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NUR3120 Patho, 2nd half, ONCOLOGY - Coggle Diagram

- - - - No detectable pulse
      - Related to hypoglycemia
      - Management
        Cardiac compression, airway management, ventilation and IV access + adrenaline
        Only adrenaline needs to given every 3-5 min in PEA
        Atropine no longer recommended for routine use in maangement of PEA.
        Sodium bicarbonate no longer recommended for prolonged cardiac arrest
        
        Drugs: Adrenaline
        Others: potassium, calcium, antidotes
    - - Regularity: Flat line
        Rate: No rate
        P-wave: No P-waves
        PR interval: Cannot measure since no P-waves
        QRS complex: No QRS complexes present
      - Extremely poor prognosis
      - Management
        Continue with chest compress and reassess after 2 minutes of CPR (5 cycles)
        Cardiac compress, airway management, ventilation, IV access + adrenaline administration
        
        After 15-20 mins, recovery from asystole are dismal. Exceptions to this are cases of near drowning, poisoniong and hypothermia
        
        Drugs: Adrenaline
    - - Regularity: R-R intervals are usually but not always, regular, rate
        Rate: atrial rate cannot be determined. Ventricles usually 150-250 beats per min
        P-wave: QRS complex not preceeded by P-waves. There are occassionally P waves in strip but not associated with ventricular rhythm
        PR interval: not measured since this is a ventricular rhythm
        QRS complex: QRS complex measures more than 0.12. QRS usually be wide and bizzare. Difficult to see separation between QRS complex and T-wave
        
        Management: defib
        
        Drugs: adrenaline, amiodarone, lignocaine, magnesium, others
    - - Regularity: no regular QRS shape because heart not able to conduct properly
        Rate: appears rapid but disorganized electrical activity prevents heart from pumping
        P-wave: no P-waves present
        PR interval: no PR interval present
        QRS complex: ventricle complex varies
        
        Management: defib
        
        Drugs: adrenaline, amiodarone, lignocaine, magnesium, others
    - - Management
        24hr ECG monitoring to detect
        Assessment, administer O2, IV access, Defib, 12 lead ECG
        
        Unstable<90/60mmHg, symptomatic
        =DRUGS/PACING
        
        First line (Drugs)
        IV atropine, 0.6mg every 3-5 mins (max 4 doses) (may cause paradoxical bradycardia)
        IV dopamine/adrenaline (to increase cardiac output)
        If not enough,
        Begin transcutaneous pacing with analgesia and sedation
        Transvenous pacing if available
        
        Stable
        90/60mmHg, asymptomatic
        =MONITOR
        
        If type II 2nd degree heart block/3rd degree heart block
        Rhythm = haemodynamic monitoring
        Transcutaneous pacing in event of deterioration
      - Various types of heart blocks causes this
        Bradycardia with pulse (HR<60)
      - Sick sinus syndrome: sinus node defective. RR pattern irregular, unable to see P-wave in some cases
        1st degree AV block: AV node delay. Sometimes PR interval more than 2 seconds (PR = 280ms)
        2nd degree AV block: increased delay at the AV node until P-wave is sometimes not conducted
        Bundle branch block: QRS widened for both right and left bundle.
        Usually left bundle brunch block.: Wider QRS complex V4,V5,V6
        Right bundle branch block: widening QRS complex in V1, V2 (R.R. pattern)
    - - Atrial flutter: atrial activity/rate more than 240-320
      - Atrial fibrillation: atrial activity/rate more than 240-320 --> embolic stroke
      - Supraventricular tachycardia: above AV node
  - - - Causes and Management of cardiac arrest (6H, 5T)
        
        6H
        
        Hypovolemia
        
        Hypoxia
        
        Hydrogen ion- severe acidosis
        
        Hyperkalemia
        
        Hypokalaemia
        
        Hypothermia
        
        Treatment
        
        Fluid resus
        2.Ventilation
        
        Give sodium bicarbonate 1mEq/kg
        
        Remove potassium/dialysis
        
        Replace potassium
        
        Warm patient
        
        5T
        
        Tablets
        
        Tamponade, cardiac
        
        Tension pneumothorax
        
        Thrombosis (Acute Coronary syndrome, acute myocardial infarct)
        
