cardiovascular disorder for nursing

1. 1
By: Tadele M. (BSc, MSc)
SU-CMHS, DEP’T of Nursing
FOR 3rd YEAR NURSING
STUDENTS, 2015 E.C
CARDIOVASCULAR DISORDER
SAMARA UNIVERSITY
CMHS DEP’T OF NURSING
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2. Lecture Outline
Management of Patients With Coronary VD
 Atherosclerosis
 Angina Pectoris
 Myocardial Infarction
Assessment and Management of Patients With VD
 Aneurysms
 Hypertension
 Varicose Veins
 Thrombotic Disorders
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3. Management of Patients With Hematologic Disorders
 Anemia
 Polycythemia
 Hemophilia
 Thrombocytopenia
 Thrombocythemia
 Leukemia
 Lymphoma
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4. Management of Patients
With Coronary Vascular
Disorders
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5. Coronary arteries
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6. Coronary Vascular Disorders
• Coronary heart disease (CHD), or
• Ischemic heart disease(IHD)
– These terms are characterized by insufficient delivery
of oxygenated blood to the myocardium (ischemia)
because of atherosclerotic coronary arteries (CAD).
– Occurs when there is an imbalance between the supply
of oxygen (and other essential myocardial nutrients) and
the myocardial demand for these substances.
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7. Coronary heart disease (CHD)
Non modifiable Risk Factors
Family history of coronary heart disease
Increasing age
Gender and Race
Modifiable Risk Factors
High blood cholesterol level
Cigarette smoking, tobacco use
Hypertension
Diabetes mellitus
Lack of estrogen in women
Physical inactivity and Obesity
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8. Coronary heart disease (CHD)
–Atherosclerosis
–Angina Pectoris
–Myocardial Infarction
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9. Coronary Atherosclerosis
• Coronary atherosclerosis is a complex inflammatory
process characterized by the accumulation of lipid,
macrophages and smooth muscle cells in intimal plaques
in the large and medium-sized epicardial coronary arteries.
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10. Coronary Atherosclerosis
• Arteriosclerosis is a thickening, or hardening, of
the arterial wall that is often associated with aging.
• Atherosclerosis, a type of arteriosclerosis, involves
the formation of plaque within the arterial wall.
• Atherosclerosis is the major cause of CAD.
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11. Coronary Atherosclerosis:Pathophysiology
The macrophages ingest lipids, becoming “foam cells” that
transport the lipids into the arterial wall.
Attraction of inflammatory cells, such as monocytes
(macrophages).
Inflammatory response, which begins with injury to the vascular
endothelium.
Smoking, hypertension, and other factors.
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12. Coronary Atherosclerosis: Pathophysiology
These deposits, called atheromas or plaques, protrude into the
lumen of the vessel, narrowing it and obstructing blood flow.
Smooth muscle cells within the vessel wall subsequently
proliferate and form a fibrous cap over a core filled with lipid and
inflammatory infiltrate.
Activated macrophages also release biochemical substances that
can further damage the endothelium, attracting platelets initiating
clotting.
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15. Coronary Atherosclerosis: Pathophysiology
• As the stenotic lesions grow, perfusion pressure distal to the
lesions decreases;
• in response, coronary arterioles dilate to maintain adequate
blood flow preventing ischemic symptoms at rest.
• During exertion the myocardial oxygen demand increases which
couldn’t be matched by the perfusion via the narrowed coronary
artery.
• The resulting myocardial ischemia results in chest pain, called
angina pectoris, which is relived by taking rest.
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16. Coronary Atherosclerosis risk factors
Genetics related to predisposition for hyperlipidemia
Low HDL-C
High LDL-C
Diabetes mellitus related to hyperglycemia
Hypertension
Smoking
Obesity
Sedentary lifestyle
Increased serum homocysteine levels (an amino acid)
Infection
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17. Coronary Atherosclerosis clinical manifestations
• The most common manifestation of myocardial ischemia is the
onset of chest pain.
• Chest pain: men report a crushing or stabbing pain in their chest,
but women say they felt pressure, tightness or aching in their
chest or back
• Significant myocardial damage may result in persistently low
cardiac output and heart failure.
• A decrease in blood supply from CAD may even cause the heart
to abruptly stop beating (sudden cardiac death).
• Dyspnea, nausea, and weakness 17
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18. Coronary Atherosclerosis Clinical Manifestations
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19. Angina chest pain
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20. Coronary Atherosclerosis: Diagnostic tests
 History
Hemoglobin or CBC, fasting blood glucose, Serum lipid
profile
Exercise stress test
Resting ECG-ST segment depression ischemia
 Radiologic/Imaging
• Chest-x ray if there is CHF
• Stress echocardiography
• Cardiac catheterization
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21. Medical management
• Advise to continue beta-blockers as first-line
medication(atenolol 50-100 mg daily).
• If beta-blockers are contraindicated, sustained release
nitrates are the preferred alternative.
• Calcium channel blockers may be an alternative
medication if the patient is unable to take beta-blockers or
nitrates (Amilodipin , nefedipine).
• ASA 85-100mg daily (unless contraindicated).
• Statins are indicated regardless of lipid levels 21
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22. Nursing management
• Physical activity
• Nutritional therapy
• Lipid-Lowering Agents
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23. Coronary Atherosclerosis prevention
• Controlling cholesterol abnormalities
• Managing hypertension
• Controlling diabetes mellitus
• Cessation of smoking
• Unless contraindicated (e.g., history of GI
bleeding), low-dose aspirin (81 mg) is
recommended for most people at risk for CAD
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24. Angina Pectoris
• Angina pectoris, or angina, is chest pain resulting
from reduced coronary blood flow, which causes a
temporary imbalance between myocardial blood
supply and demand.
• The imbalance may be due to coronary heart disease,
atherosclerosis, or vessel constriction that impairs
myocardial blood supply.
• Chest pain results from the ischemia
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25. Angina pectoris Pathophysiology
Normally, when the heart needs more oxygen, the coronary
arteries dilate to carry more blood.
However, with CAD, the narrowed vessels are unable to dilate
and supply the heart with this extra blood and oxygen.
When an increased workload is placed on the heart, as in
exercise or strenuous activity, there is an increased demand
for oxygen.
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26. Angina Pathophysiology………….ctd
If adequate blood supply to the myocardium is
restored with rest, no myocardial damage usually
occurs.
This inability to supply more blood and oxygen
causes myocardial ischemia. Chest pain results from
the ischemia but usually lasts only for a few
minutes, especially if activity is stopped.
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27. Types of Angina
• Stable angina
• Usually occurs when the work of the heart is
increased by physical exertion, exposure to cold,
or by stress.
• Angina is due to poor blood flow through
the blood vessels in the heart.
• Is the most common and predictable form of
angina.
– Stable angina is relieved by rest and nitrates.27
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28. Types of Angina
• Prinzmetal’s (variant) angina
– Is atypical angina that occurs unpredictably (unrelated to
activity), and often at night.
– The pain of variant angina is the same as in stable angina,
except it has a longer duration and can occur at rest.
– It is caused by coronary artery spasm with or without
an atherosclerotic lesion.
– It may result from hyperactive sympathetic nervous system
responses, altered calcium flow in smooth muscle, or
reduced prostaglandins that promote vasodilation.
