Hematology and Immunology Health Alterations Flashcards
(170 cards)
1
Q
hematology
A
focus on blood disorders
such as benign disorder, clotting, bleeding or malignant disorder
2
Q
components of the blood
A
red blood- carry oxygen
platelets help with clotting and healing
white blood cells- helps with infection
plasma regulate bleeding and clotting
3
Q
lymphoma
A
is a cancer that develops in white blood cells called lymphocytes. lymphocytes are the main part of the immune site that circulate in blood vessels. lymphocyte can enter blood and tissue to respond to viruses and bacteria. lymphoma develop when the white blood cells develop too rapidly and develop a mass that occurs organs and tissues
4
Q
healthy cells vs cancer cells
A
healthy cells- have short life span and regenerate. cancer cells multiple never dies and create mass and spread throughout the body
5
Q
the role of protein in blood clotting
A
- clotting factors help the platelets stick together to plug cuts and breaks at the site of the injury to stop the bleeding. if lack of clotting profuse bleeding may occur
6
Q
DVT (deep vein thrombosis)
A
occurs when a lot breaks off and travels through the circulation system. when it reaches the blood vessels it can not pass through it is called a embolism.
7
Q
sickle cell
A
red blood cells create a sickle shape
bone marrow tries to make more red cells, however, the bone marrow can not keep up with production and may cause anemia
the sickle cells and “jam up” and stick to the walls of the blood vessels.
this may lead to delayed oxygen delivery
8
Q
primary prevention
A
promoting healthy lifestyle, weight control, and physical activity
9
Q
secondary prevention
A
screening/ control of multiple risk factors
10
Q
tertiary prevention
A
CAD management after coronary event
11
Q
framingham risk scoring system
A
score each of the patients relevant risk factors such as: age sex HDL cholesterol Total choestrol systolic BP smoking status diabetic status family history ECG
12
Q
risk factors of cardiac diseases are
A
smoking and abnormal ratio of blood lipids
other factors are:
diabetes, hypertension, abdominal obesity, psychosocial factors, lack of daily consumption, diet and exercise
13
Q
possible cardiac test are
A
ECG, stress test, myocardial perfusion imaging, MRI CT and calcium score.
14
Q
examination of the cardiovascular system
A
assessment usually done on patients right side
assess heart function
signs of SOB 10-20/min
color, expression, sweating and pallor of face
upper extremities:
color, temp, capillary refill (2 sec),
Lower extremities
exam venous system
note color and temp of legs
edema
hair distribution
varicose veins
15
Q
arterial pulse
A
radial pulse, assess rhythm, quality, equality, avg 50-100
16
Q
irregular heart beat
A
a-fib, ventricular ectopic beats,
17
Q
Jugular venous pressure
A
supine position
raise to 45-degree angle
measure the angle
low JVP may mean hypovolemia due to haemorrhage
elevated JVP is elevated due to heart failure, tricuspid insufficiency, constrictive pericarditis,
https://www.youtube.com/watch?v=MZKSkVSbH8k
18
Q
pericardium
A
assesses the membrane enclosing the heart, consisting of an outer fibrous layer and an inner double layer of serous membrane
Usually done on a 30 degree angle
look for deformities of the chest
palpate apical pulse on 5th and 6th intercostal rib
19
Q
gradation of murmurs
A
Grade 1 Very faint, may be barely audible with a stethoscope in a quiet room
Grade 2 Quiet, but heard when the stethoscope is placed over the heart
Grade 3 Moderately loud
Grade 4 Loud, with palpable thrill
Grade 5 Very loud, thrill palpated easily
Grade 6 Audible when stethoscope not in contact with chest wall, thrill palpated easily
20
Q
acute coronary syndromes
A
Varied presentation across anterior chest and may be radiating to neck, jaw, shoulders or arms • Described as “pressing, squeezing, tightness, heaviness or burning” • May occur with exertion or at rest depending on degree of myocardial ischaemia • May be relieved by rest or require nitroglycerine or morphine • Sometimes accompanied by dyspnoea, sweating,
21
Q
Aortic anerysum
A
• Anterior chest pain radiating to back, abdomen or neck • Severe with a “ripping” or “tearing” feeling • Usual starts abruptly and persistent • May also have syncope, hemiplegia or paraplegia
22
Q
pericariditis
A
Usually in the precordial area with radiation to the shoulder tip and neck • Described as “sharp” or “knifelike” • Tends to be persistent and aggravated by breathing, coughing, lying down and changing position • Position changes may give some relief
23
Q
pluerisy
A
• Discomfort in chest wall overlying area of inflammation • Often severe, persistent • Described as “sharp, knifelike” • Aggravated by coughing, movements of the thorax • Lying on the involved side may provide some relief • May also be associated with other symptoms of pneumonia, pulmonary infarction or neoplasm
24
Q
oespohagpgastric disorder
A
Typically just behind the sternum, may radiate to • back • Described as “burning, squeezing” and symptoms may be similar to angina • Tends to be unpredictable and variable onset • Aggravated by large meals, lying down or bending over. Activity does not tend to exacerbate the discomfort