        Thrombosis (pulmonary)
        
        Treatment
        
        Antidote
        
        Pericardiocentesis (procedure done to remove fluid that has built up in the sac around the heart (pericardium))
        
        Needle compression of chest
        
        Resuscitation
        
        Revascularisation/PCI
        
        Thrombolytics/surgery
- - - - Hypoxaemia WITHOUT hypercapnia
        
        Diffusion limitation: idiopathic pulmonary fibrosis
        gas transfer of alveolar membrane impaired --> arterial hypoxemia --> resultant increase in alveolar-arterial oxygen differencec
        
        Alveolar hypoventilation: opoiate overdose
        Respiratory depression = hyperventilation= hypercapnia
        Increased PaCO2 = increased alveolar CO2
        
        Impaired ventilation, preserved perfusion: lobar pneumonia
        Area of lung receives little oxygen in proportion to the extent to which is being perfused. Air spaces congested wiith inflammatory exudate
        
        V/Q mismatch is partially offset by: hypoxic pulmonary vasoconstriction: Heterogeneous emphysema
        Diminished ventillation in the upper lobes
        Planning best therapy for advance COPD --> lung volume reduction surgery
        
        Impaired perfusion, preserved ventilation: pulmonary embolism (Right to left shunt)
        
        V/Q mismatch is partially offset by: hypoxic pulmonary vasoconstriction
        
        Low inspired oxygen: commercial flights
        Absence of an increase fraction of inspired oxygen, an increased PaCO2 will cause a decrease in PaO2 (hypoxemia and hyperventilation --> masked by increased inspired oxygen)
      - Common causes
        
        Low ambient O2
        
        V/Q mismatch
        
        Alveolar hypoventilation
        
        Diffusion problem
        
        (Respiratory dysfunction + cardiac pathologies)
        Asthma
        Bronchitis
        Pneumonia
        Acute pulmonary edema
        Heart failure
      - Treatment
        
        (Patient stable)
        Resting PaO2 of 7.3kPa or lower (or 8kPa if features of right ventricular failure present) should be given long term O2 for at least 15 hrs a day
    - - Hypoxaemia WITH hypercapnia
        
        Alveolar hypoventilation due to failure of respiratory muscle pump
        
        Neural respiratory drive: CNS (encelopathy, cerebral ischemia, infection. Space occupying lesion, central acting drugs, spinal cord injuries, motor neuron disease)
        Capacity of muscular pump (muscular dystrophy, inflammatory myopathies, electrolyte imbalances)
        Load
        DYSFUNCTION IN ANY OF THESE 3 PARTS
      - Common causes
        
        Increased airway resistance
        
        Reduceed WOB
        
        Decrease in area of lung for gas exchange (e.g. bronchitis)
        
        Neuromuscular problems
        
        (Pulmonary dysfunction
        CNS dysfunction
        Neuromuscular dysfunction)
        COPD
        Emphysema
      - Treatment
        
        Domiciliary NIV is indicated due to chest wall deformity, progressive neuromuscular disease and obseisity related respiratory failure
    - - Causes: pulmonary edema
        lactic acidosis
        anemia
      - Management:
        Intubation
        Mechanical ventilation
        Allow redistribution of cardiac output away from respiratory muscles and back to vital organs while shock is treated
    - - Causes: lung atelectasis
        After general anesthesia, decreases in functional residual capacity leads to collapse of dependent lung units
      - Management
        Frequent changes in position
        Chest physio
        Upright positioning
        Control of incisional and/or abdominal pain
  - - - 1: chest physiotherapy to removed trapped secretions
        bronchodilators increase airway patency and mobilzie trapped secretions
        Administer non-invasive mechaniocal ventilation
        If unable to maintain, intubation and invasive mechanical ventilation
      - 2: thorough investigations and medical interventions must be made to identify and reverse cause of ARF
      - 3: monitor for respiratory distress, ausculate
        provide supplement O2
        Position for comfort and to enhance V/Q matching
        Blood transfusion to ensure optimal Hb to transport O2
      - 4: provide adequate bed rest
        Timing of ADLs
        Addressing sepsis, restlessness,
        patient-ventilator dysynchrony: when initiation/termination of mechanical ventilator not in sync with patient. Or magnitude of mechanical assist does not respond patient's respiratory demand
      - 5: monitor for potential complications
        immobility related
        fluid/nutrition imbalance
        adverse effects from medication
        ventilator-associated complications
- - - - CONSEQUENCES
        
