NURSING REVISION NOTES 2 PATHO II UP.pptx

1. REVISION
PATHOPHYSIOLOGY II

2. CONT
• Manifestations of altered respiratory function.
• Hypoxia. An inadequate delivery of oxygen to satisfy the
metabolic requirements of the organs and cells of the body.
• Hypoxemia. Reduced levels of oxygen in the blood (decrease
in PaOa) that causes cyanosis, clubbing and polycythemia.
• Polycythemia. Increased release of erythropoietin due to
hypoxia.
– Causes increased production of red blood cells.
– In chronic obstructive pulmonary disease, leads to
increased blood viscosity, further impeding oxygenation
pf the tissues.

3. CONT
• Hypercapnia.The retention of carbon dioxide (PaCOa > 44 mm Hg).
Associated with hypoventilation (emphysema).
– Chemoreceptor stimulates the respiratory center to increase
respirations.
– Chronic hypercapnia depress the receptiveness of these chemo
receptors, leaving the stimulus for breathing to depend on peripheral
chemo receptors.
• Hypocapnia. PaC02< 30 mm Hg. Associated with hyperventilation that
removes carbon dioxide.
• Compensated respiratory acidosis. A high PCOa is counteracted by
renal retention of bicarbonate, leading to a pH that is near normal.
• Cyanosis. Insufficient oxygenation of Hgb in the lungs, manifested by a
blush discoration of the face, lips, nasolabial folds, earlobes and palate.
• Clubbing. Bulbous appearance of the fingers and toes. My be due to
hypoxia.

4. Acute Obstructive Airway Disease.
• Acute bronchitis.
• A common condition caused by infection and inhalants.
• Pathogenesis.
– Inflammation of the mucosal lining of the tracheobronchial tree
due to viral or bacterial infection.
– Increased secretion of the mucus, bronchial swelling, and
dysfunction of the cilia lead to increased resistance to expiratory
airflow, causing air trapping on expiration.
• Clinical manifestations.
• Subjective findings.
– Recent upper respiratory infection.
– Chronic lung disease.
– Smoking.

5. CONT
– Exposure to respiratory irritants.
– Mucopurulent productive congestion.
• Objective findings.
– Vital signs. Fever below 101 ° F.
– Sputum.
• Mucoid (vital).
• Mucopulent (bacterial).
– Lung. Wheezing.
Asthma.
• An episodic disorder characterized by recurrent paroxysm of wheezing and dyspnea not
attributable to other disease.

6. CONT
• Pathogenesis.
– Response is initiated by release of chemical mediators in an IgE mast cell
interaction.
– This results in increased bronchial secretion from goblet cells and in mucosal
swelling and bronchospasm.
– There are constriction of the air passages and air trapping.
• Extrinsic asthma. Affects children with a family history of allergies. Attacks
usually disappear or disease in severity and frequency as the person matures.
• Intrinsic asthma. Affects adults. Attacks are usually related to a respiratory tract
infection, exercise, or emotion. Allergy can play a part.

7. CONT
• Clinical manifestations.
• Subjective findings.
– Childhood asthma
– Inhalation of irritants.
– Respiratory infection.
– Positive family history/childhood asthma.
– Tightness in chest.
– Psychogenic factors.
– Dyspnea.
– Fatigue due to increased work of breathing.

8. CONT
• Objective findings.
• Vital signs.
– Tachypnea.
– Pulses paradoxis. Measures bronchospasm. The amount of pooling
of blood in the pulmonary vessels increases, causing the amplitude
of the arterial pulse to be exaggerated. On inspiration, arterial blood
pressure falls more than 10 mm Hg.
• Lungs. Expiratory wheeze, progressing to inspiratory and expiratory
wheeze. Production of a large amount of thick yellow or green sputum.
• Course.
– The lungs usually return to normal once the attack ha subsided and
the precipitating factors have cleared.

9. CONT
– A significant relationship exists between a asthma and
the future development of chronic obstructive lung
disease.
– Chronic Obstructive pulmonary Disease. Chronic
disease differs from acute disease in that lung tissues
do not return to normal in between exacerbations.
Pulmonary damage slowly progresses due to chronic
obstruction to airflow.

10. Chronic Obstructive Pulmonary Disease (COPD)
Bronchietasis.
• A disease of bronchi and bronchioles associated with chronic infection and
inflammation of
these passage ways.

11. CONT
• Pathogenesis.
– There is irreversible dilatation of the bronchial tree.
– The bronchial mucosa is replaced by fibrous scar tissue,
which leads to the destruction of the bronchi and permanent
dilatation of the bronchi and bronchioles.
• Clinical manifestations.
• Subjective findings.
– Childhood onset.
– An initiating event such as pneumonia or bronchitis.
– Cough.
– Symptoms of infection.

12. CONT
• Objective findings.
– Production of large amounts of mucopurulent sputum and,
occasionally, hemoptysis.
Cyst fibrosis (mucoviscidosis).
• A hereditary disorder which affects children and in which
large quantities of viscous material are secreted.
• Pathogenesis.
• The disorder affects the sweat glands, bronchi, pancreas, and
mucous - secreting glands of the small intestine.
• Secretions of tenacious mucus in the airways causes airway
obstruction that in turn causes many respiratory conditions,

13. CONT
• Clinical manifestations
• Relate to the inability to handle excessive secretions.
• To diagnose the disease, at least three of the following four criteria
are essential.
– Increased sodium and chloride in the sweat.
– Deficient pancreatic enzymes in the gastrointestinal secretions.
– Chronic pulmonary infections, especially with opportunistic
organisms such as pseudomonas aeruginosa and staphylococcus
aureus.
– Family history of the problem.
• The prognosis is variable, with survival past age 20 increasing.
Gastrointestinal and pulmonary problems are encountered
throughout life.

14. CONT
Chronic bronchitis.
• Continued bronchial inflammation with progressive increase in productive
cough dyspnea not attributable to specific causes.
• Pathogenesis.
– The bronchial mucosa becomes thickened and rigid due to vasodilatation,
congestion, and edema.
– Excessive secretion of mucus, together with narrowing of the passageways
due to inflammation, causes obstruction to maximal expiration and later to
maximal inspiration.