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29. Types of Angina
• Unstable angina
– Occurs with increasing frequency, severity, and
duration.
– Pain is unpredictable and occurs with decreasing levels
of activity or stress and may occur at rest.
– Rest does not decrease the chest pain of unstable
angina.
– Patients with unstable angina are at risk for myocardial
infarction.
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30. Factors associated with typical anginal pain:
• Physical exertion
• Exposure to cold
• Eating a heavy meal
• Stress or any emotion-provoking situation
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31. Angina pectoris:
Clinical Manifestations
• Chest pain:
Substernal or (across the chest wall); may radiate
to neck, arms, shoulders, or jaw.
• Associated manifestations:
Dyspnea, pallor, tachycardia, anxiety, and fear.
• Atypical manifestations:
Indigestion, nausea, vomiting, upper back pain
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32. Area of pain due to angina
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33. Angina pectoris: Assessment and Diagnosis
 Patient’s history
 A 12-lead electrocardiogram (ECG)
 Findings : transient ST segment depression
 Laboratory studies
 Exercise stress test
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34. 34
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35. Medical Management Pharmacologic Therapy
• Nitroglycerin
– NTG may relieve chest pain within 1 to 2 minutes.
– NTG can be administered sublingually, orally,
transdermally, intravenously, or as a lingual spray.
• Beta blockers
– Including propranolol, metoprolol, nadolol, and atenolol,
are considered first-line drugs to treat stable angina.
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36. Pharmacologic Therapy
• Calcium channel blockers
– verapamil, diltiazem, and nifedipine,
• lower blood pressure, reduce myocardial contractility,
and, in some cases, lower the heart rate, decreasing
myocardial oxygen demand.
• Aspirin
– Low-dose aspirin (80 to 325 mg/day)
• to reduce the risk of platelet aggregation and
thrombus formation.
• Oxygen Administration
– Oxygen therapy is usually initiated at the onset of chest
pain in an attempt to increase the amount of oxygen
delivered to the myocardium and to decrease pain.
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37. Angina pectoris: Nursing Interventions
• Monitor vital signs
• Assess chest pain each time the patient reports it (Remember
PQRST)
• Monitor cardiac status using a 12-lead ECG
• Record fluid intake and output. Assess for renal function.
• Place patient in a semi-Fowler's position
• Treating angina
• Reducing anxiety
• Preventing pain and Teaching patients self-care 37
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38. Exercise
• Beamlak is a 59 year old man with a history of high blood
pressure and high cholesterol. Heart disease runs in his family.
He is outside working on his farm today. He is digging out
ditches with a shovel. After a few shovels of dirt are cleared, he
begins to feel a pain in his chest and has pain down his left
arm. He recognizes this pain since he gets it every time he tries
to do any physical labor. He is frustrated and angry but stops
working and goes inside to rest. Once he's able to sit down on
the couch and relax for a few minutes, the pain resolves.
Beamlak is experiencing ?
• stable angina
• Unstable angina
• Prinzmetal's Angina
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39. exercise
• Betsegew is Dawit's son. He has been stressed about his father's
open heart surgery to restore blood flow to his heart. Betsegew
wakes up in the middle of the night with severe chest pain. He is
worried that he may have inherited his father's heart disease so he
goes to the hospital. They give him nitroglycerin and it relieves the
pain. They rule out any blockages, and he might have…?
– stable angina
– Prinzmetal's Angina
– Unstable angina
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40. Exercise
• A few weeks later, Beamlak is at home watching TV one night. He
suddenly has a crushing pain in his chest and feels sweaty. He tries
to ignore it but even after 10 minutes, the pain continues and is
getting worse. Although he has experienced chest pain before, this is
much different and he has an uncanny sense of fear for his well-
being. His wife is nearby and notices something isn't right; she
immediately calls 911. This time Dwayne is experiencing ?
 stable angina
 Prinzmetal's Angina
 Unstable angina
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41. MYOCARDIAL INFARCTION
• MI refers to the process by which areas of
myocardial cells in the heart are permanently
destroyed.
• Usually caused by reduced blood flow in a
coronary artery due to atherosclerosis and
occlusion of an artery by an embolus or thrombus.
• Necrosis (death) of myocardial cells, is a life-
threatening event.
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42. MYOCARDIAL INFARCTION
• Of the major heart diseases, myocardial infarction
(MI) or heart attack, and other forms of ischemic
heart disease cause the majority of deaths.
• Annually, approximately 785,000 people in the United
States experience their first MI; another 470,000
suffer an MI subsequent to the initial one.
• It is estimated that 195,000 silent attacks occur each
year (AHA, 2009).
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43. Myocardial infarction
• Risk factors
Age
Gender
Heredity
Race
Smoking
Obesity
Hyperlipidemia
Hypertension
Diabetes
Sedentary lifestyle, diet, and others.
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44. Myocardial infarction: Pathophysiology
Once necrosis takes place, the contractile function of the
muscle is permanently lost.
With prolonged ischemia lasting more than 20 to 45
minutes, irreversible hypoxemia causes cellular death and
tissue necrosis.
Cellular injury occurs when the cells are denied adequate
oxygen and nutrients.
Myocardial infarction occurs when blood flow to a portion
of cardiac muscle is completely blocked, resulting in
prolonged tissue ischemia and irreversible cell damage.
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45. MI: Clinical Manifestations:
• Pain. Severe, immobilizing chest pain not relieved by rest,
position change, or nitrate administration is the hallmark of
an MI.
• Persistent and unlike any other pain, it is usually described
as a heaviness, pressure, tightness, burning, constriction, or
crushing.
 Common locations are substernal, retrosternal, or
epigastric areas.
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46. MI: Clinical Manifestations:
 Shortness of breath
 Nausea or vomiting
 Heart rate >100 (tachycardia)
 Variable blood pressure
 Anxiety and Restlessness
 Pale, cool, clammy skin; sweating (diaphoresis)
 Sudden death due to arrhythmia usually occurs within first
hour 46
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47. Myocardial infarction: Diagnostic Tests
 ECG change
 Decreased pulse pressure because of diminished cardiac
output.
 Increased WBC count due to inflammatory response to injury.
 Blood chemistry:
Elevated creatine kinase MB (CK-MB)
Elevated troponin I- and troponin T-proteins
 Less than 25 ml/hr of urine output due to lack of renal blood
flow. 47
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48. Myocardial infarction: Diagnostic Tests
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49. Myocardial infarction: Medical Treatment
• Administer analgesics to
relieve pain
– Morphine
• Administer antihypertensive
to keep blood pressure low
– Hydralazine
• Administer nitrates
– Nitroglycerin
• Thrombolytics
– streptokinase
• Anticoagulants
– Heparin following
thrombolytic therapy
– Aspirin
• Administer calcium
channel blockers
– Verapamil
– Diltiazem
• Administer beta-
adrenergic blockers
– Propranolol
– Nadolol
– Metroprolol
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50. Myocardial infarction: Nursing interventions
• Monitor:
– Vital signs, oxygen saturations, intake and output
– Cardiovascular: changes or instability in pulse,
Oxygen administration
• low-fat, low-cholesterol, and low-sodium diet; no caffeine
• Fluid restriction
• Bed rest and Daily weight checks
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51. Assessment and
Management of Patients
With Hypertension
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52. 52
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53. Normal regulation of blood pressure
• Blood pressure (BP): is the force exerted by the blood
against the walls of the blood vessel.