        Impaired gas exchange = V/Q mismatch and shunting
        
        Decreased lung compliance = stiffness or poorly/nonaerated lung more than changes in PV characteristics
        
        Pulmonary hypertension
  - - - Marked by mediator induced interstitial and alveolar odedma and damagee with hyaline membrane formation
        Increase permeability to proteins
    - - Hemodynamic instability
        SIRS:
        Generalised oedema, lungs become more dense, decreased lung compliance
        Thickened alveolar membrane
    - - Increased dyspnea and RR
        Worsen within 24 hr
        Coarse bilateral crackes
        CXR reveals shows patchy infiltrates
    - - Lung completely remodelled by sparsely collageous and fibrous tissues
        Increased dead space --> poor ventilation --> increased AW pressure
- - - - Management
        IV fluids: 30ml/kg
        
        Goals
        Treatment specific and directed to insul
        Take blood culture, broad spectrum, then specific antibiotics
        Ensure patient haemodynamically stable
        Fluid resus using 2 large bore IVs: increase blood pressure (e.g. colloids)
        Ensure urine more than 30ml/hr (or insert catheter)
        Insert cecntral and miaintain central venous pressure (8-12mmHg)
      - Manifestations
        
        Hyperthermia/hypothermia
        
        Tachycardia
        
        Low blood pressure (SBP <90)
        
        Mental status changes
      - Diagnosis
        
        Blood culture: sample of blood for bacteriological culture
        Indication: determine presence of bacteria in blood/diagnose cause of sepsis
        Determine what antibiotics most effective
        Other cultures: sputum, urine, surgical wounds, invasive lines
        Full blood count
        ABg
        
        CXAR
    - - Causes
        
        AMI
        
        Myocarditis
        
        Myocardial contusion
        
        Acute aortic insufficiency
        
        Ventricular septal rupture
        
        Cardiac tamponade (space around heart fills with blood)
      - Manifestations
        Cardio
        
        Decreased capillary refill
        
        May have chest pain
        
        Pulmonary
        
        Tachypnea
        
        Cyanosis
        
        Crackles
        
        Rhonchi
        
        Skin
        
        Pallor
        
        Cool, clammy
        
        Renal
        Sodium and water retention increase
        Neurologic
        Decreased cerebral perfusion
        Gastrointestinal
        Decreased bowel sounds
        Nausea/vomiting
      - Diagnosis
        
        ECG echocardiogram
        
        Chest X-ray
        
        FBC, electrolytes, cardiac enzymes, PT/PTT studies
        
        ABG
      - Management
        Airway stability:
        Maintain respiratory function + oxygen delivery
        Maintain optimal cardiac output:
        Revasculartion + improve cardiac contractility + maintain blood pressure + cardiac monitoring
    - - Sudden onset of rapidly progressive urticaria(hives) and respiratory distress
      - Causes
        
        Drug
        
        Bee/wasp stings
        
        Latex allergy
        
        Food
      - Manifestations
        
        Pruritus, flushing, urticaria appear
        
        Throat fullness
      - Management
        Reduce immune response (immediate administration of medication)
        Maintain airway
        Fluid resus
        Cpr to treat cardiac arrest
        
