Hematology and Immunology Health Alterations Flashcards
hematology
focus on blood disorders
such as benign disorder, clotting, bleeding or malignant disorder
components of the blood
red blood- carry oxygen
platelets help with clotting and healing
white blood cells- helps with infection
plasma regulate bleeding and clotting
lymphoma
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
healthy cells vs cancer cells
healthy cells- have short life span and regenerate. cancer cells multiple never dies and create mass and spread throughout the body
the role of protein in blood clotting
- 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
DVT (deep vein thrombosis)
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.
sickle cell
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
primary prevention
promoting healthy lifestyle, weight control, and physical activity
secondary prevention
screening/ control of multiple risk factors
tertiary prevention
CAD management after coronary event
framingham risk scoring system
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
risk factors of cardiac diseases are
smoking and abnormal ratio of blood lipids
other factors are:
diabetes, hypertension, abdominal obesity, psychosocial factors, lack of daily consumption, diet and exercise
possible cardiac test are
ECG, stress test, myocardial perfusion imaging, MRI CT and calcium score.
examination of the cardiovascular system
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 veinsarterial pulse
radial pulse, assess rhythm, quality, equality, avg 50-100
irregular heart beat
a-fib, ventricular ectopic beats,
Jugular venous pressure
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
pericardium
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
gradation of murmurs
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
acute coronary syndromes
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,
Aortic anerysum
• 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
pericariditis
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
pluerisy
• 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
oespohagpgastric disorder
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
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
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
biochemical markers
creatine phosphokinase
troponin
ECG
ACS with unstable angina
ECG change: ST depression, T inversion, or transient ST elevation
Troponin normal
ACS with myocyte nercosis
ECG change ST depression, T inversion, or transient ST elevation
Troponin sightly elevated
ACS with clinical myocardial infraction
ST elevation or depression, T inversion and q wave may evolve, significantly elevated
risk stratification
assess 8 factors: grade of heart failure systolic BP HR age creatinine cardiac arrest
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.
unstable angina cont’d
anginga are diagnosed when patient’s symptoms, with evidence of cardiac disease, no ECG evidence myocardial infarction and negative troponins
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
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.
unstable agnina tx
rest and analgesia anti-ischemic therapy anti platelet therapy anticoagulant plaque stabilization
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.
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
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).
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
medication that can help reduce reoccurence of cardiovascular events
aspirin clopidogrel ACE beta blockers calcium channel blockers long acting nitrate statin
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.
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.
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
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
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
autoimmune
directed reaction directed against a person’s own tissue
immune
protected from an infectious disease
immunity
state of being protected
Immunoglobuli
Specific protein evocked by an antigen
Immunization
Administration of an agent to provide immunity
Immunologist
Medical specialist in immunology
Immunology
The science and practice of immunity and allergy
Immunize
Make resistant to infectious disease
Immunodeficiency
Failure of the immune system
Immunosuppression
Suppression of the immune response by an outside agent such as a drug
cancer
is applied only to malignant neoplasms,
associated with alterted expression of cellular genes that normally regulate cell proliferation and differentiation
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
malignant
may herald months of intensive and often uncomfortable treatment with uncertain outcomes
- potential to kill the host if untreated
anaplasia
a lack of differentiated features in a cancer cell
- a greater degree of anaplasia is correlated with a more aggressively malignant
metastasis
is invasion of local tissue to distant sites confirms the diagnosis of malignancy
tumor terminology
suffix -oma is used to indicate a benign tumor
carcinoma and sarcoma are used to indicate malignant tumors
carcinoma
refers to malignant tumors of epithelial origin
sarcoma
to malignant tumors of mesenchymal (nerve, bone, muscle) origin
adenoma
a benign tumor of glandular tissue
leukemia
refers to a malignant growth of white blood cells
apoptosis
is when normal cells respond to signals instructing them to actively destroy themselves