• It must be adequate to maintain tissue perfusion during
activity and rest.
• BP is primarily a function of
– Cardiac output (co) ---systolic
– Systemic vascular resistance- diastolic
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54. Hypertension
• Hypertension is a state of elevated systemic blood
pressure that causes marked increment of cardiovascular
risk.
• It’s a major, preventable risk factors for;
– coronary artery disease, hemorrhagic and ischemic
stroke, heart failure and chronic kidney disease.
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55. 55
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56. Hypertension………
• Hypertension is a systolic blood pressure greater than 140
mm Hg and a diastolic pressure greater than 90 mm Hg
over a sustained period;
 Based on two or more blood pressure measurements taken
in two or more contacts with the health care provider after
an initial screening
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57. 57
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58. 58
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59. Hypertension
• Risk Factors affecting blood pressure
Age
Obesity
Family history
Cigarette smoking
Sedentary lifestyle
Diabetes mellitus 59
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60. Hypertension: Etiology
Primary (essential or idiopathic) Hypertension
Diastolic pressure is 90mmHg or higher and systolic
pressure is 140mm Hg or higher in the absence of other
causes of hypertension.
Tends to be familial and is likely to be the consequence
of an interaction between environmental and genetic
factors.
It accounts for 90% to 95% of all cases of
hypertension.
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61. Hypertension: Etiology
• Secondary hypertension
– Which mainly result from renal
disease, endocrine disorder
and coarctation of the aorta
(narrowing of the aorta).
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62. Hypertension
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63. PATHOPHYSIOLOGY OF HYPERTENSION
• Various neural and humoral factors are known
to influence and regulate BP. These include:-
The adrenergic nervous system
The renin-angiotensin-aldosterone system(RAAS)
Renal function and renal blood flow
Several hormonal factors (adrenal cortical
hormones, vasopressin, thyroid hormone, insulin)
The vascular endothelium (regulates release of
nitric oxide, bradykinin, prostacyclin, endothelin).
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64. PATHOPHYSIOLOGY OF HYPERTENSION
Renin convert angiotensinogen to angiotensin I
Secretion of Renin from jaxtaglomerular cell of kidneys
and activation of beta receptors
Decrease blood flow to organs >>>>Decreased blood
pressure >>>> Decreased renal perfusion.
Increase afterload: The resistance against which the left
ventricle must eject its volume of blood during contraction.
Increase systemic vascular resistance
Risk factors
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65. PATHOPHYSIOLOGY OF HYPERTENSION
Increase cardiac output>>>Increase blood pressure
Aldosterone cause sodium and water retention
Angiotensin II: Is potent vasoconstrictor and increase
vascular resistance and Stimulate adrenal cortex to
secrete Aldestrone
Angiotensin I then converted to angiotensin II by
angiotensin converting enzymes(ACE)
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66. Hypertension: Clinical Manifestations
• Hypertension is a “Silent killer”
• Subjective data might include
Throbbing occipital headache upon walking
Fatigue and Dizziness
Drowsiness and Confusion
Vision problem
Nausea & Palpitations
Dyspnea & Nosebleeds
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67. Hypertension: Clinical Manifestations
• Objective data
– Blood pressure > 140/90 mm Hg
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68. Hypertensive Crisis: Two major forms
• Hypertensive Emergencies:
– Are acute, life-threatening, organ damage and usually
associated with marked increases in blood pressure
(BP), generally 200/120mmHg.
• Hypertensive Urgency:
– Is a situation in which there is asymptomatic severe
hypertension with no target organ damage.
– blood pressure readings are 180/110 or higher
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69. Hypertension: Assessment and Diagnostic Findings
 History and Physical Examination
 Renal Function: Serum Creatinine & Urine Creatinine
Clearance
 Electrolytes –Na+
 Blood Glucose: fasting glucose
 Serum Lipids: HDL, cholesterol levels
 Urinalysis
 ECG
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70. Hypertension: Medical Management
• Nonpharmacological(Lifestyle Interventions)
– Reduce salt intake:
– Dietary recommendations:
– Physical activity:
– Weight reduction:
– No Alcohol consumption:
– Smoking cessation:
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71. Hypertension: Pharmacologic Treatment ………
• Factors that should be considered before the selection
of an antihypertensive agent include the following:
Cost of the drug class
Patient-related factors such as the presence of major risk
factors
Conditions favoring use of specific drug category
Contraindications
Associated clinical conditions and the presence of target
organ damage.
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72. • WHO recommends initiation of pharmacological
antihypertensive treatment of individuals with a
confirmed diagnosis of hypertension and systolic blood
pressure of ≥140 mmHg or diastolic blood pressure of
≥90 mmHg.
• WHO recommends pharmacological antihypertensive
treatment of individuals with existing cardiovascular
disease and systolic blood pressure of 130–139 mmHg.
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73. Hypertension: Pharmacologic Treatment ………
• In the absence of compelling indications, the least
expensive of the following classes of drugs are
preferred as first line agents to control
hypertension:
Thiazide diuretics
Calcium channel blockers
Angiotensin converting enzyme inhibitors
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74. Hypertension: Pharmacologic Treatment ………
• Non-Emergency conditions
– First line
• Calcium channel blockers-Amlodipine, Nifedipine
Felodipine
• ACE inhibitors-Lisinopril, Enalapril and Captopril
• Thiazide diuretics-Hydrochlorothiazide
• Angiotensin receptor blockers (ARBs) –
Candesartan, Valsartan, Losartan 74
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75. Hypertension: Medical Treatment
• Follow-up and Clinical Monitoring
– Start at low doses and increase dose step by step to
maximum tolerated dose in order to achieve target BP
control.
– If on maximum, or highest tolerated dose of a single
agent, and BP is not controlled, combination therapy
should be instituted with another drug from the first-line
classes;
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76. Hypertension: Medical Treatment ………
• Treatment of Hypertensive Emergencies:
– Hydralazine, 5-10 mg IV/IM initially and refer to higher
health facility after giving one oral dose of long-acting
antihypertensive like Atenolol ( 50mg) or metoprolol
(50mg) or Propranolol (40mg).
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77. Hypertension: Medical Treatment ………
• Hypertensive Urgency
– For previously untreated patients
• Start either a low dose of a calcium channel blocker
(nifedipine) or ACE inhibitor (captopril or enalapril) or
beta blocker.
• Furosemide 20-40mg (PO or IV) can be added to the
above agents - if patient is reliable follow up can be made
every one to two days. If not reliable, admit. –
• Avoid rapid drop in blood pressure 78
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78. Hypertension: Nursing intervention
Monitor blood pressure
Record fluid intake and output.
Reduce stress by providing a quiet
environment.
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79. Hypertension: Nursing intervention
• Explain to the patient:
No smoking—smoking contributes to
cardiovascular disease, raising blood pressure.
Change to a low-sodium and low-cholesterol
Reduce alcohol
Reduce weight—decreased risk for obesity,
better BP control
Exercise.
Call health personnel when BP is elevated.
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80. Q1. The nurse is caring for a patient who has been
diagnosed with an elevated cholesterol level. The
nurse is aware that plaque on the inner lumen of
arteries is composed chiefly of what?
