bacterial acute Lymphadenitis?

A
  • The Lymph nodes are discrete enlarged and soft.

- The cut surface bulges out and is pink grey.

107
Q

What is the M/E of acute bacterial lymphadenitis?

A
  • L.N show large germinal centers containing numerous mitotic figures, sometimes a neutrophilic infiltrate & necrosis resulting in the formation of an abscess.
108
Q

What is the clinical examination of bacterial acute lymphadenitis?

A
  • They are discrete, enlarged, soft, painful and tender.
109
Q

What are the complications of bacterial acute lymphadenitis?

A

 Acute suppurative lymphadenitis

 Chronic non specific lymphadenitis

110
Q

What is example of viral acute lymphadenitis?

A
  • As in glandular fever which is presented by fever, sore throat, enlarged cervical lymph nodes.
111
Q

What is viral acute lymphadenitis misdiagnosed with?

A

lymphoma

112
Q

What are the types of chronic lymphadenitis?

A

A- Chronic non specific lymphadenitis

B- Chronic specific (granulomatous) lymphadenitis

113
Q

How does chronic non-specific lymphadenitis occur?

A
  • Occurs in lymph nodes draining foci of chronic non specific inflammation.
114
Q

What is the N/E of chronic non specific lymphadenitis?

A

 Affected nodes are matted, moderately enlarged and firm.

 Cut surface has a red tinge and is hemogenous.

115
Q

How does the reaction heal in chronic nonspecific lymphadenitis?

A

fibrosis

116
Q

Give an example for chronic specific granulomatous lymphadenitis.

A

infective granulomas

117
Q

What are the causes of lymph node enlargement?

A

1) Acute lymphadenitis
2) Chronic lymphadenitis

3) Hyperplastic lymphadenopathy:
 Follicular hyperplasia 
 Sinus histiocytosis.
 Nodes draining tumour
4) Histocytosis X: Due to proliferation of langerhan’s cells.
5) Lymphomas: either
 Hodgkin’s lymphoma
 Non Hodgkin's lymphoma
6) Secondaries: either from
 Carcinomatous 
 Sarcomatous
118
Q

What is the definition of splenomegaly?

A

enlargement of the spleen

119
Q

What is splenomegaly classified according to?

A

1- According to the rate of enlargement

2- According to the size

120
Q

What is splenomegaly classified into according to the rate of enlargement?

A

Acute and chronic

121
Q

What are the causes of acute splenomegaly?

A

Septicemia, Pyemia, Typhoid fever, Glandular fever (infectious mononucleosis).

122
Q

What are the causes of chronic splenomegaly?

A

Divided according to the etiology into:

1) Bacterial: Brucellosis, T.B., Syphilis.
2) Parasitic: Bilharziasis, Malaria, Hydatid, Leishmaniasis (kalazar)

3) Circulatory disturbances as Congestive splenomegaly, Infarction.
4) Hematological disorders as Extra medullery hemopoeisis, Hemolytic anemia, Polycythemia, Leukemia, Purpura, Hypersplenism

5) Lipid storage disorders as Gaucher’s disease, Niemenn pick disease, Hyper lipidemias.
6) Histocytosis X.
7) Amyloidosis and sarcoidosis

8) Tumors mostly lymphoma

123
Q

What are the types of splenomegaly according to size?

A

Massive splenomegaly (weight more than 1000 gm)

Moderate splenomegaly (weight 500-1000 gm)

Mild splenomegaly (weight <500 gm)

124
Q

What are the causes of massive splenomegaly?

A
 Chronic myeloproliferative disorders & chronic leukemia 
 Hairy cell leukemia
 Lymphomas
 Malaria & Gaucher disease
 Primary tumors of the spleen (rare)
125
Q

What are the causes of Moderate splenomegaly?

A
 Congestive splenomegaly
 Leukemias
 Autoimmune hemolytic anemia 
 Amyloidosis
 Niemann-Pick disease 
 Langerhans histiocytosis 
 Chronic splenitis
 Tuberculosis, sarcoidosis
126
Q

What are the causes of mild splenomegaly?

A

 Acute splenitis
 Acute splenic congestion
 Infectious mononucleosis
 Acute febrile disorders e.g. septicemia & SLE

127
Q

What is the definition of arteritis?

A
  • Inflammation of arteries
128
Q

What are the types of arteritis?

A

1- Infective

2- Non-infective

129
Q

What causes infective arteritis?

A
  • due to microorganisms e.g. (staph aureus). It may be:
    Acute as in arteries passing in area of acute inflammation or,Chronic as in arteries passing in area of chronic inflammation (endarteritis obliterans).
130
Q

What are the types of non-infective arteritis?

A
  • Polyarteritis nodosa.
  • Systemic lupus erythematosus.
  • Thromboangitis obliterans.
  • Giant cell arteritis.
131
Q

What is non infective arteritis mediated by?