15. CONT
• Clinical manifestations.
• Subjective findings.
– Cough (bronchial irritation) with copious sputum production.
– Recurrent chest infections, initially in winter but becoming
perennial.
– Cigarette smoking.
– Generally overweight.
• Objective findings.
– Skin. Marked cyanosis and edema; 'blue bloaters'.
– Lungs.
• Mild degrees of hyperinflation; rounded diaphragm.
• Marked hypercapnia.
• Severe hypoxemia (decreased P02, increased PC02).
• Percussion note resonant,
• Wheezes.

16. CONT
• Heart.
– Cor pulmonale (right-sided heart failure due to advanced
obstructive disease).
– Jugular venous distension.
– Cardiac enlargement.
– Peripheral edema.
• Bronchitis is usually associated with some degree of emphysema.
Pulmonary emphysema.
• A common, chronic pulmonary disease usually classified with
chronic bronchitis.
• Pathogenesis.
– Emphysema is characterized by a permanent enlargement of
the acinus (portion distal to the terminal bronchiole).

17. CONT
– Air becomes trapped in the sacs to edema and bronchial spasm.
– The over distention causes rupture and destruction of septal
tissue.
– The lungs become more distensible with loss of elastic recoil.Air
trapping causes an increase in airway size on inspiration and
collapse of the small airways on expiration. The gas-exchanging
surface is reduced.
• Types.
– Centrilobular emphysema. Dilation of the terminal airways.
– Pan lobular emphysema. Dilation of the alveolar sacs.
• Clinical manifestations.
• Subjective findings.;
– Cigarette smoking.
– Exposure to chemical irritants or air pollution.
– Chronic respiratory infections.
– Exertional dyspnea over a long period of time.

18. CONT
– Cough with small amount of sputum production.
– Wheezing or tightness of chest.
• Objective findings.
– Vital signs. Tachyphea at rest or mild exertion.
– Skin. Cyanosis with chronic bronchitis; flushed with emphysema
('pink puffer').
– Mouth. Possible cyanosis of lips; pursing of lips to exhale.
– Chest and lungs. Barrel chest with retraction of interspaces during
inspiration and bulging with expiration;
• decreased vesicular breath sounds;
• prolonged expiratory phase; hyperrsonance;
• decreased tactile fremitus; low, flat diaphragm; no change in
diaphragmatic excursion.
• Diagnostic test. Pulmonary function. Prolonged FEV; Decreased vital
capacity.

19. RESTRICTIVE ALTERATIONS
• Restrictive disease causes a decrease in total lung capacity and
vital capacity.
• There is difficulty with the respiratory phase of respiration.

20. Disorders of the lung Parenchyma.
• Atelectasis.
– A common, acute, restrictive disease of the lung parenchyma that involves
collapse of a previously expanded lung, or incomplete expansion at birth.
– Compression atelectasis.
• Compression of lung tissue from a source outside the alveoli.
• Examples;
• Pneumothorax,
• Pleural effusion,
• Tumors within the thorax.

21. Illustration

22. Illustration

23. Illustration

24. CONT
• Absorption atelectasis.
– Absorption of gas from the alveoli, causing the lung to collapse.
– Secretions in the bronchi and bronchioles obstruct these airways, preventing the
flow of air to the alveoli.
• Pathogenesis.
– Obstruction of bronchioles;
– Shrunken, airless alveoli;
– Reduced compliance; or right-to-left shunting, causing hypoxia.

25. Illustration

26. Illustration

27. Illustration

28. Illustration

29. Clinical manifestations
– Include;-
• Dyspnea,
• Tachycardia,
• Cough,
• Fever,
• Decreased chest wall expansion,
• Hypoxemia.

30. CONT
• Diagnostic.
– Blood gases show hypoxemia,
– Hypercapnia,
– Decreased pH.
– Chest film-Shows evidence of atelectasis.

31. Infectious disease of the respiratory tract.
• Upper respiratory tract infection.
– Upper respiratory tract is exposed to a wide variety of pathogens in its attempt to
filter the air.
– Trapped pathogens may proliferate if there is;-
• Decreased host resistance or
• Highly virulent bacteria or virus.

32. Clinical manifestations
• Inflammation of involved passageway, leading to;-
– Edema,
– Congestion,
– Necrosis of the structures.
• Lower respiratory tract infection
– Can be caused by any of the pathogens that affect the upper
respiratory tract.

33. Bacterial pneumonia
• Pneumococcal pneumonia ( streptococcus pneumoniae.).
• A common bacterial infection of the lung,
• Responsible for 30 to 80 percent of community – acquired pneumonias.
• Risk factors;-
– Malnutrition,
– Alcoholism,
– Aging

34. Illustration

35. Illustration

36. Pathogenesis.
• Acute inflammatory response leads to consolidation
(leukocytes and fibrin) of the involved area.
• Involved alveoli become airless,
• Causing perfusion with poor ventilation, but rarely cause
severe hypoxia.

37. Four steps of progression of the inflammation exudates.
– Hyperemia. Alveolar spaces become engorged with fluid and blood.
– Red hepatization. The involved lung becomes red and granular (liver like) from
the influx of red blood cells, fibrin, and polymorphonuclear leukocytes.
– Gray hepatization. The lung tissue becomes solid and grayish as leukocytes
consolidate in the alveoli.
– Resolution. Excudate is lysed and reaborded by neutrophilis and macrophages.
Lung structure and function are restored.

38. Clinical manifestations
– Fever,
– Cough,
– Pleuritic chest pain,
– Production of rusty-colored or blood-streaked. Sputum.
• Effects on the elderly.
– Bacterial pneumonia may be life threatening.
– Classic symptoms vary and may manifest themselves as
lethargy or confusion.

39. Mycoplasmal pneumonia
– Is a self-limiting disease that is a common cause of respiratory tract infections.
The mycoplasmal organism is smaller than bacteria but is not classified as a virus.
• Viral pneumonia
– Is usually mild and self-limiting in adults but may be rapidly proliferative and be
fatal in children (usually under age 2).

40. Tuberculosis.
• Caused by Mycobacterium tuberculosis (an acid-fast bacillus)
and is transmitted by droplets from persons with active
tuberculosis.
• It is more common in malnourished and aged persons.