A) Lipids and fibrous tissue
B) White blood cells
C) Lipoproteins
D) High-density cholesterol
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81. Q2. The nurse is providing an educational workshop about
coronary artery disease (CAD) and its risk factors. The nurse
explains to participants that CAD has many risk factors, some
that can be controlled and some that cannot. What risk factors
would the nurse list that can be controlled or modified?
A) Gender, obesity, family history, and smoking
B) Inactivity, stress, gender, and smoking
C) Obesity, inactivity, diet, and smoking
D) Stress, family history, and obesity
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82. Q3. The staff educator is teaching ED nurses about
hypertensive crisis. The nurse educator should explain that
hypertensive urgency differs from hypertensive emergency in
what way?
A. The BP is always higher in a hypertensive emergency.
B. Vigilant hemodynamic monitoring is required during
treatment of hypertensive emergencies
C. Hypertensive urgency is treated with rest and
benzodiazepines to lower BP
D. Hypertensive emergencies are associated with evidence of
target organ damage.
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83. Q4. The nurse is planning the care of a patient who has
been diagnosed with hypertension, but who otherwise
enjoys good health. When assessing the response to an
antihypertensive drug regimen, what blood pressure
would be the goal of treatment?
A. 156/96 mm Hg or lower
B. 140/90 mm Hg or lower
C. Average of 2 BP readings of 150/80 mm Hg
D. 120/80 mm Hg or lower
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84. Aneurysm
Definition: aneurysm ( aneurism) is a localized, blood-
filled dilation (balloon-like bulge) of a blood vessel.
Risk factors
Diabetes
Obesity
Hypertension
Tobacco use
Alcoholism
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85. Types of Aneurysm
Aortic aneurysms: is a localized sac or dilation formed at a
weak point in the wall of the aorta.
1. Abdominal aortic aneurysms(AAA):
o Aneurysm that occurs in the part of the aorta that's
located in the abdomen,
o AAAs accounts for 3 in 4 aortic aneurysms.
2. Thoracic aortic aneurysms(TAA):
o An aneurysm that occurs in the part of the aorta that's
located in the chest and above the diaphragm
o TAAs account for 1 in 4 aortic aneurysms.
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86. 3. Cerebral aneurysms
Aneurysm occurs in an artery in the brain,
A ruptured brain aneurysm causes a stroke.
4. Peripheral Aneurysms
Aneurysms that occur in arteries other than the aorta
and the brain arteries
Location- popliteal, femoral, & carotid arteries.
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87. Causes and risk factors
Aging,
Smoking,
High blood pressure,
Atherosclerosis
Vasculitis
Family history
Trauma or injury
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88. Signs and Symptoms
Abdominal Aortic Aneurysms
 A throbbing feeling in the abdomen
 Deep pain in the back or the side of the abdomen
 Pain in the abdomen that lasts for hours or days
AAA ruptures,
 Sudden, severe pain in the lower abdomen and back; nausea and
vomiting; clammy, sweaty skin; lightheadedness; and a rapid
heart rate when standing up.
 Internal bleeding lead to shock.
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89. Thoracic Aortic Aneurysms
Pain in the jaw, neck, back, or chest
Coughing, hoarseness, or trouble breathing or swallowing
TAA ruptures or dissects, sudden, severe pain starting in the
upper back and moving down into the abdomen.
Diagnosis
HX and P/E
AAA -throbbing mass in the abdomen.
Tender and very painful when pressed.
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90. Ultrasound
CT scan
MRI
Treatment
Beta blockers and calcium channel blockers
Open abdominal or open chest repair and
 Endovascular repair.
Prevention- avoid risk factors
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91. Hematologic Disorders
• Hematology is the study of blood and blood-
forming tissues.
• This includes bone marrow, blood, spleen,
and lymph system.
93
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92. Bone Marrow
• Blood cell production (hematopoiesis) occurs
within the bone marrow.
• Bone marrow is the soft material that fills the
central core of bones.
• All three types of blood cells (red blood cells
[RBCs], white blood cells [WBCs], and platelets)
develop from a common hematopoietic stem cell
within the bone marrow.
94
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93. 95
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94. Erythrocytes (Red Blood Cells)
• It is a biconcave disk that resembles a soft ball
compressed between two fingers.
• Mature erythrocytes consist primarily of
hemoglobin.
• The oxygen-carrying hemoglobin molecule is
made up of four subunits, each containing a
heme portion attached to a globin chain.
• Iron is present in the heme component of the
molecule.
96
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95. Erythrocytes (Red Blood Cells)
• Erythropoiesis
–Erythropoietin
–Vitamin B12 and Folic Acid
–Intrinsic factor
97
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96. ANEMIA
• Anemia is a deficiency in the number of
erythrocytes (red blood cells [RBCs]), the
quantity or quality of hemoglobin, and/ or the
volume of packed RBCs (hematocrit).
• As a result, the amount of oxygen delivered to
body tissues is also diminished.
• Anemia is not a specific disease state but a
sign of an underlying disorder.
98
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97. ANEMIA…..
• Anemia is a manifestation of an underlying
pathological condition.
• It results from:
1. Under production
2. Increased destruction/Hemolysis
3. Blood loss /bleeding
4. Multifactorial : a combination of these
99
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98. ANEMIA…..
Accurate history provides information crucial to the diagnosis of
the underlying cause.
• Nutritional /Dietary history
• Underlying diseases
• Blood loss : GI or Genito urinary blood loss
• Family history of anemia
• Exposure to drugs/toxins E.g. - Methyldopa
• Geographical location, pregnancy
100
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99. ANEMIA
• Cause of anemia
101
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100. ANEMIA
• Cause of anemia
102
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101. ANEMIA
• Cause of anemia
103
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102. Classification of Anemias
• Anemia may be classified in several ways
–Pathogenic classification
(Causes of anemia)
–Morphologic classification
104
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103. Classification of Anemias based on etiology
• Hypoproliferative (Resulting From Defective RBC
Production)
– Iron deficiency anemia
– Vitamin B12 deficiency anemia
– Folate deficiency anemia
– Aplastic anemia
• Bleeding (Resulting From RBC Loss)
– Bleeding from gastrointestinal tract, epistaxis
(nosebleed), trauma, bleeding from genitourinary
tract (eg, menorrhagia)
• Hemolytic (Resulting From RBC Destruction)
– Hemolytic anemia
– sickle cell anemia
– thalassemia
105
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104. Morphologic classification of anemia
• Microcytic
– Iron deficiency
– Thalassemia
• Normocytic
– Aplastic anemia
– Hemolytic anemia
– Anemia of chronic disease
• Macrocytic
– Megaloblastic
– Vitamin B12 deficiency…Pernicious anemia
– Folate deficiency 106
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105. ANEMIA: Clinical Manifestations
• Weakness, or fatigue, general malaise
• Dyspnea, tachycardia, palpitation, angina,
• dizziness, exercise and cold intolerance
• Tinnitus, vertigo, throbbing headache,
• Pallor skin, mucous membranes, conjunctiva, nail
beds
107
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106. ANEMIA: Assessment and Diagnostic Findings
• Hematocrit
–Male: 42–52%
–Female: 35–47%
• Hemoglobin
–Male: 13–18 mg/dL
–Female: 12–16 mg/dL
108
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107. Criteria of anemia in adults at sea level
109
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108. ANEMIA: Assessment and Diagnostic Findings
• Mean cell volume(MCV)
–MCV is average size of RBC
–MCV = Hct x 10
RBC (millions)
–If 80-100 fL, normal range, RBCs
considered normocytic
–If < 80 fL are microcytic
–If > 100 fL are macrocytic
110
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109. Hypoproliferative Anemias
–Iron deficiency anemia
–Vitamin B12 deficiency anemia
–Folate deficiency anemia
–Aplastic anemia
111
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110. Iron deficiency anemia
• Iron deficiency anemia occurs when body iron
stores become inadequate for the needs of
normal RBC production (erythropoiesis)
• It is the most common type of anemia in all age
groups, and it is the most common anemia in the
world.