        Drugs: IM adrenaline, anti-histamine drug, corticosteroids
        
        Nursing action
        
        Patient edu
        
        Epinephrine
    - - Causes
        
        Non hemorrhagic: vomiting, diarrhoea, bowel obstruction, burns
        Hemorrhagic: GI bleed, trauma, massive hemoptysis, ectopic pregnancy, post-partum bleeding
      - Signs and symptoms
        
        Altered or decreased loss of consciousness
        
        Anxiety and restless
        
        Decreased urine output
        
        Delayed capillary refilll
        
        Increased heart and respiratory rate
        
        Pale, cool and clammy skin
        
        SBP <90mmHg
      - Diagnosis
        
        Bloods and radiological
      - Management
        Control bleeding
        Fluid restoration
        Maintain blood pressure
        Maintain patient airway
        
        Nursing management
        
        Close monitoring
        
        Awareness of normal/abnormal observation results
        
        Ensure emergency equipment available
        
        Psychological care (support for patients and relatives)
        
        Info
        
        Management of skin integrity
        
        Nutritional intake
        
        Personal care
        
        Patient positioning
  - - - SIRS criteria
        (mets any of these 2)
        
        Temp >38 or <35
        
        HR >90 (Normal 60-100)
        
        RR>20/ PCO2 <32 (Normal 35-45)
        WBC >12000 or <4000
      - Sepsis: SIRS with presumed/confirmed infectious process
      - Severe sepsis: at least one of the organ dysfunction
    - - Management is fluid replacement
        But if bp not picking up even after that = septic shock (sepsis + BP)
        Multi organ disorder syndrome (septic shock + organ failure)
- - - - CO2 from cellular respiration
        CO2 + H2O = H2CO3
        H2CO3 = H+ HCO3-
        More H+ now change pH = either increase/decrease rate + depth of ventilation
    - - Acids (other than H2CO3) can be excreted only by kidney
        Kidney can adjust blood bicarbonate by increasing secretion/reabsorption + producing new bicarbonate if necessary
    - - Location: ICF+ ECF
      - Consists of:
        
        Carbonic acid-bicarbonate
        
        Hemoglobin
        
        Phosphates, proteins
  - - - Respiratory acidosis
        pH<7.35, pCO2 >45mmHg
        Due to hypoventilation = accumulation of CO2 (combines with H2O to form carbonic acid)
        May require mech ventilation if renal buffer is ineffective
        
        Causes:
        
        Brainstem trauma
        
        CNS depressant drugs
        
        Impaired respiratory muscle formation
        
        Lung disorders e.g. pneumonia, emphysema
        
        Treatment:
        
        Correct underlying disorders
        
        Drugs
        Opiates: Naloxone (antidote for opiates) AND/OR
        Benzodiazepines: flumazenil (antidote) max 5 doses per series. May repeat series at 20 min intervals
        
        ABG
        Every 12-24 hrs a pH improves
        Basic metabolic panel
      - Metabolic acidosis
        pH <7.35, HCO3 <22mEq/l
        
        Causes:
        
        Conditions when large amt of metabolic acidsss are produced (lactic acids, ketoacid, salicylic acid)
        
        Impaired ability to excrete H+ by kidney, e.g. severe kidney damage
        
        Treatment:
        
        May require HCO3- replacement + sodium/water deficits corrected
        
        Sodium bicarbonate goals: (must monitor) HCO3- to 10meq/L + pH 7.20
    - - Respiratory alkalosis
        pH> 7.45, pCO2 <35mmHg
        Due to hyperventilation
        
        Causes:
        
        Anxiety, fear, pain
        
        Respiratory stimulants (doxapram)
        
        CNS lesions
        
        Increased metabolic demands (fever, thyrotoxicosis)
        
        Treatment:
        
        Manage cause
        
        Hold suspected drugs
        
        Initiate oxygen therapy in patients with severe hypoxemia (pO2 <40mmHg)
        
        Treat theophylline overdoses appropriately
      - Metabolic alkalosis
        pH >7.45, HCO3>26 mEq/L
        Due to either loss of H+ or excess HCO3-
        