41. Pathogenesis
– Bacterial invasion leads to;-
• Scarring,
• Reduced compliance,
• Reduced lung function.

42. Clinical manifestations
– Evening fever with night sweat,
– Cough with sputum production,
– Malaise,
– Weight loss
– Hemoptysis.
– The disease may spread, involving other structures meninges, kidneys, bones.
• Diagnostic tests;
– Chest film findings
– Positive skin test.

43. Aspiration pneumonia
.
• Inhalation of gastric contents, food. Water or blood into the
tracheobronchial system.
• Most frequently occurs with near-drowning.

44. Pathogenesis.
• Pneumonia results when the material is propelled into the alveolar system.
• Chemical irritation from the aspirant leads to;-
– Bronchospasm,
– Necrosis,
– Fibrosis of airways.

45. Clinical manifestations
• Abrupt signs of bronchospasm,
• Dyspnea,
• Tachycardia,
• Tachypnea,
• Cyanosis.

46. Illustration

47. Pulmonary edema
• Accumulation of serous or serosanguinous fluid in the interstitial
spaces and alveoli of the lungs.
• Pathogenesis.
• Edema occurs in two stages.
– Interstitial edema. Fluid accumulates in the peri-bronchial and
perivascular spaces with increased lymphatic flow.
– Alveolar edema. Blood plasma fills the alveoli as interstitial
hydrostatic pressure exceeds the colloid osmotic pressure of
the pulmonary arteries.
– Lungs lose compliance, greatly increasing the elastic work of
breathing.

48. CONT
• Clinical manifestations
• May initially include wheezing, paroxysmal
nocturnal dyspnea (PND) , and dry cough.
• The condition may progress to dyspnea,
orthopnea,wheezing, moist rales, and rapid
shallow with pink-tinged sputum
production.

49. Traumatic Injuries of the chest wall.
• Common results of automobile accidents and other injuries.
• Simple rib fracture.
– Pathogenesis.
• Aspiratory pain causes voluntary splinting, which restricts total volume and
increases respiratory rate.
• Chest strapping further reduces compliance, and narcotics may depress the
respiratory drive and cough reflex.
• Elderly people with underlying disease are at risk for atelectasis, pneumonia,
or respiratory failure.

50. Fracture of several ribs.
– Pathogenesis.
• There is instability of the involved area of the chest wall.
• As the chest inspires, intra-thoracid pressures is lowered.
– The area of the chest wall is sucked in.
– The under lying lung tissue does not expand, impairing
gas exchange and reducing compliance.
• During expiration, the chest wall may expand as intra-
thoracic pressure increases, creating a paradoxic movement
(fluid chest).

51. Pleura Disorders
• Pleural effusion.
– Accumulation of excess fluid in the pleural cavity, resulting from trauma or
disease.

52. Illustration

53. Illustration

54. Illustration

55. Illustration

56. Related terminology
• Transudate.
– Accumulation of fluid due to a rise in pulmonary venous pressure, hypoproteinemia,
or pressure from a tumor on the vena cava.
• Hydrothorax. The accumulation of pleural transudates.
• Empyema. Effusion contains purulent material.
• Fibro thorax. Fibrous of the lung and chest wall.
• Hemothorax. Frank blood in the pleural fluid ( trauma).
• Excudate.
– Fluid that has a higher specific gravity and protein content.

57. Illustration

58. Pathogenesis.
– Accumulation of fluid in the pleural space secondary to altered
hydrostatic or oncotic forces.
• Clinical manifestations
– Unequal chest expansion,
– Dullness
– Reduced breath sounds,
– Chest discomfort,
– Dyspnea of large effusion.

59. Pneumothorax.
• Air in the pleural space from an opening in the;-
– Chest wall (through parietal pleura)
– From the lungs ( through the visceral pleura).
• Pathogenesis.
– Pressure in the potential pleural space is normally lower than intra-alveolar
pressure.
– A break in the integrity of the pleura causes air to rush to the area of lowest
pressure, the pleura space
– A portion of the lung collapses.

60. Illustration

61. Illustration

62. Illustration

63. Spontaneous pneumothorax
– A sudden pneumothorax that occurs when there is a
communication between the alveoli, through the parietal
pleura to the pleural space.
– Air is released into the pleural space (I,e., a ruptured bled
indicates a client with emphysema.

64. Tension pneumothorax
• A progressive build-up of air in the pleural space, causing a life-threatening
condition.
• The lung collapses, with displacement of the mediastinum.
• Clinical manifestations
– Dyspnea
– Chest pain,
– Tracheal deviation with a mediastinal shift toward the unaffected side,
– Unequal chest expansion,
– Reduced breath sounds on affected side.

65. Illustration

66. Pathogenetic Process of Arteries.
• Atherosclerosis.
• Atherosclerosis is a disease affecting the smooth muscle of the inner; layer of the
large-and medium-sized arteries.
• It impedes arterial blood flow to the affected extremity.
• Chronic occlusive disease due to atherosclerosis is called atherosclerosis obliterans.

67. Illustration

68. Illustration

69. Illustration

70. Illustration

71. Illustration

72. Illustration

73. CONT
• Pathogenesis.
• A fatty streak composed of lipid material is deposited on the
intima of arteries.
• The lesion progresses to form an atheroma or an atheromatous
plaque composed of fatty material, collagen fibers, and
connective tissue.
• It may thrombose and hemorrhage or combine with other
atheroms to form a large mass.
• Occluding or partially occluding arterial blood flow.
Atherosclerosis obliterans most commonly affects aortoiliac,
femoral-popliteal, and popliteal-tibial vessels..

74. CONT
• Clinical manifestations.
• Symptoms usually occur after 50-70 percent of the affected vessels
are occluded.
• The level of claudication depends on the level or arterial
obstruction.
• Subjective findings.
• Specific age. Frequency increase with advancing age (50-70 years).
• Specific diet. Diets high in calories and saturated fats cause
hyperlipidema.
• Specific sex. Increased incidence in males until age 75 or older.
• Family history of cardiac disease or PVD
• Diabetes mellitus or hypertension.
• Certain lifestyle. Type A personality carries an increased risk

75. CONT
• Certain habits such as smoking.
• Pain. Pain to ischemia distal to the lesion is known as
intermittent claudication.
• It is described as an achy, cramping pain that occurs after a
certain amount of exercise (a number of block or stairs) and is
relieved with rest.