A
  • These inflammatory and often necrotizing vascular lesions are usually mediated by immune mechanism (immune complex deposition).

“Type III hypersensitivity reaction”

132
Q

What is the definition of polyarteritis nodosa?

A
  • It is a necrotizing inflammation of small and medium sized arteries caused by immune complex hypersensitivity reaction. It is marked by destruction of arterial media and internal elastic lamina resulting in aneurysmal nodules.
  • Mostly affects kidney, heart, GIT, CNS and musculoskeletal vessels. “Biopsy is taken for diagnosis”
133
Q

What are the complications of polyarteritis nodosa?

A
  • Ischemia: It may be chronic due to fibrosis or acute due to thrombosis.
  • Rupture due to fibrinoid necrosis leading to heamorrhage. “Acute”
  • Aneurysms due to weak fibrosed media. “Chronic”
134
Q

What is the definition of systemic lupus erythrematous?

A
  • Multi-system disease, type III hypersensitivity (immune complex).

“Mainly affects females in middle age”

135
Q

What are the affected blood vessels in SLE?

A
  • Small arteries, arterioles or even venules are affected nearly all-over the body.
136
Q

What is the fate of SLE?

A
  • Death is usually due to:
    1. Hypertension
    2. Renal failure
137
Q

What is giant cell arteritis? (Temporal arteritis)

A
  • It seen in medium to large sized arteries with granuloma formation.

“Mainly affects males, especially in temporal artery”

138
Q

What is Thromboangitis obliterans? (Buerger’s disease)

A
  • It is an acute inflammation (followed by chronic) involving small to medium-sized arteries of the extremities extending to adjacent vein and nerve.
139
Q

What is the cause of Thromboangitis obliterans?

A
  • Hypersensitivity to tobacco products with hereditary predisposition.

“More in Jewish”

140
Q

What are The complications of Thromboangitis obliterans?

A
  • Ischemia which may lead to intermittent claudication (chronic ischemia) and gangrene (acute ischemia).

“Pain after walking for some time”

141
Q

What is the definition of atherosclerosis?

A
  • Chronic degenerative disease characterized by formation of intimal fibro- fatty plaques
142
Q

What is the most common arterial disease?

A
  • Atherosclerosis
143
Q

where is atherosclerosis more common?

A
  • More common in developed countries
144
Q

What is the pathogenesis of atherosclerosis?

A

1- Reaction to injury formulation

Injury (or dysfunction) of endothelium leads to…
• Entry of monocytes and lipids (hyperlipoproteinemia) to subendothelium.
• Platelet adhesion and aggregation.

2- Release of mitogenic factors from platelets and
macrophages…..proliferation and migration of smooth muscle fibers.

3- Monocytes and smooth muscle cells engulf lipid and
cause lipid deposition into the lesion.

4- Necrosis in the deeper part.

145
Q

What is the N/E of atherosclerosis?

A
  • Sites: Small, medium, and large arteries
  • Aorta, especially descending *Coronaries and cerebrals
  • Femoral , renal, superior mesenteric and internal carotids.
  • Uncomplicated atheroma: “unit lesion for atherosclerosis”
    disc-like patches. Color ranges from yellow to white according to relative amount of fat covered by glistening intima. more around the mouths of the branches.
  • Complicated atheroma: calcification, ulceration, thrombosis
146
Q

What is the M/E of atherosclerosis?

A
  • Intimal lesions:
    Subendothelial fibrous cap, formed of proliferated smooth muscle cells, foam cells and extra cellular matrix, Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam cells), necrotic debris and calcification.
  • Medial lesions:
    Internal elastic lamina: disrupted
    Media: atrophy “due to pressure”
    Vascularisation of plaque
  • Adventitia: lymphocytic infiltrate “to fight infection”
147
Q

What are the complications of atherosclerosis?

“ACUTE”

A

1- Narrowing of vascular lumen…chronic ischemia.

2- Superimposed thrombosis…acute ischemia.

3- Ulceration with liberation of fatty core … acute ischemia, athero emboli, DIC.

4- Pressure atrophy of the media with fibrosis….weakening of the wall …. Aneurysm.

5- Dystrophic calcification.

148
Q

What is the definition of aneurysms?

A
  • Localized abnormal dilatation of arterial wall forming a sac.
149
Q

What is the iteology of aneurysms?

A

 Due to weakening of the wall and/or increase of blood pressure.

 It may be true or false.

150
Q

What is the pathogenesis of aneurysms?

A
  • Two processes are responsible for aneurysm formation:
    1. Weakening of arterial wall which may be: “سديت”
    congenital: As Berry aneurysms of brain (cerebral arteries).
    traumatic: As arterio-venous fistula. “Like a bullet”

Inflammation: As polyarteritis nodosa, T.B. syphilis, emboli of subacute bacterial endocarditis, and bilharziasis.

Degenerative: As atheroma and intracerebral microaneurysm in hypertension.