• RBCs are small (microcytic) and the patient has
mild symptoms of anemia, including weakness
and pallor.
112
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111. Iron deficiency anemia: Causes
1. Chronic blood loss from Uterine, esophageal varices,
peptic ulcer disease; aspirin ingestion
2. Increased demands: Prematurity in newborns ,Rapid
growth ( as in adolescent ) ,Pregnancy
3. Mal absorption of iron: Gastrectomy, Celiac disease
4. Poor diet⇒ Contributory factor in many countries
113
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112. Iron deficiency anemia:
Clinical Manifestations
Specific symptoms
• Pica: craving for unusual food substance (geophagia)
• Increased GI absorption of lead – lead poisoning
• Koilonychia – spooning of the finger nails
114
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113. Iron deficiency anemia:Diagnostic Studies
 History and physical examination
 Hct and Hgb levels
 RBC count, including morphology
 Reticulocyte count
 Serum iron
 Serum ferritin
 Serum transferrin
115
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114. Iron deficiency anemia:
Medical management
• Increasing the oral intake of iron from food sources (e.g.,
red meat, organ meat, egg yolks, kidney beans, leafy green
vegetables, and raisins).
• An adequate diet supplies about 10 to 15mg of iron per
day.
• If iron losses are mild, oral iron supplements, such as
ferrous sulfate, are started. Ferrous sulphate, 325mg
116
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115. Iron deficiency anemia: Medical
management
• In some cases, oral iron is poorly absorbed or poorly
tolerated, or iron supplementation is needed in large
amounts.
• In these situations, IV or, infrequently, intramuscular (IM)
administration of iron may be needed.
• When iron deficiency anemia is severe, iron solutions can
be given IV or IM.
117
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116. Iron deficiency anemia: Nursing Management
• Because iron is best absorbed on an empty stomach, the patient
is instructed to take the supplement an hour before meals.
• Taking iron-rich foods with a source of vitamin C (eg, orange
juice) enhances the absorption of iron.
• Antacids or dairy products should not be taken with iron,
because they greatly diminish its absorption.
• Iron supplements are usually given in the oral form, typically as
ferrous sulfate.
118
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117. Megaloblastic anemias
 Megaloblastic anemias are a group of disorders caused by
impaired DNA synthesis and characterized by the presence of
large RBCs.
 When DNA synthesis is impaired, defective RBC maturation
results.
 The RBCs are large (macrocytic) and abnormal and are
referred to as megaloblasts.
 Macrocytic RBCs are easily destroyed because they have
fragile cell membranes. 119
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118. MEGALOBLASTIC ANEMIAS
• Caused by deficiencies of vitamin B12 or folic acid
–Vitamin B12 deficiency anemia
–Folic acid deficiency anemia
120
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119. Vitamin B12 deficiency anemia
Cause
Vitamin B12 deficiency occurs when inadequate vitamin
B12 is consumed, or, more commonly, when it is poorly
absorbed from the GI tract
Anemia resulting from failure to absorb vitamin B12
which is caused by a deficiency of intrinsic factor
121
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120. Vitamin B12 deficiency anemia:
Clinical Manifestations
Pallor or slight jaundice and weakness develop.
GI manifestations include a sore, red, beefy, and shiny
tongue; anorexia, nausea, and vomiting; and abdominal
pain.
Patients with pernicious anemia may also have
paresthesias in the feet and hands and poor balance and
reduced vibratory and position senses.
122
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121. Vitamin B12 deficiency anemia: Clinical
Manifestations
123
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122. Vitamin B12 deficiency anemia
Diagnostic Studies
 Clinical
 The RBCs appear large (macrocytic) and have abnormal
shapes.
 Serum folate levels
 A serum test for anti-IF antibodies
124
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123. Vitamin B12 deficiency anemia:
Medical Management
 Dieting Vegetables
 Intrinsic factor replacement
 IM injections of vitamin B12
A typical treatment schedule consists of 1000 mcg/day of
cobalamin IM for 2 weeks and then weekly until the
hemoglobin is normal, and then monthly for life.
 High-dose(2 mg/day) oral vitamin B12 and sublingual vitamin
B12are also available for those in whom GI absorption is intact.
125
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124. Folic acid deficiency anemia
Folic acid is stored as compounds referred to as folates.
The folate stores in the body are much smaller than those of
vitamin B12, and they are quickly depleted when the dietary
intake of folate is deficient (within 4 months).
Folate is found in green vegetables and liver.
Folate deficiency occurs in people who rarely eat uncooked
vegetables
126
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125. Folic acid deficiency anemia: Causes
Poor nutrition
Especially a diet lacking green leafy vegetables,
liver, yeast, dried beans, and nuts
Alcoholism
Pregnancy
Hemolytic anemias
Drugs: Chemotherapy, anticonvulsants
127
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126. Folic acid deficiency anemia:
Clinical Manifestations
Pallor, progressive weakness and fatigue, shortness of
breath, and heart palpitations.
No neurologic symptoms occur with folic acid deficiency
anemia, helping differentiate it from vitamin B12
deficiency anemia.
128
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127. Folic acid deficiency anemia:Medical Management
 Increasing the amount of folic acid in the diet
 Administering folic acid daily.
Folic acid, 1 to 5mg P.O., daily for 1-4 months, or
until complete hematologic recovery.
 Folic acid is administered intramuscularly only to people
with malabsorption problems.
130
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128. Aplastic anemia
• Aplastic anemia is a disease in which the patient has
peripheral blood pancytopenia and hypocellular bone
marrow.
• Because of failure of the bone marrow to produce these
cells.
• Therefore, in addition to severe anemia, significant
neutropenia and thrombocytopenia also occur.
131
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129. Aplastic anemia: Etiology
Aplastic anemia can be congenital or acquired, but most
cases are idiopathic.
Infections and pregnancy can trigger it, or it may be
caused by certain medications, chemicals, or radiation
damage.
Certain antibiotics (chloramphenicol), and
chemotherapeutic drugs.
132
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130. Aplastic anemia: Clinical Manifestations
• Fatigue, pallor, progressive weakness, exertional
dyspnea, headache, and ultimately tachycardia
and heart failure.
• Platelet deficiency leads to bleeding problems;
bleeding gums, excessive bruising, and nose
bleeds may be the initial symptoms.
• A deficiency of WBCs increases the risk of
infection, causing manifestations such as sore
throat and fever.
133
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131. Aplastic anemia: Assessment and
Diagnostic Findings
• Complete blood count (CBC) is done to determine
blood cell counts, hemoglobin, hematocrit, and RBC
indices
• Iron levels and total iron-binding capacity are
performed to detect iron deficiency anemia.
