dr.

Jacky J

ACIDS BASE BALANCE
 Acids are H+ donors.
 Bases are H+ acceptors, or give up OH- in
solution.
 Acids and bases can be:
• Strong – dissociate completely in
solution
 HCl, NaOH
• Weak – dissociate only partially in
solution
 Lactic acid, carbonic acid

2

 Homeostasis of pH is tightly controlled
 Extracellular fluid = 7.4
 Blood = 7.35 – 7.45
 < 6.8 or > 8.0 death occurs
 Acidosis (acidemia) below 7.35
 Alkalosis (alkalemia) above 7.45

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 Acids take in with foods  Acids produced by metabolism of lipids and proteins  Cellular metabolism produces CO2.  CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3- 4 .

1. Buffer systems Take up H+ or release H+ as conditions change Buffer pairs – weak acid and a base Exchange a strong acid or base for a weak one Results in a much smaller pH change 5 .

: H2CO3 HCl + NaHCO3 ↔ H2CO3 + NaCl NaOH + H2CO3 ↔ NaHCO3 + H2O 6 . Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)  Maintain a 20:1 ratio : HCO3.

↔ H2PO4-  OH.↔ H2O + H2PO42- 7 . + H2PO4. Major intracellular buffer  H+ + HPO42.

work in blood and ISF  Carboxyl group gives up H+  Amino Group accepts H+  Side chains that can buffer H+ are present on 27 amino acids. 8 . Includes hemoglobin.

but only works with volatile acids  Doesn’t affect fixed acids like lactic acid  CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-  Body pH can be adjusted by changing rate and depth of breathing 9 . Exhalation of carbon dioxide  Powerful.

pH balance fails 10 . Can eliminate large amounts of acid  Can also excrete base  Can conserve and produce bicarb ions  Most effective regulator of pH  If kidneys fail.

 Buffers function almost instantaneously  Respiratory mechanisms take several minutes to hours  Renal mechanisms may take several hours to days 11 .

12 .

N.Causes 3.Fate 7.Sites 6. .Definition 2.Composition 4.1.Types 5.B.

The formation of a solid mass (compact mass) .Composed of the blood elements. . .During life.In circulating blood.Thrombosis is: .In a blood vessel or heart. . .

There are 3 major factors which predispose to thrombosis (Virchow’s triad) 1.Slowing & turbulence of blood flow 3.Endothelial damage 2.Changes in blood composition .

Virchow triad in thrombosis .

Endothelial damage: . The injured endothelium becomes swollen with rough surface.This is the most important factor in thrombus formation. .Endothelial damage may be: Mechanical. inflammatory. 2. . or degenerative.Staisis: There is slowing of blood flow in the heart as in mitral stenosis and in blood vessels as in varicose veins.1.

.Changes in composition of blood: . .3. as in leukaemia → ↑ viscosity of blood → staisis → thrombosis. (polythycaemia) → ↑ viscosity of blood → staisis → thrombosis. .↑ W.C.B.B.Cs. after operations.g.↑ platelets e.↑ fibrinogen as in pregnancy.↑ R. .

.Platelets leave the blood stream.Soon. .They form laminae. fibrin accumulates around them with red and white blood cells. agglutinate and adhere to the damaged endothelium. .. which are arranged vertical to the blood stream and called lines of Zhan.

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 According to the color & composition of thrombi  According to the site of thrombus:  According to presence or absence of bacteria: .

3.Pale thrombus: formed only of platelets and fibrin.According to the color & composition of thrombi: 1. .Red thrombus: formed mainly of red cells and fibrin. 2.Mixed thrombus: containing all blood elements.

4.According to the site of thrombus: 1.Arterial thrombus: found in atherosclerosis and aneurysm.Capillary thrombi . 3. 2.Venous thrombus (the most common): formed in veins as in varicose veins and after major abdominal operations. either in the heart chambers called mural thrombus or on the heart valves called vegetations.Cardiac thrombus: found in the heart.

.Septic thrombus: containing pyogenic bacteria.Aseptic thrombi: without bacteria. 2.According to presence or absence of bacteria: 1.