76. CONT
• Mechanism;
• Activity
• ↓
• Increased oxygen demand to the muscle
• ↓
• Ischemia distal to the lesion
• ↓
• Anaerobic metabolism
• ↓
• Production of lactic acid
• ↓
• Pain
•

77. CONT
• Night pain. Usually occurs after lumen is 75 percent occluded. Pain
may be described as a shock like sensation traveling along the nerves,.
• Heaviness and fatigue in the affected leg.
• Poor healing of wounds of the feet.
• Objective findings.
• Peripheral vascular exam.
• Impaired arterial pulsations below the level of obstruction.
• May be associated with a bruit. Scales;
– 0 nonpalpable
– 1 weak and thready
– 3. normal
– 4 full and bounding
–

78. CONT
• Cool extremity due to lack of warmed, oxygenated blood flow.
• Color changes;
– Pallor and mottling as the active muscle “steals” blood flow from
skin.
– Rubor (advanced disease) due to reactive hyperemia within the
arterioles.
– Postural changes. When the affected extremity is raised 45 degrees
for 60 seconds, becomes abnormally blanched. In the dependent
position, a delay indicates ischemia (normal color return in 10
seconds).
• Atrophic skin. Shiny skin with minimal hair. Particularly on the dorsum
of the feet and toes.
• Ridged, brittle nails.
• Ulceration over pressure points. Pale base with erythematous margin.
• Edema Occurs with advanced disease, with legs in a dependent
position.

79. CONT
• Wasting of leg muscles.
• Complications.
– Forty percent of persons with atherosclerosis obligations
develop a type of thrombophlebitis of superficial non-
varicose veins.
– Permanent venous occlusion occurs, but the inflammation
subsides one to three weeks.
• Diagnosis.
– Angiography involves the use of a contrast material of high
capacity to determine the precise location and extent of the
disease.

80. CONT
– Doppler ultrasound uses a dopper recorder to detect the
velocity of flow within a segment of an artery.
– Translumber aortography.

81. Aortic aneurysm.
• A localized dilation occurring in a weakened area of the medial layer of an artery.
• It is mainly atherosclerotic but may also occur from congenital defects (Marfan’s
syndrome), infections (syphilis), and trauma.
• Pathophysoilogy.
– A fusiform aneurysm produces a circumferential dilation of the vessel.
– The fills with necrotic debris and thrombus.
– Calcium infiltrates the area. The medial layer is weakened. The radius increases
and the vessel dilates.
– The wall tension rises, further dilating the vessel.

82. CONT
• Complications.
– Rupture.
– Embolism to a peripheral artery.
– Pressure on the surrounding structures.
– Obstruction of the blood flow to the organs supplied
by the tributary arteries.

83. Illustration

84. Abdominal aortic aneurysm (AAA).
• The most common type of aneurysm, occurring distal to the renal arteries and
extending to the aortic bifurcation.
• The iliac arteries may be included.
• It is usually atherosclerotic.

85. Illustration

86. Clinical manifestations.
• The person is usually asymptomatic.
• A pulsatile mass may be palpated in the umbilical region to the left
of the midline.
• Peripheral circulation is decreased.
• Large aneurysms may produce epigastric discomfort or an ileus or
intestinal obstruction.
• Rupture may cause abdominal or back pain and symptoms of
hemorrhagic shock.
• Prognosis.
• Small, asymptomatic aneurysms may not require surgery.
• A symptomatic aneurysm that has progressed to 4-6 cm required
surgical repair.

87. Thoracic aneurysm.
• A fusiform aneurysm usually located in the arch and
descending segments of the thoracic aorta.
• It is usually atherosclerotic.
• Clinical manifestations.
– Initially asymptomatic
– Dull, aching thoracic pain as the aneurysm expands.
– Hoarseness and coughing due to compression of the
recurrent laryngeal nerve.
– Dysphagia due to esophageal compression.
• Prognosis.
• Thoracic aneurysm require surgical repair.

88. Illustration

89. Illustration

90. Dissecting aneurysm (dissecting hematomas).
•
• Blood flows between the intimal layer and the adventitial layer
of the vessel through an intimal tear and/or degeneration of the
medial layer.
• The aneurysm usually occurs in the ascending aorta in
individuals with hypertension (80%).
• Clinical manifestations.
• The person usually complains of a sudden onset of severe
chest pain radiating to the back, abdomen, and thighs.
• Prognosis.
• The mortality rate is high during the first two weeks after
rupture.
•

91. Saccular aneurysm.
• An out pouching of one side of an artery, commonly associated with syphilis or
congenital malformations rather than atherosclerosis.

92. Raynaud’s disease.
• Paroxysmal episodes of bilateral ischemia of the digits.
• Raynaud’s phenomenon is a vasospastic disorder producing ischemia and
usually has no underlying pathologic basis.
• Pathogenesis.
• Spasm and constriction of the small arteries or arterioles of the extremities
result in intermittent pallor and cyanosis of the skin and extremities.
• In the advanced stages, the intima of the digital arteries becomes
thickened.

93. CONT
• Clinical manifestations.
• Subjective findings.
– Certain sex. Raynaud’s disease primarily affects young women.
– Family history.
– Certain age. The disease usually affects women of child-bearing
age.
– Certain habits. Smoking.
– Bilateral cyanosis of fingers in response to cold or stress.
– Numbness’, tingling, and throbbing of the fingers.
• Objective findings.
• Classically, the three stages noted are the following;
– Pallor due to vasoconstriction of the arterioles.
– Cyanosis due to retarded blood flow of poorly oxygenated blood in
dilated capillaries.
– Rubor due to reactive hyperemia.

94. HYPERTENSION
• Hypertension is an abnormal elevation of systolic and/or diastolic
blood pressure. It usually follows insidious course, affecting nearly
20 percent of the U.S. adult population.
• Pathogenesis.
• Determinants of arterial blood pressure.
– Blood pressure is directly proportional to the cardiac output and
the amount of peripheral resistance in the arterioles.
– Any change in either will alter the blood pressure.
– Cardiac output (C) x total peripheral resistance (MAP).
• Factors that increase blood pressure.
– Increased sympathetic activity. Sympathetic nerve fibers release
norepinephrine. Causing vasocontraction and increasing blood
pressure. Epinephrine increases cardiac contractility.