• Bone marrow examination is done to diagnose
aplastic anemia.
134
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132. Aplastic anemia: medical Management
Bone marrow transplant (BMT)
Immunosuppressive therapy
Supportive therapy: blood transfusion
135
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133. Hemolytic Anemias
Hemolytic anemia
Sickle cell anemia
Thalassemia
136
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134. Hemolytic Anemias
 Hemolytic anemias are characterized by premature
destruction (lysis) of RBCs.
 When RBCs break down, iron and other by-products of
their destruction remain in the plasma.
 RBC lysis (hemolysis) may occur within the circulatory
system or due to phagocytosis by WBCs such as
circulating monocytes and macrophages in the spleen.
137
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135. Hemolytic Anemias
• Hemolytic anemia has various forms.
Inherited forms include
– Sickle cell anemia
– Thalassemia
– Hereditary spherocytosis.
Acquired forms include
– Autoimmune hemolytic anemia
– Anemia associated with hypersplenism.
138
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136. Sickle cell disease (SCD)
• In healthy adults, the normal hemoglobin molecule
has two alpha chains and two beta chains of amino
acids.
• Normal adult hemoglobin is called hemoglobin A
(HbA).
• Normal adult red blood cells usually contain 98% to
99% HbA, with a small percentage of a fetal form of
hemoglobin (HbF).
139
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137. Sickle cell disease (SCD)
• The main problem in Sickle cell disease is the
formation of abnormal hemoglobin chains.
• In SCD, at least 40% (and often much more) of the total
hemoglobin is composed of an abnormality of the beta
chains, known as hemoglobin S (HbS).
– Hemoglobin S (Hgb S), results from the substitution of
valine for glutamic acid on the β-globin chain of hemoglobin
• HbS is sensitive to changes in the oxygen content of
the RBC.
140
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138. Sickle cell disease (SCD)
141
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139. 142
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140. Sickle cell disease (SCD)
• When RBCs having large amounts of HbS are exposed to
decreased oxygen conditions, the abnormal beta chains
contract and pile together within the cell, distorting the
shape of the RBC.
• These cells assume a sickle shape, become rigid, and
clump together, causing the RBCs to become “sticky” and
fragile.
143
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141. Sickle cell disease (SCD)
• These clumps form masses of sickled RBCs that
block blood flow.
• leads to further tissue hypoxia (reduced oxygen
supply) and more sickle-shaped cells, which then
leads to more blood vessel obstruction and
ischemia.
144
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142. Sickle cell disease (SCD)
Conditions that cause sickling include
• Hypoxia,
• Dehydration,
• Infections,
• Venous stasis,
• Pregnancy,
• Alcohol consumption,
• High altitudes
145
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143. Sickle cell disease (SCD)
• The average life span of an RBC containing 40% or
more of HbS is about 12 to15 days, much less than
the 120-day life span of normal RBCs.
• This reduced RBC life span causes hemolytic
(blood cell–destroying) anemia in patients with
sickle cell disease.
146
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144. Sickle cell anemia
147
A normal red blood cell
• Sickle cell anemia is a severe hemolytic anemia
that results from inheritance of the sickle
hemoglobin gene.
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145. 148
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146. Sickle cell anemia: Clinical Manifestations
• Sickling causes general manifestations of hemolytic
anemia, including pallor, fatigue, jaundice, and irritability.
• Obstruction of blood flow triggers vasospasm that halts
all blood flow in the vessel.
• Vaso occlusive crises are painful and last an average
of 4 to 6 days.
• Infarction of small vessels in the extremities causes
painful swelling of the hands and feet; large joints also
may be affected.
149
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147. Sickle cell anemia: Assessment and
Diagnostic Findings
150
• Low hematocrit and sickled cells on the smear.
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148. Sickle cell anemia: Medical Management
• Peripheral Blood Stem Cell Transplant
• Pharmacologic Therapy: Hydroxyurea, Arginine??
• Daily folic acid replacements??
• Antibiotics for infection
• Supportive Therapy:
– Pain management
– Adequate hydration
– Supplemental oxygen
– Transfusion Therapy
151
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149. 12/28/2023 Tadele M 155

150. Varicose veins
Definition: varicose veins are veins that have become enlarged
and tortuous.
Pathophysiology
 Varicose veins may be considered primary (without
involvement of deep veins) or secondary (resulting from
obstruction of deep veins)
 Calf Skeletal muscle contraction helps blood to be perfused
against gravity
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151. If only the superficial veins are affected, the person may
have no symptoms but may be troubled by the appearance
of the dilated veins.
Causes and risk factors
Age and Pregnancy
Sex and Genetics
Obesity and Standing for long periods of time
Crossing knees
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152. Sign & symptoms
 Twisted and bulging; often like cords on legs
 An achy or heavy feeling in legs
 Burning, throbbing, muscle cramping and swelling in
lower legs.
 Worsened pain after sitting or standing for a long time
 Itching around one or more of veins
 Skin ulcers near ankle
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153. 12/28/2023 Tadele M 159

154. Complications
 Ulcers (ankles).
 Blood clots.
Diagnosis
History & physical exam
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155. Treatment of VV
Self-care: exercising, losing weight, not wearing tight
clothes, elevating your legs, and avoiding long periods
of standing or sitting.
Manual Compression
 Compressive bandage
Legs above heart
 urgery – vein transplant, repair
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156. Thrombotic Disorders: DVT
• Venous thrombosis is a condition in which a blood clot
(thrombus) forms on the wall of a vein, accompanied by
inflammation of the vein wall and some degree of
obstructed venous blood flow.
• Deep vein thrombosis (DVT) is the formation of a blood
clot (thrombus) in a deep vein, predominantly in the legs.
162
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157. DVT:
Factors Associated with Venous Thrombosis
• Immobilization: myocardial infarction, heart failure,
stroke, postoperative
• Surgery:
• Cancer:
• Trauma:
• Pregnancy
• Hormone therapy: oral contraceptives, hormone
replacement therapy
• Coagulation disorders
163
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158. DVT: Etiology……….
• Three important factors (called Virchow’s triad) in the
etiology of venous thrombosis :
(1) Venous stasis
(2) Damage of the endothelium (inner lining of the vein)
(3) Hypercoagulability of the blood
164
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159. DVT: Pathophysiology
Platelets and fibrin form the initial clot. Red blood cells
are trapped in the fibrin meshwork, and the thrombus
propagates (grows) in the direction of blood flow.
Vessel trauma stimulates the clotting cascade. Platelets
aggregate at the site, particularly when venous stasis is
present.
Three pathologic factors, called Virchow’s triad: stasis of
blood, vessel damage, and increased blood coagulability.
165
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160. DVT: Pathophysiology
Fibroblasts eventually invade the thrombus, scarring the
vein wall and destroying venous valves. Although patency
of the vein may be restored, valve damage is permanent,
affecting directional flow
Initially the thrombus floats within the vein. Pieces of the
thrombus may break loose and travel through the
circulation as emboli.
The inflammatory response is triggered, causing
tenderness, swelling, and erythema in the area of the
thrombus.