25
chest wall pain
May be related to a minor injury and can be anywhere along costal cartilages or elsewhere in the thorax • Severity is variable and feels like a stabbing, sticking, aching discomfort • May be aggravated by movement of the chest, arms and trunk There may be localised tenderness
26
clinical examination regarding cardiac issue
• • Airway – assess for any signs of airway obstruction and treat airway obstruction as an emergency. Administer oxygen at a high concentration as soon as possible. Breathing – look, listen and feel for signs of breathing problems. An increased breathing rate may be the first physiological observation to alter in the deteriorating patient (Smith et al. , 2002). Count the respiratory rate while assessing the depth and pattern of breathing. Lifethreatening conditions (acute severe asthma, pneumothorax and pulmonary oedema) must be treated immediately. Provide breaths with a pocket mask or bag-mask to any patient who has stopped breathing or has inadequate breathing. Circulation – do a rapid general examination of the patient noting colour of hands and feet and temperature of the hands. Measure CRT. Take a blood pressure and look for other signs of decreased cardiac output such as a change in level of consciousness. Any patient with a suspected ACS should be treated initially with oxygen, aspirin, nitroglycerine and morphine. A 12-lead ECG should be recorded. Disability – assess the patient’s conscious level quickly using AVPU: A lert, responds to V ocal stimuli, responds to P ainful stimuli or U nresponsive. Hypoxia, hypercapnia and cerebral hypoperfusion are common causes of unconsciousness.
Exposure – look at the patient exposed from head to toe and consider anything else that may be causing chest pain (e.g. injury, trauma)
.
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diagnostic procedure
```
chest xray
echo
exercise tolerance test
myocardial Perfusion scintigraphy
coronary angiogram
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28
biochemical markers
creatine phosphokinase
troponin
ECG
29
ACS with unstable angina
ECG change: ST depression, T inversion, or transient ST elevation
Troponin normal
30
ACS with myocyte nercosis
ECG change ST depression, T inversion, or transient ST elevation
Troponin sightly elevated
31
ACS with clinical myocardial infraction
ST elevation or depression, T inversion and q wave may evolve, significantly elevated
32
risk stratification
```
assess 8 factors:
grade of heart failure
systolic BP
HR
age
creatinine
cardiac arrest
```
33
unstable angina
With unstable angina the flow of blood in the coronary arteries is markedly reduced, leading to the patient experiencing pain at rest or on minimal exertion. This difference in symptoms can be explained by the different nature of atherosclerotic plaque in the coronary arteries. The plaque of stable angina is intact but reduces the size of the lumen of the artery, limiting the rate at which blood can flow through it. In contrast, the coronary artery plaque in unstable angina may have ruptured or eroded, exposing the plaque core to blood flow. This core, which includes lipid, vascular smooth muscle cells, lymphocytes and modified macrophages called foam cells, is highly thrombogenic (Falk et al ., 1995). Its exposure causes platelet activation, thrombin production and fibrin deposition, resulting in thrombus formation in the artery, markedly reducing the lumen and blood flow. In addition, plaque content and small emboli from the thrombus may migrate, occluding smaller vessels distal to the rupture. It is the presence of thrombus in the artery that makes unstable angina an ACS. However, there are other critical events that may lead to unstable angina; it may present as troponin-negative and may arise because a coronary stenosis has grown so tight that it limits the blood supply, or in multi-vessel coronary disease the worsening of a single lesion can disrupt the balance of a potentially critical blood supply. The trigger for the rupture or erosion of plaque in unstable angina is unclear. The relative contributions of plaque contents to its stability and also inflammatory processes have been proposed as causes. The inflammatory marker C-reactive protein may be elevated in unstable angina. While a widespread, large quantity of plaques can lead to unstable angina, it is clear that atherosclerotic plaque is subject to dynamic processes and that plaque rupture and erosion occur without the patient suffering pain, often many times. Indeed, one study has demonstrated that a significant number of people without symptoms have evidence of plaque rupture and erosion in their coronary arteries (Falk et al ., 1995). The finding that plaque which ruptures may not be causing a flow-limiting stenosis prior to rupture suggests the quality, rather than quantity, of the plaque is more important (Braganza and Bennett, 2001). The pain of unstable angina arises from myocardium that is ischaemic, i.e. there is insufficient oxygen to meet tissue demands. In stable angina this may be due to increased tissue demand, for example on exercise, with blood flow limited by atheroma.