95. CONT
– Abnormal rennin theory. The release of rennin stimulates
the release of aldosterone and causes arterial
vasoconstriction. An excess of rennin is present in 50-70
percent of adults who have hypertension.
– Increased blood volume.
• Excessive salt intake and abnormal Na+
metabolism lead
to Na and water retention.
• Renal or hormonal dysfunction may expand blood
volume.
– Aortic impedance. Resistance regulated by the aorta valve
and the elasticity of the aorta wall.
– A genetic predisposition for arteriolar thickening, which
increases peripheral resistance.

96. CONT
• Clinical Manifestations.
• Early hypertension is usually asymptomatic.
• If symptoms occur, the disease is usually far advanced
and complications may have developed.
• Subjective findings.
– Previously diagnosed hypertension.
– Family history hypertension, stroke, transient ischemia
attacks, kidney disease, or diabetes mellitus

97. CONT
– Specific age. The frequency and severity of hypertension
increase with age.
– Specific race. Proportoinary, blacks have twice the incidence
of hypertension as whites.
– Specific sex. Men are affected more than women until women
reach middle age.
– Certain lifestyle.
• Low socioeconomic status.
• Low educational level.
• Type A personality. Individuals who are competitive and
aggressive have high levels of stress.
• Sedentary lifestyle.

98. CONT
– Certain habits
• Cigarette smoking. Nicotine causes the sympathetic release of
catecholemines.
• Obesity. A diet high in calories, salt, and saturated fats may cause
obesity, which increases the heart’s workload.
– Headache in the accompanied by nausea, vomiting, and metal confusion.
– Nocturia or hematuria if renal dysfunction is present.
– Blurred or impaired vision if retinal changes have occurred

99. CONT
• Objective findings.
• General appearance.
• Blood pressure. Hypertensive levels vary with age.
– Borderline from 140/90 mm Hg to 160/95 mm Hg.
– Mild. Diastolic pressures of 95-104 mm Hg.
– Moderate. Diastolic pressure of 105-114 mm Hg.
– Severe. Diastolic pressure of 115 mm Hg or greater.
– Malignant. Diastolic pressure of 130 mm Hg or greater.

100. CONT
• Eyes. Keith-Wagener classification. Provides objective clues to the
progression of the disease.
– KWI--mild congestion of retinal blood vessels with minimal
arteriolar narrowing.
– KW2--mild congestion causes significant narrowing of the
arterioles. Arteriovenous nicking (AV nicking) occurs when lipid
infiltration causes thickening of the arterioles. The vein is
invisible for a short segment on either side of the arteriole.
– KW3--flame-shaped hemorrhages and cotton and exudes.
– KW4--all of the above with papilledema.
• Heart.
– Apical impulse is displaced laterally if cardiomegaly is present.
– ECG changes.

101. CONT
• Complications,
• Untreated hypertension damages the small arterioles and
causes target organ dysfunction
– Stroke. An increase in blood pressure may cause dilation of the
small vessels. These weak areas bulge and develop aneurysms.
Rupture causes hemorrhage into the brain parenchyma.
– With hypertension, the arterial wall becomes infiltrated with
lipoids and thickens, concealing a segment of the vein on
either side of the overlying artery.
– Myocardial infarction. A myocardial infarction may result
from atherosclerosis due to injury to the endothelium.
– Renal failure. Progressive damage to the kidneys may be a
result of sustained blood pressure elevation.

102. CONT
– Congestive heart failure. A prolonged increase in cardiac
workload causes cardiac hypertrophy. The heart may
eventually decompensate and end heart failure.
– Encephalopathy. There may be leakage of water and
electrolytes from the capillaries of the brain, causing
cerebral edema and papilledema (optic disc swelling).
• Diagnosis.
• Elevated blood pressure readings at three separate times at
least on week apart.
• ECG or chest roentgenogram may show evidence of cardiac
hypertrophy associated with congestive heart failure.

103. CONT
Essential Hypertension (primary or Idiopathic).
• Persistent elevation of blood pressure with no known cause. Ninety
five percent of individuals with blood pressure have this type.
Secondary Hypertension.
• Continuous elevation of blood pressure resulting from a primary
disease process.
• Causes.
– Renovascular hypertension. Renal ischemia produced by an
obstruction of one or both of the renal arteries activating rennin.
– Renal parenchyma disease.
– Cushing’s disease. An excessive secretion of adrenocorticotropic
hormone (ACTH) from the adrenal cortex increases blood
volume.

104. CONT
•
– Primary aldosteronism. An excessive secretion of
aldosterone causes hypervolemia due to salt and water
retention
– Pheochromocytoma. A rare tumor of the adrenal
medulla causes an increased secretion of epinephrine
and norepinephrine. Hypertension is usually malignant.
– Coarctation of the aorta. A congenital constriction of
the aorta causes a constriction in the flow of blood. It
produces marked elevation of blood pressure in the
upper pressure.

105. CONT
Benign Hypertension.
• A gradual increase in blood pressure. (it is not really benign, in that it may
become markedly elevated and cause permanent damage if untreated).
Malignant Hypertension.
• A rapidly progressive form of uncontrollable blood pressure elevation that
causes rapid and severe systematic complications.
• The condition is not preceded by benign hypertension, nor is it related to
cancer (as the name may imply).

106. Erythropoiesis.
• Erythrocytes.
– Mature red blood cells that are non-nucleated,
– Biconcave disks,
– Able to pass through very small capillaries, and
contain hemoglobin, which carries essential gases
to and from tissues.
–

107. Development of erythrocytes.
• After infancy, the bone marrow becomes the principal site of
red blood cell production.
• Maturation process is from stem cell to mature erythrocyte.
– Pro-erythroblast. Immature stem cell with a large nucleus.
– Basophilic erythroblast. Nucleus becomes smaller;
hemoglobin synthesis begins.
– Polychromatic erythroblast. Nucleus continues to shrink
and become more dense; red hemoglobin appears.
– Late orthochromatic norm oblast. Hemoglobin synthesis is
almost complete, constituting 34 percent of cell volume;
nucleus shrinks and becomes external to cells.