Thrombus Clot 1.Friable and dry 3.Pale. pale red or red 4.Occurs in stagnant blood blood during live during life or after death 2.Loosely attached 3.No lines of Zhan .Soft and moist 4.May show lines of Zhan 5.Red and yellow 5.Occurs in circulating 1.Firmly attached 2.

DEFINITION CAUSES & TYPES .

.● Definition Embolus: An insoluble (solid. Embolism: Is the process of impaction of the embolus in a narrow vessel. liquid or gaseous) mass circulating in the blood stream.

3.Detached thrombi (thrombo-embolism) 2. 5.Fat embolism: The fat of the bone marrow reaches the circulation after fracture of bones. . 6.g.Tumor emboli: groups of tumour cells penetrate the wall of blood vessels especially veins.● Causes & Types: 1.Amniotic fluid embolism. 4. bilharzial worms and ova.Air embolism: due to injury of neck & chest veins.Parasitic emboli: e.

e.the embolus coming with venous return to be impacted in lung causing pulmonary embolism but instead of that it will pass from right side of heart to its left side through septal defect then pass to systemic circulation.Portal embolism 3.Pulmonary embolism 2. Sites of impaction: 1.Systemic embolism 4. .Paradoxical embolism i.

Nature of the embolus (septic or aseptic). . Effects depends upon: 1.Size of the embolus.State of the collateral circulation in the affected site. 3. 2.

Size of the embolus. 2.State of the collateral circulation in the affected site.Nature of the embolus (septic or aseptic). 3. Effects depends upon: 1.  Effects of pulmonary embolism: Big embolus Medium sized embolus Small embolus .

3.Size of the embolus.State of the collateral circulation in the affected site.Nature of the embolus (septic or aseptic).  Effects of pulmonary embolism: Big embolus Medium sized embolus Small embolus Acute Rt sided Heart failure Sudden death . Effects depends upon: 1. 2.

 Effects depends upon: 1.State of the collateral circulation in the affected site.Nature of the embolus (septic or aseptic). 3. 2.  Effects of pulmonary embolism: Big embolus Medium sized embolus Small embolus Acute Rt sided healthy lung Heart failure no effect Sudden death .Size of the embolus.

 Effects of pulmonary embolism: Big embolus Medium sized embolus Small embolus Acute Rt sided healthy lung congested lung Heart failure no effect lung infarction Sudden death .Size of the embolus. Effects depends upon: 1.State of the collateral circulation in the affected site. 3.Nature of the embolus (septic or aseptic). 2.

Nature of the embolus (septic or aseptic). 2. 3.  Effects of pulmonary embolism: Big embolus Medium sized embolus Small embolus Acute Rt sided healthy lung congested lung no effect Heart failure no effect lung infarction Sudden death . Effects depends upon: 1.Size of the embolus.State of the collateral circulation in the affected site.

In criminal abortion → air may pass into uterine veins 4. . but 50-100 cc. . 2. the high pressure increases the amount of gasses dissolved in the blood of the divers. Rare and may result from: 1.Injury to the large neck veins.Caisson’s disease (decompression sickness): .During cardiothoracic surgery → air may enter veins 3.Small amount of air is harmless. nitrogen form emboli in the blood vessels. interferes with cardiac contraction and causes acute heart failure. gases esp. .In deep dives.If decompression is done rapidly. Air is sucked by the negative pressure in the thorax.

(2) Trauma to adipose tissue (infl. or burns). (3) Trauma to a grossly fatty liver. (4) Major surgery. . Rare condition  Causes include: (1) Bone fractures and crush limb injuries.

Definition: Deficient arterial blood supply to an organ or tissue due to partial or complete occlusion of its artery.Chronic ischemia (partial or gradual ischemia) .Acute ischemia (complete or sudden ischemia) 2. Types: Ischemia may be either: 1.

g. Effects: depends on the efficiency of collaterals: ● Sudden occlusion of end arteries or arteries with poor collaterals → infarction or gangrene. 4.Twisting of the pedicle of a movable organ e.Arterial spasm as in ergot poisoning.Thrombosis or embolism. intestinal loop. ● Sudden occlusion of arteries with efficient collaterals may not cause tissue damage. (most common) 2.Causes: Sudden complete arterial occlusion by: 1.Surgical ligature of the artery. . 3.