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unstable angina cont'd
anginga are diagnosed when patient’s symptoms, with evidence of cardiac disease, no ECG evidence myocardial infarction and negative troponins
35
symptoms of a unstable angina
angina is chest pain, which is often described as a tight or heavy pain. There may be associated pain in the arms, more commonly the left arm, and the throat or jaw. The pain of unstable angina differs from the pain of stable angina in that either: • • the pain lasts more than 20 minutes at rest the patient has developed new angina pain that severely limits mild physi• cal activity, such as walking or climbing stairs or which occurs at rest (Campeau, 1976) the patient with stable angina now experiences anginal pain that severely limits mild physical activity, such as walking or climbing stairs or which occurs at rest, this is commonly described as crescendo angina the patient has developed angina pain following a myocardial infarction (Bassand et al ., 2007). • Less frequently, the presenting symptoms of unstable angina include breathlessness, palpitations, epigastric discomfort, shoulder or neck pain and syncope. Some patient groups, notably women, diabetics and elderly patients, are more likely to describe atypical symptoms
36
assessment of unstable angina is
rapid ABCDE evaluation and the recording of vital signs taking a focused patient history investigations including a 12-lead ECG routine baseline blood chemistry.
37
unstable agnina tx
```
rest and analgesia
anti-ischemic therapy
anti platelet therapy
anticoagulant
plaque stabilization
```
38
non- st segment elevation myocardial infarction
similar to a unstable angina
In NSTEMI, cardiac enzyme blood tests are abnormal, indicating that at least some actual cell damage is occurring to heart muscle cells. The patient with NSTEMI will be experiencing the same critical events that led to disruption in the cardiac blood supply, which include unstable plaque and thrombus in their coronary arteries and critical coronary stenosis that is limiting the blood supply; in multi-vessel coronary disease, the worsening of a single lesion can disrupt the balance of a potentially critical blood supply.
39
pathogensis of NSTEMI
The common underlying causative mechanism is sudden fissuring, erosion or rupture of the cap of an atherosclerotic plaque in a coronary artery. Subendothelial collagen becomes exposed and promotes platelet adhesion, aggregation and activation. A surrounding fibrin-rich thrombus develops around the platelets and is accompanied by a complex set of reactions including vasoconstriction, inflammation and micro-embolism (Edwards and Pitcher, 2005). The result is reduced coronary arterial blood flow, but the pathological and clinical consequences are variable, depending on whether occlusion of the coronary artery is partial or total, the degree of collateral blood flow to the affected myocardium and the mass of myocardium affected
40
sings and symptoms of NSTEMI are
chest pain
SOB
nausea
vomiting
diaphoresis (sweating)
palpitations anxiety or sense of impending doom a feeling of being acutely ill
non-specific ECG changes – ST segment depression/T wave inversion ( see Figures 6.3 and 6.4) raised troponin levels (amount released reflects extent of myocardial damage).