108. CONT
• .
– Reticulocyte. Nonnucleated immature cell, usually remains in marrow
one day then in bloodstream on day before becoming a mature red
blood cell.
– Mature erythrocyte emerges and has a life span of approximately 120
days.
Hemoglobin.
• Hemoglobin is a protein that contains iron and red pigment; its function is
to carry oxygen from the lungs to the tissues.
• The disk shape of the erythrocytes provides a large surface area for gas
exchange to take place.
Substances. Needed for erythropoiesis.
• Substances essential for the production of red blood cells (RBCs) and
hemoglobin include;
– Amino acids,
– Iron, copper, pyroxide, cobalt,
– Vitamin B12, and folic acid.

109. CONT
• Vitamin B12 is essential for the synthesis of DNA molecules in immature
RBCs. B12 must be bound to an intrinsic factor for its absorption of RBCs.
• Iron is essential for the production of heme molecules, and about 65 percent of
body iron is present in hemoglobin.
– Iron is absorbed in the duodenum by transferring and stored in the liver as
ferritin.
Energy production in erythrocytes.
• Even without a nucleus, RBCs are metabolically active and require energy to
maintain osmotic stability, maintenance of iron, and modulation of hemoglobin
function.
• Mature RBCs cannot synthesize nucleic acids, carbohydrates, lipids, proteins,
and there are no mitochondria.
• Energy of red blood cells is generated by glucose metabolism by anaerobic and
aerobic pathways.
•

110. CONT
• Function of red cells in oxygen and carbon dioxide
transport.
– Most of the oxygen in blood combines with the heme
portion of hemoglobin, forming oxyhemoglobin.
– Oxygen saturation in hemoglobin is about 95 percent.
– This oxygen is released in tissue, which has an oxygen
pressure of about 40 mm Hg.
• Carbon dioxide is transported from tissues in two major
ways.
– Twenty to 25 percent in combination with hemoglobin as
carbominomoglobin.
– Seventy percent in the dissolved form of bicarbonate.

111. CONT
• Carbon dioxide diffuses into the RBC and combines with water to
form carbonic acid, which dissociates into free hydrogen and
bicarbonate ions.
• Free hydrogen is a powerful acid-base buffer, and bicarbonate
diffuses into the plasma to attach to a positive ion in the RBC.
• As bicarbonate diffuses into the plasma, it is replaced by chloride
shift, which results in greater amount of chloride in various RBCs
than in arterial cells.
Factors influencing erythropoiesis.
• Erythropoiesis is regulated by the;
• Number of circulating red blood cells,
• The PO2 of arterial blood,
• A negative feedback system with hypoxemia as the stimulus for the
release of erythropoietin hormone from the kidney.

112. Antigenic properties pf erythrocytes.
• More than 30 red blood cell antigens have been identified.
• Antigenic properties are genetically determined and therefore
individualized.
• The antigens in one person’s blood may react with the plasma or cells
of another, especially during or after blood transfusion, causing
hemolysis or agglutination.
• Classification of blood is according to antigens present on he red cell
membrane. A, B, or Rh.
– Type O—no antigens. Universal donor.
– Type A or B—one antigen.
– Type AB—both antigens, Universal recipient.
– Rh+ -, Refers to the presence or absence of certain antigens on the
red blood cell. About 90 percent of the U.S. population is Rh+.

113. Destruction of erythrocytes.
• Aging cells begin to fail at glucose metabolism and may
rupture at tight spots in the circulation due to a fragile cell
membrane or through intravascular destruction.
• After lysis of the cell, hemoglobin is reduced; the iron is
recycled; and the remainder is reduced to bilirubin.
Erythrocytosis.
• Myeloproliferative disorders
• Refer to various syndromes that are characterized an
abnormal increase in the number of red blood cells in
circulation called erythrocytosis. Causes of erythrocytosis are
the following;
– Hypoxemia. Stimulates marrow to produce more red blood
cells. Hypoxemia may result from pulmonary diseases,
heavy smoking, or high-altitude acclimation.

114. CONT
• Prognosis. Varies, depending on clinical management of
complications of increased blood components and volume.
Fourteen to 20 percent of persons affected with polycythema Vera
develop leukemia.
Anemia’s.
• Anemia is a condition in which there is a reduction in the number
of circulating RBCs, or in hemoglobin concentration, or in the
volume of packed red cells (hematocrit), or a combination of these
factors.
• Categorization.
• Anemia’s are classified according to etiology and/ or morphology.
Morphologic classifications are;
– Normocytic, normochronic. Normal size and color of RBCs.
– Microcytic, hypochromic. Decreased size and color of RBCs
due to less than normal hemoglobin.

115. CONT
• Microcytic. Large size of RBCs.
• Anisocytosis. Variations in size of RBCs.
• Poikilocytosis. Variations in shape of RBCs.
A plastic anemia.
• Results from reduced bone marrow function whereby stem
cells do not mature.
• Etiologies include
– Genetic failure of bone marrow,
– Injury to stem cell.
– Radiation, or chemical agents such as cytoxic drugs,
antimicrobial agents, anticonvulsants, and anti-inflammatory
drugs.

116. CONT
Clinical manifestations.
• Symptoms are associated with progressive anemia and
decreased oxygen transport and include;
– Weakness,
– Dyspnea,
– Headaches,
– Syncope.
• Thrombocytopenia is a variable symptom, but many clients
present with recurrent infections due to leucopenia and a
compromised immune response.

117. CONT
Diagnostic tests include
• Blood studies
• Bone marrow aspiration.
Prognosis varies,
• Depending on causative agent or response to bone marrow
transplantation.
• Infection and hemorrhage are the most common causes of death.
Red blood cell aplasia
• Is much rarer that a plastic anemia.
• It is characterized by a severe normocytic, normochromic anemia.
• Causative factors include immunologic alterations, drug, or viral
infections.
• Red blood cell aplasia may be preukemic or be a result of end-
stage renal failure.