166
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161. DVT: Clinical Manifestations
 Calf pain
 Tenderness
 Swelling
 Red or Warm Leg
 Dilated Veins
 Low Grade Fever
 Cyanosis of affected extremity
 A positive Homan’s sign 167
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162. DVT: Clinical Manifestations
168
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163. DVT: Complications
• The major complications of deep vein
thrombosis are:-
Chronic venous insufficiency
Pulmonary embolism.
169
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164. DVT: Assessment and Diagnostic Findings
History & Physical examination
Doppler ultrasound of leg and pelvic veins
Magnetic resonance imaging (MRI)
D-dimer: Normal results: <250 ng/mL
Blood Laboratory Studies
170
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165. DVT: Assessment and Diagnostic Findings
• Blood Laboratory Studies
171
Test Normal Value DVT Value
WBC 4,000 – 11,000 Increased
Platelet 150,000 –
400,000 per ul
Increased
PT 11.0 - 12.5 sec Decreased
APTT 30 - 40 sec Decreased
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166. DVT: Medical Management
• Pharmacologic
• Acute treatment : First line
– Unfractionated heparin (UFH), 5000 U, IV, bolus then 250
U/Kg/dose, BID or 17,500U SC, BID (for an average adult) PLUS
Warfarin (starting simultaneously with heparin), 5 mg P.O., daily
with regular dose adjustment
Chronic treatment
– Warfarin,
– Prophylaxis is indicated for many medical and
surgical patients who are hospitalized. 172
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167. DVT: Nursing Management
• Monitoring and Managing Potential
Complications
–Bleeding
–Thrombocytopenia
–Drug Interactions
173
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168. DVT:Nursing Management
• Providing Comfort
– Elevation of the affected extremity, graduated
compression stockings, and analgesic agents for pain
relief are adjuncts to therapy.
– They help improve circulation and increase comfort.
– Warm, moist packs applied to the affected extremity
reduce the discomfort associated with DVT.
174
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169. 175
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170. Leukemia
• The term leukocytosis refers to an increased level
of leukocytes in the circulation.
• Leukemias are neoplasms of hematopoietic cells
proliferating in the bone marrow initially
• then disseminate to peripheral blood, lymph
nodes, spleen, liver etc.
• Lymphomas differ from leukemias in that,
lymphomas arise primarily from lymph nodes
• but spread to blood and bone marrow only in
"leukemic phase” of the diseases.
176
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171. Epidemiology and incidence
• Leukemia is the general term used to
describe a group of malignant disorders
affecting the blood and blood-forming
tissues of the bone marrow, lymph system,
and spleen.
• Leukemia occurs in all age-groups.
177
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172. Epid.con’ted…
• Are higher in whites than in people of other racial and
ethnic groups.
• Overall, men are more likely to develop leukemia than
women.
• AML accounted for approximately 25% of all
leukemias in adults and 15%-20% in patients age ≤
15 years.
178
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173. Etiology
Mostly unknown
High level radiation/toxin exposure
Exposure to chemicals and drugs
 Bone marrow hypoplasia genetic factors
Immunologic factors
 Environmental factors(viruses) and the interaction of
theses
179
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174. Pathophysiology
• Leukemia is a type of cancer with uncontrolled
production of immature white blood cells (usually
blast cells) in the bone marrow.
• As a result, the bone marrow becomes
overcrowded with immature, nonfunctional cells
and production of normal blood cell is greatly
decreased.
180
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175. Pathophysiology…
• The cells are abnormal and excessive
• bone marrow stops normal production of red
blood cells, platelets, and mature leukocytes.
• Anemia, thrombocytopenia, and
leukopenia result.
181
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176. Con’ted…
• Leukemic cells can also be found in the
spleen, liver, liver nodes and central
nervous system.
• Without treatment, the client dies of
infection or hemorrhage.
182
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177. Assessment & diagnosis of leukemia
Physical examinations: looking for physical signs of
leukemia, such as pale skin from anemia, swelling of
lymph nodes, and enlargement of liver and spleen.
Blood tests: analyzing a patient's blood sample through
CBC
Bone marrow test
183
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178. Management of leukemia
Common treatments used to fight leukemia
 Chemotherapy is the major form of treatment of leukemia
 Targeted therapy
 Radiation therapy
 Bone marrow transplant
 Immunotherapy
 Engineering immune cells to fight leukemia
184
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179. 185
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180. Lymphoma
 Lymphoma is cancer of the lymphatic system
 The lymphatic system is the body's disease-fighting
network.
 It includes the lymph nodes, spleen, thymus gland
and bone marrow.
 The main types of lymphoma are Hodgkin's
lymphoma and non-Hodgkin's lymphoma.
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181. Classifications of lymphoma
Non-Hodgkin's lymphoma:
 Cancer that starts in the lymphatic system.
 The condition occurs when the body produces too many
abnormal lymphocytes, and can form growths (tumors)
throughout the body. a type of white blood cell.
 Symptoms include swollen lymph nodes, fever, stomach
pain or chest pain.
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182. Classifications of lymphoma…
Hodgkin's lymphoma
 It is a type of cancer that affects the lymphatic system
 In which lymphocytes grow out of control, causing
swollen lymph nodes and growths throughout the body
 Hodgkin lymphoma is marked by the presence of Reed-
Sternberg lymphocytes
 In non-Hodgkin lymphoma, these cells are not present.
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183. Diagnosis of lymphoma
A diagnosis of lymphoma is confirmed by tissue
biopsy
Commonly used methods include
Excisional biopsy is considered the "gold standard"
as it allows for the assessment of whole lymph node
architecture through fine-needle aspiration
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184. Management of lymphoma
Treatment may involve
Chemotherapy,
Medication,
Radiation therapy
Rarely stem-cell transplant.
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185. SHOCK
• Is a condition in which system blood pressure is
inadequate to deliver oxygen and nutrients to
support vital organs and cellular function.
• It is characterized by inadequate tissue perfusion, if
untreated results in cell death.
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186. SHOCK
• Adequate blood flow to the tissue and cell requires
the following components:-
• Adequate cardiac pump
• Effective circulatory system
• Sufficient blood volume
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187. Quiz 5%
1. What are three important factors (Virchow’s triad)
in the etiology of venous thrombosis?
2. What are the complications of DVT?
3. What are the difference between Leukemia and
lymphoma?
4. List and discuss types of shock
5. Write at least 3 clinical manifestations of shock?
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188. Types of shock
• Hypovolemic shock
• Cardiogenic shock
• Circulatory shock
• Septic shock
• Neurologic shock
• Anaphylactic shock
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189. Types of shock: Hypovolemic shock
–The most common type
–Characterized by a decreased in intravascular
volume
–Risk factors
• Trauma
• Surgery
• Vomiting
• Diarrhea
• Hemorrhage
• Burn
• Dehydration
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190. Types of shock
• Hypovolemic shock…..Pathophysiology
• Risk factor
• Decreased blood volume
• Decreased venous return
• Decreased stroke volume
• Decreased cardiac out put
• Decreased tissue perfusion
–Shock 196
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191. Types of shock
• Cardiogenic shock
–Occur when the heart’s ability to contract and to
pump blood is impaired and the supply of oxygen
is inadequate for the brain and other vital organs.
–Clinical manifestation
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192. Types of shock
• Cardiologic shock….Pathophysiology
• Decreased cardiac contractility
• Decreased cardiac out put
• Decrease stroke volume
• Decreased systemic tissue perfusion
»Shock
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193. Types of shock
• Circulatory shock
–Occur when blood is mal distributed in the body.