41
treatment for NSTEMI
pain relief
-IV morhpine/diamorphine
stabilizing nausea with antimetic suchas cyclizine or metocloppramide
anti platelet agents
-such as aspirin, platelet ADP receptor such as clopiogderl or prasugel
glycoprotein llb/ illa inhibitor
Anti-thrombin agents
- heparin(blocks thrombin production, can reduce thrombus formation,
- LMWH
Anti-ischemic agents decrease myocardial oxygen use by decreasing heart rate, lowering BP, decrease left ventricular contraction and increase vasodilationand improve pain relief. medication such as nitrate, beta blockers, calcium channel blockers
42
medication that can help reduce reoccurence of cardiovascular events
```
aspirin
clopidogrel
ACE
beta blockers
calcium channel blockers
long acting nitrate
statin
```
43
st segment elevation myocardial infarction
STEMI is defined by myocardial necrosis consistent with myocardial ischaemia indicated by persistent ST segment rise. Patients presenting with STEMI may go on to develop Q waves on their ECG and show a rise in biomarkers indicative of cardiac necrosis (European Society of Cardiology, 2008; Thygesen et al ., 2007). This finding will be determined by the speed of reperfusion and resultant myocardial necrosis.
44
pathogensis of STEMI
is a cardiac necrosis caused by a cessation of blood flow to the myocardium. This is usually the result of a blockage to one of the major epicardial coronary arteries supplying the myocardium with oxygenated blood. Commonly the blockage is caused by a blood clot (thrombus) that forms over a ruptured atherosclerotic plaque. When a vulnerable atherosclerotic plaque ruptures, a chain of events occurs resulting in coronary artery occlusion and a medical emergency. If the thrombus fully occludes the coronary artery then STEMI will occur (Moser and Riegal, 2008). Other less common causes of STEMI include coronary artery spasm, coronary dissection, coronary embolism and pericardiac interventions. Anaemia, arrhythmias, hypertension and hypotension can also lead other myocardial injury.
When the blood flow to the myocardium deteriorates, myocardial oxygen demands exceed those of supply and the myocardial cells begin an immediate process of demise.
45
signs and symptoms of STEMI
Patients suffering from STEMI will present in a variety of ways depending on:
• the size and location of the infarct
• the degree of chest pain experienced
• the response of the autonomic nervous system to injury • the patient’s co-morbidities and previous experience.
Generally patients will present with:
chest pain nausea and possible vomiting dyspnoea (breathlessness) anxiety or a feeling of “impending doom” diaphoresis (sweating) pallor.
Most of the common presenting symptoms will result from the activation of the autonomic nervous system in response to injury, pain and anxiety. Sympathetic nervous response can lead to peripheral vasoconstriction causing the patient to look pale, and feel cool and clammy.
As blood is moved away from the skin’s surface during vasoconstriction, a film of sweat may appear over the patient’s skin. This fluid would normally be invisible as it is evaporated by the warm blood flowing near to the skin’s surface. Inhibition of insulin production can lead to an increase in blood glucose (Richards, 2005). Heart rate, respiration rate and blood pressure may increase to varying degrees as part of the sympathetic nervous response. Occasionally patients may experience a parasympathetic nervous response (more common in inferior and posterior infarcts; see below) and experience a low heart rate and blood pressure. Relaxation of the sphincters in the
46
chest pain assessment (PQRST)
P
Precipitating or Palliating factors
Qualitative factors Findings associated with STEMI Pain constant, can start at rest, unrelieved by rest, breathing or movement
Region and Radiation Tightness, heaviness, pressure, constriction, burning, difficult to pin point (clenched fist over central chest normally used to demonstrate – Levine’s sign)
Severity and associated Symptoms Retrosternal, radiating to anywhere from the lower jaw to the epigastrium but commonly ulner aspect of the arms and hands
Timing Ranges from “worse pain ever” to mild pain. Measure using a numerical rating scale from 1 to 10. Associated symptoms include sweating, dyspnoea, nausea, vomiting, weakness, anxiety, pallor Lasts in excess of 20 minutes
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treatment for STEMI
Aspirin 150–325 mg oral (ESC, 2008) - Platelet aggregation inhibitor Recommends administering oxygen therapy to those who are breathless or showing signs of heart failure
Oxygen therapy ESC (2008) BTS (2008) - Recommend that oxygen should not be used to treat breathlessness but hypoxaemia: only be given for hypoxaemic patients to • maintain saturations of 94–98% or 88–92% initially for patients at risk of hypercapnic respiratory failure • be delivered via nasal specula at 2–6 l/min or simple face mask at 5–10 l/min Nurses should give oxygen as prescribed and document clearly the rate of oxygen administered and oxygen saturations achieved
Pain relief with IV morphine (AHA, 2008) - Comfort of the patient and reduced workload of the myocardium
Diamorphine 2.5–5.0 mg IV is given at 1 mg/min followed by 2.5 mg doses until pain is relieved (Jowett and Thompson, 2007). - • Both pain and anxiety will stimulate sympathetic nervous response resulting in peripheral vasoconstriction, increased venous return and subsequently increased myocardial workload.