        Causes:
        
        Prolonged vomiting, gastric suction
        
        Excessive antacid usage
        
        Treatment:
        
        Treat underlying cause + hold suspected drugs (May require Cl- or K+ replacement)
        
        IF ECF volume contracted:
        Normal saline at appropriate rate for degree of volume depletion
        Replace potassium as needed
        If ECF volume overload
        
        No renal insufficiency: Actetazolamide: 250-375 daily
        
        If ARF/ESRD: hemodialysis/peritoneal dialysis
        
        Hyperaldoteronissm: spironolactone/amiloride
  - - - pH =acidosis/alkalosis
        
        PaCO2 = hypercapnia?
        
        HCO3 =
        
        Match CO2/HCO3 with pH to determine case of acid base disturbance
        
        Determine if HCO3 went the opposite way of pH
        
        Analyze PaO2 = hypoxemia?
        
        Only difference between partially and fully compensated states is whether pH has returned to normal
- - - - Low risk = > 4.88
        Moderate risk = 3.85-4.88
        High risk = <3.85
  - - - Provide respiratory support
- - - - Continuou Positive Airway Pressure (CPAP)
        
        Positive pressure applied. Respiration rate, inspiratory flow, tidal volume controlled by patient
        Increase functional residual capacity and improve oxygenation by opening alveoli at the end of inspiration
      - Pressure Support (PS)
        
        Senses patient's inspiratory effort and delivers pressure support = larger tidal volume
        Inflation volume, respiratory frequency =
        Augment spontaneous breathing
      - Synchronised Intermittent Mandatory Ventilation (SIMV)
        
        Tidal volume/pressure delivered by MV while allowing patient to breathe spontaneously
    - - Continuous Mandatory Mode (CMV)
        
        Tidal volume delivered by mechanical ventilator
        Breaths will be initiated when patient fails to do them on their own at a set timing
      - Pressure controlled Ventilation (PCV)
        
        Set using pressure, inspiratory time and inspiratory rate
        Inspiratory flow is not constant, but pressure is constant
  - - - Oxygen concentration (FiO2): fraction of inspired O2 delivered to patient (21-100%)
        Positive End Expiratory Pressure (PEEP): positive pressure delivered at end of expiration of ventilator breath (3-5 cmH2O)
        Inspiratory:Expiratory ratio: length of inspiratory and expiratory ratio (e.g. 1:2 to 1.1.5)
        
        Senitivity: Presure trigger (0.5-1.5cmH2O below baseline)
        Flow trigger (1-3L/min below baseline)
    - - Barrel trauma
        Volume trauma (excessive volume in alveoli)
        Atelac trauma (repeated opening and closing of alveoli)
        = pneumothorax, subcutaneous emphysema
    - - Refer to doc
        
        Sedation
    - - Continuous monitoring of patient's haemodynamic status
        
        Mean Arterial Pressure (MAP)
        
        BP, HR, cardiac rhythm
        
        SpO2, temperature
        
        Loss of consciousness - Sedation score (Richmond Agitation Sedation Scale RASS)
      - Monitor ABG closely
      - Troubleshoot alarm triggers: High pressure (thick secretions)/low pressure (loose connection of ventilator tubings)
      - VAP bundle
        
        Head of bed elevation
        
        Oral care with chlorhexidine
        
        Stress ulcer prophylaxis
        
        Daily sedation assessment an spontaneous breathing trials
        
        Deep venous thrombosis prophylaxis
      - Maintain humidification of ventilated gas for patient with heat mmoisture exchanger (HME) = change a per hospital protocol
        Refer to PT for chest percussion, suctioning and follow up-care
        Perform ETT ssuctioning every 4 to 8 hrly and when necessary
        Prevent decubitus ulcer: perform 2hrly turning and nurse patient on air mattress
        Allay stress on patient family
      - Evaluation and documentation
        