  1. Stretching of the weakened wall: by increased pressure (hypertension)
151
Q

What are the types of aneurysms?

A
  • True & false
152
Q

What is the definition of true aneurysm?

A
  • The wall of the aneurysmal sac is part of the arterial wall.
153
Q

What is the definition of false aneurysm?

A
  • The wall of the sac is not the vessel wall.
154
Q

What is the shape of true aneurysm?

A
  • It may be saccular or fusiform.
155
Q

What are examples of true aneurysm?

A

❖ Syphilitic aneurysm of thoracic aorta: It may be saccular or fusiform.

❖ Atherosclerotic aneurysm of abdominal “weaker than thoracic” aorta: It is fusiform.

156
Q

What are examples of false aneurysm?

A
  • It may be of fibrous tissue after traumatic rupture of artery and organization of the hematoma, or arterio-venous fistula.
157
Q

What are the complications of aneurysm?

A

1- Pressure on surrounding: More with syphilitic and produce superior mediastinal syndrome manifested by dyspnea, dysphagia and hoarseness of voice.

2- Rupture: More with atheromatous (internal heamorrhage)

3- Thrombosis and organization and may be embolization.

158
Q

What is the site of dissecting aneurysm?

A
  • Occurs only in the aorta with splitting of the media into two parts inner and outer and in between blood accumulates (producing 2 telescoped tubes).
159
Q

What is the cause of dissecting aneurysm?

A
  • It is due to medial damage by Erdheim’s medial necrosis, Marfan’s syndrome and may be atherosclerosis.
160
Q

What is the pathogenesis of dissecting aneurysm?

A

Weakness of the aortic media.
1- Blood enters the media either from tear in the sliding intima over a weak loose media.

2- Due to rupture of unsupported vasa vasorum.

3- The blood accumulates and splits the weak media into outer and inner layers forming the walls of the aneurysm.

161
Q

What is the fate of dissecting aneurysm?

A

1- Healing may occur either by clotting and organization of the blood in the media or rupture into the lumen of Aorta.

2- Rupture of the aneurysm with fatal hemorrhage.

3- Extension into the aortic branches and may narrow their opening leading to ischemia.

162
Q

What are the types of aortic aneurysms?

“ASD”

A

1- Atheromatous aneurysms: Commonest, occur in descending abdominal aorta below the level of renal artery, It is fusiform.

2- Syphilitic due to diffuse syphilitic lesions in tertiary syphilis: It occurs in arch of aorta and may be saccular or fusiform.

3- Dissecting.

163
Q

What are the types of cerebral aneurysms?

“My Coin”

A

1- Congenital berry aneurysms at circle of Willis (small, multiple):

  • Occur in the circle of Willis at sites of medial weakness at the bifurcations.
  • They are the most common cause of subarachnoid hemorrhage.

2- Intra-cerebral micro-aneurysms of benign hypertension.

3- Mycotic aneurysms due to emboli of subacute bacterial endocarditis.

4- Atheromatous.

164
Q

What is the definition of varicose veins?

A
  • It is dilatation, elongation, thickening and tortousity of veins.
165
Q

What are the sites of varicose Viens?

A

1- Superficial veins of the lower limbs (Long saphenous vein): in persons who spend much of their time standing.

2- Varices of the esophagus:

  • Veins of lower 1/3 oesophagus and cardia of the stomach.
  • Found in portal hypertension as in liver cirrhosis or bilharzial fibrosis.

3- Hemorrhoids: varices of the internal or external hemorrhoidal plexus of the rectum (piles )

4- Varicocele: varices of the pampiniform plexus of the spermatic cord

5- Caput Medusa: around the umbilicus.

166
Q

What is the pathogenesis of varicose veins?

A

Is divided into Predisposing & exciting factors

167
Q

What are the predisposing factors for varicose veins?

A
  • Congenital weakening of veins or valves.

- Familial tendency.

168
Q

What are the exciting factors for varicose veins?

A
  • The increased venous pressure leads to stretching of the venous wall.

This may be due to either:
1- Prolonged standing (effect of gravity) as in police soldiers: It affects long saphenous vein.

2- Chronic constipation and straining at stool: It leads to piles

3- Obstruction of venous return: As in cases of liver cirrhosis, bilharzial fibrosis, pressure by pregnant uterus, enlarged prostate, cancer rectum ….. Etc.

169
Q

What are the complications of varicose veins?

A
  • Local chronic venous congestion and persistent edema in limbs and secondary ischemic skin changes, including stasis dermatitis and ulcerations.
  • Hemorrhage: Haematemesis and melena from esophageal varices.
  • Thrombosis and embolism.
  • Varicose ulcers which are premalignant (gives rise to squamous cell carciroma).
    ❖ It occurs in the lower inner part of the leg above medial malleolus.
  • Inflammations leading to septic thrombophilibitis, septic emboli and pyemia.