Metoclopramide 5–10 mg or cyclizine 50 mg IV - Clopidogrel 300–600 mg loading dose followed by 75 mg daily thereafter Indications and current debateThese drugs need to be given by appropriately trained staff, clearly documented following local controlled drug policy and their effects monitored and documented to guide further treatment Can be given with morphine to reduce the risk of nausea and vomiting (Cam, 2002)
Patients undergoing PPCI There is conflicting guidance on whether clopidogrel should be given for STEMI patients receiving thrombolysis. The ESC (2008) recommends a loading dose of 300 mg if
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autoimmune
directed reaction directed against a person's own tissue
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immune
protected from an infectious disease
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immunity
state of being protected
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Immunoglobuli
Specific protein evocked by an antigen
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Immunization
Administration of an agent to provide immunity
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Immunologist
Medical specialist in immunology
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Immunology
The science and practice of immunity and allergy
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Immunize
Make resistant to infectious disease
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Immunodeficiency
Failure of the immune system
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Immunosuppression
Suppression of the immune response by an outside agent such as a drug
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cancer
is applied only to malignant neoplasms,
| associated with alterted expression of cellular genes that normally regulate cell proliferation and differentiation
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benign
growth is received with great relief inasmuch as the tumor is generally easily cured
- do not invade adjacent tissue or spread to distant sites
- encapsulates my connective tissue
- as a general rule benign cells more closely resemble their tissue type of origin
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malignant
may herald months of intensive and often uncomfortable treatment with uncertain outcomes
- potential to kill the host if untreated
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anaplasia
a lack of differentiated features in a cancer cell
| - a greater degree of anaplasia is correlated with a more aggressively malignant
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metastasis
is invasion of local tissue to distant sites confirms the diagnosis of malignancy
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tumor terminology
suffix -oma is used to indicate a benign tumor
| carcinoma and sarcoma are used to indicate malignant tumors
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carcinoma
refers to malignant tumors of epithelial origin
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sarcoma
to malignant tumors of mesenchymal (nerve, bone, muscle) origin
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adenoma
a benign tumor of glandular tissue
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leukemia
refers to a malignant growth of white blood cells
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apoptosis
is when normal cells respond to signals instructing them to actively destroy themselves
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malignant phenotype
these abnormal behaviour can be summarized as follow:
- cancer cells proliferate despite lack of growth-initiating signals from the environment
- cancer cells escape signals to die and achieve a kind of immortality in that they are capable of unlimited replication
- cancer cells lose their differentiated features and contribute poorly or not at all to the function of their tissue
- cancer cells are genetically unstable and evolve by accumulating new mutation at a much faster rate than normal cells
- cancer cells invade their local tissue and overrun their neighbors
- perhaps worst of call, cancer cells gain the ability to migrate from their site of origin to colonize distant sites where they do not belong
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cancer risk factors
```
tobacco use
nutrition
-fat
- fiber
- alcohol
- antioxidants
```
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carcinogens
cancer-causing agent were identified by demonstrating their mutagenic potential
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two groups of cancer critical genes
1. gain of function mutation which is whether over-activity of the gene contributes to cancer
2. loss of function- to little gene activity is the problem
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proto-oncogenes
which normally code for components of the cellular growth-activating pathways
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oncogene
a proto-oncogene in its mutant, overactive or over-exposed
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tumor-suppressor genes
genes in the second category of cancer-related genes which normally inhibit cell proliferation
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the majority of proto-oncogenes described to date code for component of cell signaling systems that promote cell proliferation