        Evaluate
        
        Patient respirator status and ABG results
        
        LOC from sedation vacation to determine readiness for weaning off MV
        
        Haemodynamic reading
        
        Oral hygiene and mucosa
        
        Documentation
        
        MV settings and observations in charts and nurses note
        
        Expected patientt outcomes:
        
        able to maintain airway patency and adequate gassses exchange
        
        Free from complications from MV (VAP, ventilator induced injury)
- - - - Philadelphia chromosome associated with chronic myelogenous leukemia (CML): translocation between chromosome 9 and 22
      - Down syndrome (Trisomy 21)
        Klinefelter syndrome (karotype 47, XXY)
        Bloom syndrome (genomic instability)
        Fanconi anemia (15 genes found)
    - - Primary immunodeficiencies
        
        Wiskott-Aldrich syndrome (X-linked recessive disease)
        Louis-Bar syndrome (Gene located at 11q22.3)
      - Secondary immunodeficiencies (acquired)
        
        Cytotoxic agents
        
        Radiation therapy
        
        Organ transplantation
        
        HIV
        
        Exogenous factors
        
        Physical (ionizing radiation)
        
        Chemicals (benzene)
        
        Viruses (T-cell leukemia, Epstein-Barr virus)
  - - - Clinical features
        
        Lymph nodes enlargement
        Common symptoms of intoxication (fever, profuse night sweat, weight loss)
        Lymph nodes pathology: loss of characteristic pattern, atypic cells
        Can transform to leukemia (RARE, only when more than 25% of blast cells in bone marrow)
      - Types
        
        Hodgkin lymphoma
        
        Malignant disorder of lymph nodes, characterized by presence of Reed-Sternberg cells (B cells from germinal centers in lymph nodes) malignant, tend to spread
        Epstein-Barr virus frequently found in genome of transformed Reed-Sternberg cells
        
        Types
        
        Rare lymphocyte predominance type
        
        Classical Hodgkin lymphoma (95%)
        
        Clinical features
        
        Painless lymphadenopathy
        Fever
        Night sweats
        Pruritus
        Weight loss
        Malaise
        
        Cervical lymph nodes most common site of lymph node enlargement
        
        Staging: Ann Arbor staging sysyem for lypmhomas
        
        A: No symptoms
        B: symptoms: fever, drenching night sweats, weight loss (more than 10% of body weight over 6 months)
        
        Cause of death
        
        Compression of vital organs by enlarged lymph nodes
        Secondary infection
        Cachexia (loss of skeletal and muscle mass)
        Amyloidosis (protein amyloid build up in organs)
        Organ dysfunction
        
        Non-hodgkin lymmphoma
        
        No Reed-Sternberg cells
        Majority of NHL arise from lymph nodes but they can originate in any lymphoid tissue
        Occur in males, older adults usually
        
        Clinical features
        
        (Similar to painless lyphadenopathy)
        Painless lymphadenopathy
        Fever
        Night swwwweats
        Wweight loss
        Malaise
        Pruritus
        
        Types/classification
        
        Cell size and morphology
        
        Degree of maturity
        
        Cytogenesis (T and B cells)
        
        Involvement of lymph nodes
        
        Degree of malignancy and prognosis (low intensity, aggressive, highly aggressive)
        
        Most common: diffuse large B cell lymphoma
        2nd most common: follicular lymphoma
        
        HL vs NHL (refer to docs)
        
        Pattern of spread: Contiguous/Non-contiguous
        Extranodal disease: Uncommon/More common involvement of gastrointestinal tract, testes, bone marrow
        Site of disease Mediastinal common/Medistianal less common
        Bone marrow uncommon/Bone marrow common
        Liver involvement uncommon/Liver involvement common
        Extent of disease: Often localized/Rarely localized
        B symptoms: Common/Uncommon
        
        B symptoms: FEVER, DRENCHING SWEATS (night sweats), WEIGHT LOSS (more than 10% body weight over 6 months)
        
        Burkitt's lymphoma
        
        Endemic variant occurs in equatorial Africa. Associated with Epstein-Barr virus and translocation of gene MYC
        