.Pressure on the artery by enlarged lymph node. atrophy followed by fibrosis. tumor .. . 2. 3.Causes: Incomplete arterial occlusion by: 1.Atherosclerosis. etc. ● With efficient collaterals no tissue damage occurs. intermittent claudication..cellular degeneration.pain on exercise: angina pectoris.End arteritis oblitrans as in chronic inflammation. . Effects: depends on the efficiency of collaterals: ● With inefficient collaterals: .

Definition Causes Types Pathological features Fate Examples .

Definition An infarct is an area of coagulative necrosis (liquefactive in the brain) caused by sudden ischemia. .

Causes 1. testes or ovaries. .Strangulation or twisting of an organ as in loops of intestine.Thrombosis that may occur inside diseased arteries. 3. 2.Embolism.

liver and intestine.The red color is due to hge in the substance of the infarct. .Liquefactive infarcts: .Types of infarcts: 1.Occur in vascular organs as the lung. heart and spleen.Red infarcts (hemorrhagic): .Occur in the brain and spinal cord.Pale infarcts: . 3. . 2.Are more common and occur in firm and less vascular organs as the kidney.

 Site: The infarct is subcapsular.● Gross picture:  Shape: The infarct is wedge shaped or pyramidal. red and pale. raised when recent due to edema and depressed when healed due to fibrosis. .  It is surrounded by a red zone of inflammatory hyperemia.  Size: depends on the size of the occluded vessel.  Color: Infarcts are of two types. The base is directed towards the surface of the organ.

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 Next: structural details are lost but the outlines are preserved. .  Lastly: necrotic tissue appears as granular pink debris.  The infarct is surrounded by a red zone of inflammatory hyperemia.● Microscopic picture:  Early: the cells show various post-necrotic changes.

. ESR  Elevation of certain serum enzymes as transaminase in myocardial infarction.● General reactions: Infarcts are associated with general reactions in the form of:  Fever  Leucocytosis  Increased sedimentation rate.

Large infarct: Gets surrounded by a fibrous capsule and its substance may show dystrophic calcification.Small infarct: Necrotic tissues are removed by macrophages. . granulation tissue fills the defect followed by fibrosis.

Definition
Causes
Types
Effects
Haemostasis

Definition:
Escape of blood outside the blood vessels
or cardiac chambers.
(loss of blood from circulation)

1- Trauma: involving the heart and blood vessels.
2- Diseases of blood vessels:
a) Hypertension.
b) Varicose veins: as piles.
c) Degeneration: as atheroma and aneurysm.
d) Infection: as tuberculosis.
e) Malignant cells invading blood vessels.
3- Haemorrhagic blood diseases: as haemophilia,
purpura, leukaemia and scurvy.

I. Internal haemorrhage III. Interstitial haemorrhage . External haemorrhage II.

4.Hematemesis: Vomiting of blood.Bleeding per rectum: passage of red blood with stool 6.Metrorrhagia: Irregular uterine bleeding unrelated to menses 9.Escape of blood outside the body. 7. 5.Melena: Presence of dark digested blood in stools.Menorrhagia: Excessive or prolonged menstrual bleedin 8.Hematuria: Blood in urine.Epistaxis: Bleeding from the nose. 3. 2.Bleeding from skin .Hemoptysis: Coughing of blood. 1.

Hematocele: Hge.Bleeding into body cavities. 4.Hemothorax: Hge into the pleural sac. into a joint cavity. into pericardial sa 3. into tunica vaginalis sac.Hemoperitoneum: Hge. into peritoneal sac. 2.Hemopericardium: Hge. 5.Hemoarthrosis: Hge. 1. .