these components can be lump in for four categories
- growth factors
- receptors
- cytoplasmic signaling molecules
- nuclear transcription factors
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rb gene
a tumor-suppressor gene that blocks cell division by binding transcription factors
78
the P53 gene
is a common tumor-suppressor gene is found in cells
| binds to damaged DNA and stall cel division
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brca1 and brca2
is a tumor-suppressor gene that has been identified through studies of inherited predisposition to certain types of cancer
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multistep nature of carcinogensis
- initiation
- promotion
- progression
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effects of cancer on the body
```
hair loss
pain
cachexia (overall weight loss and generalized weakness)
deficits immune system competence
anemia
leukopenia
and thrombocytopenia
bone marrow suppression`
paraneoplastic syndorme
```
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Leukopenia
refers to decrease in circulating white blood cells
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thrombocytopenia
is a deficiency in circulating platelets, which are important mediators of blood clotting
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paraneoplastic syndorme
include hypercalcemia, Cushing syndrome secondary to excess adrenocorticotropic hormone secretion and hyponatremia and water overload
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cancer therapy
```
surgery
radiation therapy
drug therapy
immunotherapy
gene and molecular therapy
stem cell transplantation
```
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components of the immune system
1. skin and mucous membrane
2. mononuclear phagocyte system
3. the lymphoid system
4. bone marrow
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leukocytes
are responsible for locating and eliminating pathogens and foreign molecules
88
chemical mediators are
complement, kinins, clotting factors, cytokines and chemokins
which aided inthier task of bodily defense
89
antigens are
marcomolecular that provokes an immune system response
90
neutrophils and macrophages
are mediators of innate defense.
91
b and T lymphocytes
are the agents of specific immunity
92
hematopoiesis
formation of blood cells
93
b lymphocyte
is formed in the bone marrow
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t lymphocyte
form in the thymus, located in the anterior mediastinum overlying the heart
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secondary lymphoid organs
tonsils, spleen, lymph nodes and lymphatics, peyer patches
96
leukocytes
- primary effector cells if the immune system
| - formed in bone marrow
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cytokines
are produced in the bone marrow, and influences cell development
98
Neutrophils
types on WBC
| first to appears after injury
99
lymphocyte
immune system
100
phagocytosis
ingestion and destruction of pathogens by leukocytes
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Eosinophils
reacts to allergic reaction, parasite infection
102
basophils
contains histamine, mediate types I allergic reaction, initate inflammation
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monocytes
are immature macrophages that circulate the blood
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macrophages
migrates from the blood vessels to sites int he lymphoid tissue, secrete a # of cytokines that stimulate inflammation.
105
two main immune disorders
deficient immune response and excesive iummune response
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excessive immune response
is over-functioning or hyperfunctioning such as auto immune and hypersensitivity disorders.
107
deficient immune responses includes
```
disorders in which the immune response is ineffective because of disease-causing genotypes or secondary/acquired dysfunction
examples
- severe combined immunodeficiency
Digeorge syndrome
selective immunoglobulin A deficiency
HIV/AIDS
```
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hypersensitivity disorders
described mechanisms of injury, or how the injury occurs, which may or may not involve autoimmunity
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autoimmunity
is a general term that is used when the immune system attacks its own tissue
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important factors in the development of autoimmune disorders
- genetic factors
- environmental triggers
- pharmacotherapies
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enviromental trigger
viruses can activate b cells, decrease function of t cells, contribute to the development of antigentic mimicry, or insert viral components on cell surfaces and trigger immune reaction
-environmental and work stress
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corticosteroids
decrease the number of lymphocytes and crease antibody formation, as well a alter the functional activity of lymphocytes
113
four types of hypersensitivity
type 1: atopic anaphylactic
type 2: cytotoxic, cytolytic
types 3 immune complex
type 4 delayed hypersensitivity
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type 1 atopic
mediated by igE
complement activation: no
immune response: ag plus IgE, leading to mast cell degranulation
peak action 15-30 min
serum transferability yes
cell transferability no