118. Hemolytic anemia.
• Characterized by RBCs with a life span of 20 days or less.
Abnormalities of red cell membrane.
• Hereditary sphecytosis (HS) is an inherited condition in
which red cells are spheric and prematurely destroyed in the
spleen, resulting in jaundice, splenomegaly, and signs of
anemia.
• Acquired immune hemolytic anemia. Results from RBC
destruction by the immune system and is diagnosed by the
Coombs’ test.
• Indirect Coombs’ test is often used as a screening test for
antibodies while cross-matching blood for transfusions and
may be related drugs such as penicillin, quinidine, quinine,
and methyldopa.

119. CONT
• Glucose – 6 – phosphate dehydrogenase G-6-PD) deficiency
is a deficiency of the enzyme necessary for converting
glycerol to glucose.
• When the affected is given certain drug or has a viral bacterial
infection or diabetic ketoacidosis, hemolytic anemia may
result.
Increased rigidity causing abnormal flow.
• Sickle-cell trait. Sickle cell anemia. An inherited chronic form
of anemia occurring almost exclusively in black and
characterized by abnormal crescent-shaped erythrocytes.

120. CONT
• Pathogenesis.
• In sickle-cell anemia a faulty hemoglobin ( HbS ) results from
an amino acid substitution on the beta chain of the globin
molecule.
• With increased oxygen demand, this hemoglobin is
deoxygenated, becomes crystallized, and takes on bizarre
shapes, causing blockages in small blood vessels and
compromising blood supply.
• These events further the cycle of increased oxygen demand
and increased sickling.

121. CONT
• Hemolysis of sickled cells reduces the life span of the RBCs
to 10-15 days; these damaged RBCs become trapped in the
spleen and may eventually infarct the entire organ.
Clinical manifestations
• Include jaundice, impaired growth and maturity,
• Increased susceptibility to infections, chronic leg ulcers, joint
pain. Abdominal pain.
• Neurologic complications, severe anemia and renal
impairment.
• Prognosis for sickle-cell anemia is improving.

122. CONT
Thelassemias
• Are hereditary anemia s that cause defects in hemoglobin
synthesis, resulting in a hypochromic , microcytic anemia classified
as major and minor.
• Thalassemia major, found in children, is characterized by
ineffective erthropiesis and peripheral hemolysis, which stimulates
enlargement of the red marrow to increase RBC formation.
• Clinical manifestations
• Include fatigue, splenomegaly, severe anemia, enlargement of the
heart, jaundice, hepatomegaly, and “chipmunk” face.
• The disease is associated with growth retardation.
• Prognosis varies,
• but life expectancy is about 17 years.
• Thalassemia minor is usually characterized by a mild anemia only.

123. CONT
• Direct physical trauma. May induce self-limiting hemolytic anemia’s.
• Causative factors include physical blows, prolonged exercise, and
artificial cardiac valves.
Maturation. Failure anemia.
• Pernicious anemia.
– Results from a vitamin B12 deficiency that may occur from a
decreased dietary intake or from malabsorption of vitamin B12 due
to atrophy of the gastric mucosal cells or lack of secretion of the
intrinsic factor.
• Pathogenesis.
– Normal maturation of RBCs is dependent on adequate amounts of
vitamin B12 for the synthesis of DNA molecules. Without B12
macrocytic anemia results, due to ineffective Erythropoiesis.

124. CONT
• Clinical manifestations
• Include anorexia, failure, dysnea irritability, and soreness of the
tongue. mild neorogic changes occur rarely and may persist after
treatment with vitamin B12 supplement.
• The schilling test is used to measure the absorption of vitaminB12.
Folic acid anemia.
• Folic acid anemia is similar in pathogenesis to pernicious anemia.
• It results from a dietary lack of folic acid and is associated with
alcoholism, chronic malnutrition, and pregnancy.
• Clinical manifestations
• Include anemia, smooth red tongue, and stomatitis which clear
with dietary replacement of folic acid.

125. CONT
Microcytic hypochromic anemia. Iron deficiency anemia
• Iron deficiency anemia is a common type of anemia whereby
there is a deficiency in hemoglobin synthesis due to a lack of
iron.
• Etiology. Increased iron loss from acute or chronic bleeding,
decreased dietary intake, or a malabsorption syndrome.
• Clinical manifestations
• Include fatigue, tachycardia, irritability, pallor, sore tongue, or
stomatitis.
• Late manifestations include cardiac murmurs, congestive
heart failure, hair loss, and pearly sclera.

126. CONT
Post hemorrhagic anemia
• Is a normocitic, normochromic anemia that results from acute
or chronic blood loss that in turn causes movement of
interstitial fluid to the capillaries, resulting in dilution of RBCs
and inadequate oxygenation of tissues.
• The bone marrow is stimulated to produce more RBCs, but
supportive transfusions may be necessary.
Laboratory and Diagnostic Tests.
• Hematologic studies.
• Hemoglobin. Reflects the oxygen-binding capacity of blood;
varies with sex and age.

127. CONT
• Red blood cells. Responsible for transporting oxygen and carbon
dioxide. Their counts vary in the same direction as hemoglobin.
• Packed cell volume or hematocrit. Refers to the ratio of packed
cells to total volume in a centrifuged sample. Hematocrit is used
to calculate blood volume and total red blood cell mass.
• Erythrocyte sedimentation rate (ESR). Refers to the rate at
which RBCs settle from a plasma sample when mixed with an
anticoagulant. The rate at which RBCs settle is directly related to
the function of fibrinogen and globulin. ESR is increased in
inflammatory conditions and may serve as a differential
diagnostic aid in acute myocardial infarction, angina pectoris,
rheumatoid arthritis, and osteoarthritis.

128. CONT
• Mean corpuscular volume (MCV) measures the volume size
each red blood cell.
• Mean corpuscular hemoglobin (MSH) refers to the amount
of hemoglobin by weight in the average red blood cell.
• Mean cell hemoglobin concentration 9MCHC) refers to the
hemoglobin content in the average red blood cell.
• Reticulocyte count is the measurement of young,
nonnucleated precursors of erythrocytes and is indicative of
bone marrow function.
• Bone marrow studies are used to diagnose or trace the
progress of blood disorders

129. Illustration

130. Illustration

131. HEMOSTASIS
• Arrest of bleeding or circulation
• Process to prevent and stop bleeding-meaning to keep blood
within damaged blood vessel opposite of hemorrhage).
• First stage of wound healing.
• Involves coagulation-blood changing from a liquid to a gel.