1.Petechial haemorrhage: escape of small amount of blood of capillary origin → small spots of haemorrhage.Hematoma: escape of large amount of blood causing a swelling. 2. 3. .Ecchymosis: escape of moderate amount of blood → a bigger patch of haemorrhage.Bleeding into interstitial tissue spaces.

.Then.BiIiverdin gives the area a green color but is soon absorbed in the blood.Interstitial haemorrhage is at first dark red (arterial blood) or bluish (venous blood). .The hemosiderin left gives the area a brown color and is gradually removed by macrophages. . hemoglobin breaks down into biliverdin and hemosiderin. so the color changes to yellow and gradually fades away. ..

Causes microcytic hypochromic anemia. ● Repeated small amounts (chronic hge): . .reflex ↑ heart rate 2.) → Is compensated by: 1. .g. in piles and peptic ulcers.withdrawal of tissue fluids into the blood.reflex vasoconstriction in the skin.M. 5.Proteins are added from the liver. ● Massive amount: → hemorrhagic shock.e. muscles & GIT 3.blood cells are added by the hyperplastic B. 4.● Small amount: No effect. ● Moderate amount: (< 750 ml.

When severe. diarrhea or increases in insensible water losses. Children. whereas dehydration denotes loss of plasma-free water disproportionate to the loss of sodium. Dehydration  Dehydration or volume depletion is classified as mild. . especially those younger than 4 years old. moderate or severe based on how much body fluid is lost. Volume depletion denotes lessening of the total intravascular plasma. Potassium and other electrolytes including buffers líke phosphates need to be considered. dehydration is a life-threatening emergency. are more susceptible to volume depletion as a result of vomiting.

or both.  Lethargic or comatose. concentrated urine is dark yellow.  Low or no urine output. .  Markedly sunken fontanelles (the soft spot on the top of the head in a baby).Dehydration can be caused by losing too much fluid. Dehydration is classified as mild. not drinking enough water or fluids.  Not producing tears. Vomiting and diarrhea are common causes.  Dizziness.  Sunken eyes. moderate or severe based on how much body's fluid is lost. Symtons include:  Dry or sticky mouth.

However.  Volume depletion denotes lessening of the total intravascular plasma. and dehydration can exist with or without volume depletion . characterized by vomiting and diarrhea. other causes of dehydration may include poor oral intake due to diseases such as stomatitis. The distinction is important because volume depletion can exist with or without dehydration. Pathophysiology  Pediatric dehydration is frequently the result of gastroenteritis. insensible losses due to fever. or osmotic diuresis from uncontrolled diabetes mellitus. whereas dehydration denotes loss of plasma-free water disproportionate to the loss of sodium.

but sodium and other solutes are not. Free water is replenished. An example is a child with diarrhea who has been given tap water to replete diarrheal losses. Volume depletion can be concurrent with hyponatremia. This is characterized by plasma volume contraction with free water excess. .

If intravascular free water excess is not corrected during volume replenishment. the shift of free water to the intracellular fluid compartment may cause cerebral edema. The degree of volume depletion may be clinically overestimated. baking soda. . but free water has not. boiled milk. Serum sodium levels less than 120 mEq/L may result in seizures. plasma volume contracts with disproportionate further free water loss. An example is the child with diarrhea whose fluid losses have been replenished with hypertonic soup. Volume has been restored. or improperly diluted infant formula. With true dehydration. In hyponatremic volume depletion. the person may appear more ill clinically than fluid losses indicate.

coma. cerebral shrinkage occurs instead of cerebral edema. . hypernatremic volume depletion may result in serious central nervous system (CNS) effects as a result of structural changes in central neurons. at least a 10% volume deficit exists with hypernatremic volume depletion. Usually. the patient may appear less ill clinically than fluid losses indicate. The degree of volume depletion may be underestimated. For this reason. volume restoration must be performed gradually over 24 hours or more. As in hyponatremia. Gradual restoration prevents a rapid shift of fluid across the blood-brain barrier and into the intracellular fluid compartment. In hypernatremic volume depletion. This may result in intracerebral hemorrhage. seizures. and death. However.