genetic mechanisms familial, High IgE level, HLA-linked ir genes, general hyperresponsiveness
cause of reaction t-cell deficiency, abnormal mediator feedback, environmental factors and Ag
manifestation: asthma, rhinitis, atopic, eczema, bee sting reaction
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type two
mediated by IgM or IgG
complement activation: yes
immune response: surface ag and Ab leading to killer cell cytotoxic action or complement medicated lysis
peak action 15-30 min
serum transferability yes
cell transferability no
genetic mechanismsHKA linked in come cases
cause of reaction exposure to Ag or foreign tissue cell or grafts
manifestation: ABO transfusions, hemolytic disease of new born myasthenia gravis
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type3 immune complex
mediated by IgG
complement activation: yes
immune response: Ag0ab complex in tissues complement activate and PMNs activated and PMN's attracted
peak action 6 hr
serum transferability yes
cell transferability no
genetic mechanisms familial (auto immune), HLA specificities
cause of reaction persistent infection extrinsic environment, auto immune
manifestation: glomerulonephritis, SLW, farmer's lung arthritis vasculitis
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type 4: delayed hypersensitivity
mediated by Tdth lymphocytes
complement activation: no
immune response: ag sensitized t cell release lymphokins, leading to inflammatory reactions, and attract macrophages which release mediator
peak action 24-48 hr
serum transferability no
cell transferability yes (t cells)
genetic mechanisms unknown
cause of reaction intradermal , epidermal, dermal ag
manifestation: Gullain Barre, Tb testing, contact dermatitis, MS
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IgE
is produces by specialized plasma B cells and circulates in very small amounts in the blood
when exposed to an allergen, the host produces more IgE
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possible causes of human anaphyalxis
penicillin, other antibiotics, radiographic contrast media aspirin, indomethacin and other analgesics, allergenic extracts, serum proteins, insulin and other hormones, vaccines, enzymes, local anesthetics, Hymenoptera (stinging) insects. honey bees, fire ants, hornets, yellow jackets, nuts, seafood, eggs, fruit, tartrazines, yellow dye, inorganic chemicals, nickel, aluminum and Zinc
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isoimmunity
a condition in which the immunes system reacts against antigens on tissue from other members of the same species.
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leukemia
can be conceptualize as circulating tumor that disseminated from the beginning of the disease process and primarily involve the blood and hone marrow
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Lymphoma
tends to localize in lymph tissues but is often disseminated to other sites at the time of diagnosis
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Plasma cell myeloma
is a malignant transformation of B cell plasma cells and has a predilection to form localized tumors in bony structures
124
malignancies of the blood-forming tissues and lymphatic structure often present with non-specific symptoms such as
malaise, weakness, unexplained fever, night sweats, and recurrent infections
125
symptoms of lymphoma and some leukemias are
non-tender lymph node
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WBC malignancies are found
by chance during routine assessment of the CBC
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classification of myeloid neoplasms
myeloproliferative disease
myelodysplastic/ myeloproliferative disease
myelodysplastic syndrome
acute myeloid leukemia
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classification of lymphoid neoplasms
b cell neoplasms
t and NK cell neoplasms
Hodgkins lymphoma
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common symptoms of hematologic malignancies
fever, weight loss, night sweats, itching, fatigue, bone pain, abdominal fullness, bleeding, bruising, frequent infection, headache, nausea, vomiting, enlarged spleen, enlarged liver, enlarged lymph modes, hyperplasia of gums, anemia, thrombocytopenia, leukopenia, blood smear, elevated uric acid, elevated alkaline, hypercalcemia,
130
treatment of hematolgic neoplasms
relies primarily on the use of combination chemotherapy to eradicate malignant cells and stem, cells transplant to rescue and restore bone marrow function, `
131
the goal of chemotherapy
is to induce ling term remission that is the absence of any detectable neoplastic cell in the body
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`chemotherapy agents
work by disrupting some aspects of DNA synthesis or cell replication and induce apoptosis
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chemotherapy
usually involves two or three phases
1. remission induction
2. postremission or consolidation phase
3. remission maintenance phase
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myeloid neoplasms
results from transformation and proliferation of a precursor stem cell in the bone marrow. in many cases the abnormal stem cell is multipotent and causes the overproduction of more than one cell type, resulting in myeloproliferative disease.
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myeloid characteristic
are neoplastic cell that are morphologically and functionally abnormal.