        Sporadic variant (non-African) NHL found outside of Africa, more with translocation of gene MYC
        
        Immunodeficiency-associated: associated with HIV infections, occurs in setting of post-transplant patients who are taking immunosuppressive drugs
        
        Pathology: areas of monomorphic cells with coarse chromatin and prominent nucleoli
    - - Cells
        
        Lymphoid
        
        NK, B cell, T cell
        
        Myeloid
        
        Myeloblast --> basophil, esiionphil, neutrophil
        Megakaryoblast --> platelets
        Erythroblast --> RBCs
        Monoblast --> monocyte
        
        Classification based on origin of malignant cells + maturity of malignant cells and clinical signs
        AML = Acute myeloid leukemia
        ALL = Acute lymphoblastic leukemia
        CML = Chronic myeloid leukemia
        CLL: Chronc lymphoblastic leukemia
        
        Acute: all ages
        Sudden
        Weeks to months
        Blasts, some mature forms predominant cells
        Mild to severe anemia/thrombocytopenia
        WBC count: variable
        
        AML
        
        85% in adults
        "Pyoid" bone marrow (pus like)
        Primarily bone marrow
        pia mater - neuroleukemia (rare)
        
        Leukemic infiltration of pia mater --> Leukemic infiltration leads to occlusion of CSF ways --> intracranial hypertension (blast cells in CSF)
        Lumbar puncture used to detect leukaemic cells in CSF
        
        French-American British (FAB) AML classification
        M0: Minimally differentiated
        M7: Acute megakaryocytic leukemia
        People are usually stage M2: AML with differentiation (8-21 translocation)
        
        Responds fairly well to treatment, worse prognosis than ALL
        
        ALL
        
        85% in children
        Crimson-red bone marrow
        Primarily lymph nodes (and thymus)
        pia mater (typical)
        
        Causes of death
        
        Hemmorhages in vital organs
        Complications associated with necrotic and ulcerative processes in GIT
        Secondary infection
        Suppression of bone marrow function
        Complications of therapy
        
        Chronic: Adult
        Insiduous
        Months to years
        Mature forms of predominant cells
        Mild anemia and thrombocytopenia
        WBC count: increased
        
        CML
        
        Others:
        Chronic erythroleukemia
        erythremia
        polycythemia vera
        
        30-40 years
        'Pyoid' bone marrow (pus-like)
        Spleen enlargement
        Philadelphia chromosome present
        
        Blast crisis is typical
        
        Blast crisis: large clusters of blasts seen in bone marrow. Blast cells have spread to tissues/organs beyond bone marrow
        --> pancytopenia, fever, poor appetite --> looks like acute leukemia
        
        Responds poorly to chemo
        
        CLL
        
        No blast crisis
        
        40-60 years (never in children)
        Crimson-red bone marrow
        Lymph nodes enlargement
        Philadephia chromosome absent
        
        Others:
        lymphomatosis of skin
        paraproteinemic leukemias
        
        Usually malignant tumour of B cells
        
        Cause of death
        
        Secondary infection
        Organ dysfunction
        Compression of vital organs by enlarged lymph nodes
        Complications of therapy
      - Main patho features
        
        Proliferation of atypical clone of hematopoietic cells
        
        Originate from the precursors of granulocytes, not able to differentiate into normal blood cells
        
        Bone marrow is affected primarily
        
        Bone marrow infiltration leads to suppression of: leukopoiesis, thrombocytopoisesis, erythrogenesis
        
        Atypical cells found in blood
        
        Atypical cells infiltrate organs
        
        How is bone marrow suppressed?
        Occupy a lot of space in the marrow, prohibit production of cells (PANCYTOPENIA)
      - Clinical features
        
        Fever
        
        Weight loss
        
        Night sweats
        
        Itching
        
        Fatigue
        
        Bone pain
        
        Bleeding episodes
        
        Frequent infections
        
        Other clinical features
        
        Leukemic infiltrates in BM, liver, spleen, lymph nodes and otherr organs with their enlargement
        