132. Illustration

133. Illustration

134. Illustration

135. Illustration

136. Stages of hemostasis
• Occurs in four stages.
– Vasoconstriction.
– Formation of a hemostatic platelet plug.
– Blood coagulation.
– Clot formation.

137. Illustration

138. Illustration

139. Illustration

140. Vasoconstriction.
• Refers to contraction of a particular blood vessel, resulting in decrease flow of blood
in or out of an injured vessel.
• Mechanisms of control.
– Nervous reflexes.
– Local myogenic spasm stimulated by direct damage to the wall, and Release of
serotonin from platelets.

141. Illustration

142. Hemostatic platelet plug formation
– Blood vessel damage.
– Results in a disrupted endothelial lining and exposed
collagen,
– Which reacts with platelets causing a viscous
metamorphosis.
– Platelet changes include;-
• Swelling,
• Irregularity of shape
• Increased stickiness, and
• Secretions that enhance attraction of other platelet,
thereby forming a platelet Plug,
– Which stops a small tear in a vessel until fibrin threads are
formed from the Coagulation process.

143. Illustration

144. Illustration

145. Illustration

146. Illustration

147. CONT
• Characteristics and physiology of platelets.
– Platelets are formed in bone marrow
– Released into circulation with a concentration of about 140,000 to 340,000 per
– Platelets have four functional regions.
• Peripheral zone.
– Includes;
– Cell membrane –
» Has properties of adhesion,
» Platelet/ collagen interaction results in platelets sticking to site of
injury, and aggregation, the calcium-requiring process of platelet-
platelet collection.

148. CONT
– Sol-gel zone.
• Platelet cytoplasm matrix
– Allows for contraction
– Changes in shape
– Secretory functions.
– Organelle zone.
• Acts as a storage area for;-
– Enzymes,
– Serotonin,
– Calcium and protein constituents .
– Membrane systems region.
• Allows for plasma substances to enter
• Cellular products to be released or secreted.
• Contractility of platelets allows shape changes, internal changes,
and clot formation.

149. Illustration

150. Blood coagulation
• Process that changes circulating substances within blood into insoluble gel.
• Gel plugs leaks in blood vessels and stops loss of blood.
• The process requires;-
– Coagulation factors-manufactured by the liver
– Calcium -available in the blood and from intracellular sources
– Phospholipids- prominent components of cellular and platelet membranes,
provide a surface upon which chemical reactions of coagulation take place

151. Coagulation Pathways
• Intrinsic pathway
– Initiated by events that take place within the lumen of blood vessels.
– Requires only elements (clotting factors, Ca++, platelet surface etc.)
found within, or intrinsic to the vascular system.
• Extrinsic pathway
– Other route to coagulation.
– Requires Tissue Factor (tissue thromboplastin), a substance which is "extrinsic
to", or not normally circulating in the vessel.
– Released when the vessel wall is ruptured.

152. Illustration

153. CONT
• Whether Extrinsic or Intrinsic pathway starts coagulation, completion of the process follows a
common pathway.
• Common pathway involves activation of factors:
– X,
– V,
– II,
– XIII
– I.
• Both pathways are required for normal hemostasis
• There are positive feedback loops between the two pathways that amplify reactions to produce
enough fibrin to form a lifesaving plug.
• Deficiencies or abnormalities in any one factor can slow the overall process, increasing the risk of
hemorrhage.

154. Coagulation factors
• Numbered in order of discovery.
• 13 numerals but only 12 factors.
• Factor VI was subsequently found to be part of another factor.
– Factor I - fibrinogen
– Factor II - prothrombin
– Factor III - tissue thromboplastin (tissue factor)
– Factor IV - ionized calcium ( Ca++ )
– Factor V - labile factor or proaccelerin
– Factor VI - unassigned
– Factor VII - stable factor or proconvertin

155. CONT
– Factor VIII - antihemophilic factor
– Factor IX - plasma thromboplastin component, Christmas factor
– Factor X - Stuart-Prower factor
– Factor XI - plasma thromboplastin antecedent
– Factor XII - Hageman factor
– Factor XIII - fibrin-stabilizing factor

156. CONT
• Liver must be able to use Vitamin K to produce Factors II, VII, IX, and X.
• Dietary vitamin K is widely available from plant and animal sources.
• Also produced by normal intestinal flora.
• Deficiency is rare but may occur:
– In newborns because they must first develop normal flora to produce Vitamin K,
or
– When the flora is disturbed by broad-spectrum antibiotics.

157. Hodgkin’s disease.
• Type of lymphoma in which cancer originates from a specific type of white
blood cells called lymphocytes.
• Symptoms may include;-
– Fever,
– Night sweats,
– Weight loss.
• Often there will be non-painful enlarged lymph nodes in the neck, under the
arm, or in the groin.

158. Illustration

159. Illustration

160. Illustration

161. CONT
• Unknown etiology that occurs in several forms;
• Latent,
• Acute,
• Localized,
• Splenomegalic
• Lymphogranulomatosis.
• It is characterized by the proliferation of large Reed-Sternberg cells.

162. Classification
• Lymphocyte predominant;- There is diffuse replacement by
lymphocytes.
• Mixed type;- shows lymphocytic and histiocytic cell patterns.
• Lymphocyte depletion;- shows a predominant pattern of large
malignant cells.
• Nodular sclerosing ;-shows extensive scarring.

163. Staging.
• By bone marrow aspiration and splenectomy.
– I--localized to a single group of nodes, above or below
the abdomen.
– II--two non-continous groups of nodes, above or
below the diaphragm.
– III--nodes above and below the diaphragm.
– iv--invasion of other tissues, usually to bone marrow
or liver.

164. Illustration

165. Illustration

166. Clinical manifestations
.
• Include;-
– Fever,
– Chills,
– Night sweat,
– Weight loss,
– Anorexia,
– Pruritis,
– Enlarged, palpable lymph nodes.
• Prognoses
• Good with combination therapies of surgery for splenectomy, chemotherapy, and
radiation.