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chronic lymphoid leukemia
is a neoplastic transformation of a mature peripheral b cell that affects adults primarily and has an insidious onset,
usually asymptomatic
disease in certain genotypes is associated with long survival times and does not require therapy
- managed with stem cell transplantation or administration and if monoclonal antibodies
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acute lymphoid leukemia
affects children primarily has an acute onset, responds well to therapy and has a good prognosis,
is associated with transformation of precursor to blasts int he bone marrow. ALL often manifests with bone pain infections, and tendency to bleeding. a significant number of children with ALL have CNS involvement, and intrathecal chemotherapy is necessary
138
plasma cell myeloma
is caused by malignant transformation of antibody-secreting B lymphocytes. usually affect older adults. ,malignant plasma cells all secrete the same monoclonal antibody, and detection of this antibody in the blood or urine aids in diagnosis
139
reed sternberg
cells on histologic examination, cells originate from b cells in the germinal center of lymph nodes
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hodgkins disease
is characterized by malignant transformation of B cells in lymph nodes called reed Sternberg cells. spread of malignant cells occur along predictable contiguous pathway, most commonly, a single cervical lymph node is involved initially with a low progression to near by nodes
141
HIV
human immunodeficiency virus
- caused by a retrovirus
- defected cell-mediated immunity, especially the decrease on CD4 or T-helper/inducer lymphocytes
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AIDS
acquired immunodeficiency syndrome
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types of HIV
HIV 1
| HIV 2
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three modes of transportation for HIV
intercourse, parenteral transmission and blood products
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prevention of HIV
safe sex
sterile needles
PPE
146
aoiotosis
trigger automatic preporgrammes t cell death
147
anergy
cause the cell to stop dividing and decrease the cell's ability to fight new infections
148
syncytium
process of cell death occurs when multiple uninfected cells become fused together with infected cells by the virus- this can lead to a large # of cell deaths from a single event `
149
clinical manisfestation of HIV
all body system are affected by HIV
early HIV infection is characterized by fever, chills, headaches, nausea, vomiting, diarrhea, fatigue, weakness, arthralgia, sore throat, stiff neck, photophobia, irritability and rash
malnutrition, elevated metabolic rate, chronic inflammation, malabsorption, anorexia, diarrhea caused by cryptosporidium, ulcers, yeast infections, pneumonia, Td and resp distress. HPV herpes, neoplastic, peripheral neuropathy, headache, apathy, cervical dysplasia, pelvic inflammation, CMV retinitis, impaired physical growth
150
treatment for HIV
antiretroviral medication are nucleoside reverse transcriptase inhibitors (NRTI_ ninnucleoside reverse transcriptase inhibitors (NNRTI), protease inhibirotrs, fusion inhibitors and CCR5 antagonists
151
hemotopoiesis
make or form blood compornents
| all cells originate from stem cells
152
hemotophic stem cells are divided in two categories which are
myeloid group and lymphoid group
153
lymphoid cells create
t cells
| b cells
154
different types of myeloid cell
```
red blood cell (erythrocyte)
megakaryocyte /platelet
Monocyte (a type of WBC) (kills the antigen)
Neutrophil (main component of pus)
basophil (eosinophil)
```
155
-blast
are premature cell
156
-cyte
are matured cell
157
Leukemia is
the cancer of the blood cells
158
other S and S of leukemia
decrease RBC, Decrease platelet, decrease WBC
159
thrombocythemia
too many platelet or thrombocyte in the blood.
160
sings and symptoms of thrombocythemia
headache, slurred speech dizziness, numbness or burning to hands and feet, bleeding, splenomegaly
161
extra note
no clotting can create bruising.
162
inr
high inr - potential bleeding, blood to clotting to slowly
| low inr- potential clotting to fast
163
high inr
treatment is vitamin K to help increasing clotting in the blood
164
treatment of thrombocythemia
aspirin, hydroxyurea or interferon (decrease production of megakaryoblasts), platelet pheresis
165
attenuated
a process of weakening the degree of virulence of disease organism
166
line of defence
anatomic barriers
inflammatory repsonse
immune response
167
lymphokines
one of the chemical factors produced and relased by t cells that attrack macrophages to the site og infection or inflammation and prepare them to attack
168
plasmapheresis
removal of plasma that contains components causing or thought to cuase disease
169
innate immune system
phagocytes, natural killer,
170
humoral immunity
a form of immunity response to antigens such as bacteria or foreign bodies