        Manifestations of anemia
        
        Necrotic processes in mucosa: necrotic angina, stomatitis, gingivitis, ulcers in stomach
        
        Hemorrhagic syndrome resulting from: vessel wall infiltration, thrombocytopenia/anemia, low fibrinogen
        
        Physical assessment
        Enlarged spleen
        Enlarged liver
        Enlarged lymph nodes
        Hyperplasia of gums
        
        Laboratory
        Anemia/polycythemia
        Thrombocytopenia/thrombocythemia
        Leukopenia
        Pap smear = wbc in premature stages (BLASTS not cytes)
        Hypercalcemia
      - Hairy Cell leukemia: rare, chronic type of leukemia
        
        2% adult leukemia, HIGHLY TREATABLE
        55 years, predominance of males
        B-cell phenotype, presence of peculiar cells with hair like projections on surface
        hairy cells in peripheral of blood as well as pancytopenia
        Splenomegaly common finding
    - - Originates from bone marrow but tendency to invade bones and form multiple tumour sites --> FRACTURES, HYPERCALCEMIA
        
        Usually affects adult men
        
        Excessive production of light chain antibody fragments by malignant plasma cells result in accumulation in blood and urine
        When found in urine, these light chain fragments are called Bence Jones protein --> diagnostic for multiple myeloma
      - Patho
        
        Diffuse/focal myeloma infiltrates
        Rare in long bones. Usually in flatbones, spine
        
        Cause of death: myeloma nephropathy (myeloma contracted kidney): main cause of de ath
      - Monoclonal gammopathies (MGUS):62% patient asymptomatic, very mild pancytopenia
        25% of MGUS patients progress to malignant disease
        But can progress to myeloma (period of 20 years) because of microeneviroonmental changes in bone marroww
        Serum electrophoresis (monitor closely), check Bence Jones protteins
      - Clinical features
        
        Asymptomatic until fairly advanced
        Only complaint: Frequent infections
        Protein in urine
        High serum calcium levels
        Bone pain usually first symptom
        Anemia, recurrent infection, bleeding tendencies --> bone marrow depression
        Renal insufficiency is a complication experienced by approximately 50% of patients with plasma cell myeloma
        
        ALL, CLL Plasma cell myeloma, REFER TO DOCS
  - - - ADVANTAGES
        Preserve organ
        Function preservation
        Cosmeetic preservation
        No operative modality
      - Routes
        EExternal beam
        3D conformal radiation
        Intensity modulated
        Image guided
        Intra-operative
        Bracyhtherapy
        Stereotactic radiotherapy
      - Side effects
        General: damage to epithelial tissues + fatigue
        Late: fibrosis
        Specific: site specific
    - - Stimulate/supress immune system
        Interfere with tumour cells abiility to survive/metastasize
      - How does it help?
        
        Targeted therapy
        Range of modes of action
        Inhibit signalling pathway that causes cell division
        Prevents formation of tumour blood vessels
        Prevent the production of particular enzymes which stop cell from dividingh
        
        Examples of targeted therapy
        Monoclonal antibodies (type of immunotherapy)
        Rituximab: lymphomas (block a specific target on the outside of target cells + send toxic substances to cancer cells)
        Tyrosine kinase inhibitors
        Her2 positive
        Herceptin
    - - Combination chemotherapy to eradicate malignant cells to rescue and stem cell transplant restore bone marrow function
      - Bone marrow transplantation: due to intense chemo, some amount of bone marrow suppression and bone marrow failure
        
        Given IV, go to host bone marrow to multiply and produce functional white blood cells Own host's stem cells stored in bank and reintroduced after chemo (autologous type --> patient's own stem cells)
        (allogenic --> closely related relatives)Autologous better: side effects reduced but recurring problem is higher than allogenic
        
        Anemia complication of leukemia and chemotherapy
        Administrationf erythropoietein
      - Thrombocytopenia (platelet deficiency) --> give fresh frozen plasma or pooled platelets --> restrict activities + prevent themselves from getting into injured