–The displacement of blood volume causes a
relative hypovolemic because not enough blood
returns to the heart which leads to subsequent
inadequate tissue perfusion.
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194. Types of shock
• Circulatory shock….Pathophysiology
• Vasodilatation
• Misdistribution of blood volume
• Decreased venous return
• Decreased stroke volume
• Decreased cardiac out put
• Decreased tissue perfusion
»Shock 200
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195. Types of shock: Circulatory shock
• Septic shock
– The most common type and caused by wide
spread of infection.
– Its dangerous low blood pressure through the
action of bacterial lipopolysaccharide called
endotoxin.
– Endotoxin activate the enzyme nitric oxide
synthase with in macrophage.
– Nitric oxide synthase produces nitric oxide
which promotes vasodilatation which decrease
blood pressure.
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196. Types of shock: Circulatory shock
• Neurologic shock
• Vasodilatation occur as a result of a loss of
sympathetic tone.
• Caused by:-
–Spinal cord injury
–Spinal anesthesia
–Nervous system damage
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197. Types of shock: Circulatory shock
• Anaphylactic shock
–Caused by sever allergic reaction that are foreign
to the body and immediate reaction cause massive
vasodilatation and increase capillary permeability
–Widespread release of histamine cause
vasodilatation.
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198. SHOCK…Signs and Symptoms
 Pale or bluish skin and mucus membrane(cyanotic skin)
 Cool clammy extremities, Weakness.
 Rapid and weak pulse (HR)
 Rapid and shallow breathing
 Low blood pressure.
 Restlessness, anxiety severe thirst, Fever and vomiting
 Hypotension, Tachypenia
 Kidneys-decrease urine out put –renal failure-death
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199. Medical management: Hypovolemic shock
• Infusion of fluid (Normal saline or Ringer lactate) 1-2
liters fast; reassess the patient for adequacy of treatment; if
needed repeat the bolus with maximum tolerated dose being
60 – 80 ml/kg with in the first 1 – 2 hr.
– If due to hemorrhage, apply transfusion of packed Red
Blood Cells (RBC) or whole blood 20ml/kg over 4 hrs,
repeat as needed until hgb level reaches 10gm/dl and the
vital signs are corrected.
• Correct the underlying cause of fluid loss
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200. Medical management: Cardiologic shock
• Dopamine, 5-50mcg/kg/min IV diluted with
dextrose 5% in Water, or in sodium chloride
solution 0.9%;
• Improve the cardiac function by increasing
cardiac contractility: Nitroglycerine
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201. Thrombocytopenia
 Thrombocytopenia (low platelet level) can result from
 Decreased production of platelets
 Increased destruction of platelets
Clinical Manifestations
 Bleeding and petechiae usually do not occur with platelet
counts greater than 50,000/mm3, although excessive
bleeding can follow surgery or other trauma.
 When the platelet count drops below 20,000/mm3,
petechiae can appear, along with nose and gingival bleeding,
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202. Cont…d
 Excessive menstrual bleeding, and excessive bleeding
after surgery or dental extractions.
 When the platelet count is less than 5000/mm3,
spontaneous, potentially fatal central nervous system
or gastrointestinal hemorrhage can occur.
 If the platelets are dysfunctional due to disease or
medications (eg, aspirin), the risk of bleeding may be
much greater even when the actual platelet count is not
significantly reduced.
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203. Diagnostic Findings
 Examining the bone marrow via aspiration and biopsy.
 When platelet destruction is the cause of
thrombocytopenia, the marrow shows increased
megakaryocytes
 Another cause of thrombocytopenia is sequestration.
 Approximately one third of the circulating platelets are
within the spleen, and a greatly enlarged spleen results
in increased sequestration of platelets.
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204. Medical Management
 If platelet production is impaired, platelet transfusions
 If excessive platelet destruction occurs, transfused
platelets will also be destroyed, and the platelet count
will not rise.
 The most common cause of excessive platelet destruction
is Idiopatic thrombocytopenic pupura (ITP)
 In some instances splenectomy can be a useful
therapeutic intervention,
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205. HEMOPHILIA
 Two inherited bleeding disorders, hemophilia A and hemophilia
B are clinically indistinguishable
 Hemophilia A is caused by a genetic defect that results in
defective factor VIII
 Hemophilia B stems from a genetic defect that causes defective
factor IX.
 Hemophilia is a relatively rare disease; hemophilia A, which
occurs in 1 of every 10,000 births, is three times more common
than hemophilia B
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206. HEMOPHILIA…
 Both types of hemophilia are inherited
 The disease is recognized in early childhood, usually in
the toddler age group.
 However, patients with mild hemophilia may not be
diagnosed until they experience severe trauma or
surgery.
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207. Clinical Manifestations
 Hemorrhages into various parts of the body.
 Hemorrhage can occur even after minimal trauma.
 The frequency and severity of the bleeding depend on
the degree of factor deficiency as well as the intensity
of the precipitating trauma.
 Spontaneous hemorrhages, particularly hemarthroses
and hematomas, can frequently occur in patients with
severe factor VIII deficiency
 These patients require frequent factor replacement
therapy.
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208. Clinical Manifestations
 About 75% of all bleeding in patients occurs into joints.
 The most commonly affected joints are the knees, elbows,
ankles, shoulders, wrists, and hips.
 pain in a joint , swelling and limitation of motion.
 Hematomas, which results in decreased sensation,
weakness, and atrophy of the area involved.
 Spontaneous hematuria and gastrointestinal bleeding can
occur.
 The most dangerous site of hemorrhage is in the head
(intracranial or extracranial).
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209. Medical Management
 In the past, the only treatment for hemophilia was
infusion of fresh frozen plasma,
 Now factor VIII and factor IX concentrates are
available to all blood banks.
 It is crucial to initiate treatment as soon as possible
so that bleeding complications can be avoided.
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210. Q1. A patient with a hematologic disorder asks the
nurse how the body forms blood cells. The nurse
should describe a process that takes place where?
• A) In the spleen
• B) In the kidneys
• C) In the bone marrow
• D) In the liver
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211. Q2. Through the process of hematopoiesis, stem cells
differentiate into either myeloid or lymphoid stem cells.
Into what do myeloid stem cells further differentiate?
• A) Leukocytes
• B) Natural killer cells
• C) Cytokines
• D) Platelets
• E) Erythrocytes
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212. Q3. A patients electronic health record states that the
patient receives regular transfusions of factor IX.
The nurse would be justified in suspecting that this
patient has what diagnosis?
• A) Leukemia
• B) Hemophilia
• C) Hypoproliferative anemia
• D) Hodgkins lymphoma
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213. THE END!!!
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214. References
• Brunner & Suddarth's Textbook of Medical-Surgical
Nursing, 11th edition.
• Brunner & Suddarth’s textbook of medical-surgical nursing.
2010, 12th ed.
• Porth’s pathophysiology. Concepts of Altered Health States,
2014 ,9th edition.
• Sharon L. Lewis, Shannon Ruff Dirksen, Et Al .Medical-
surgical Nursing: Assessment And Management Of Clinical
Problems, 2014, Elsevier Inc. Ninth Edition
• Medical surgical nursing. patient centered collaboration
care, 7th edition
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215. Thank You for Being
Patient Till the End
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