Oncology Flashcards
type of blood cancers
- leukemias
- lymphomas
- plasma cell disorder
solid tumor types
- diff. by type (breast, prostate, colon, lung-most common)
types of cancer treatments
- chemo
- immunotherapy
- radiation
- surgery (solid only)
- stem cell transplant
- CAR-T therapy
what are blood cancers
- malignancy originating from hematopoietic (blood producing) cells in the bone marrow
types of myeloid blood cancer
-MDS, AA, AML, CML
Types of lymphoid blood cancer
-acute lymphocytic leukemia, MM, lymphomas
acute leukemia
abnormal blood cells are immature blood cells (blasts) that cant carry out their normal function and they multiply rapidly which means it can worsen quicker
DX of acute leukemia
- peripheral blood tests (blasts)
- bone marrow biopsy
- lumbar puncture
- imaging
systemic symptoms of acute leukemia
- weight loss
- fever
- lots of infections
lung symptoms of acute leukemia
-sob
Muscular symptoms of acute leukemia
-WEAKNESS
bone and joint symptoms of acute leukemia
-pain and tenderness
psychological symptoms of acute leukemia
- fatigue
- loss of appetite
lymph node symptoms of acute leukemia
-swelling
spleen and liver symptoms of acute leukemia
-enlargement
skin symptoms of acute leukemia
- night sweats
- easy bleeding and bruising
- purplish patches or spots
difference between AML and ALL
- AML: fatigue, DIC, Bleeding (sicker on presentation)
- ALL: hepatosplenomegaly
B-symptoms
- will be seen with lymphoid lineage cancers (ALL, lymphomas, CLL)
- unintentional weight loss
- drenching night sweats
- fever (unknown why)
- painless lymphadenopathy
chemo induction phase
- initial chemo treatment
- meant to induce remission
- response to induction can predict outcomes/response to future treatment
chemo consolidation phase
- goal to eradicate disease that is below the level of detection
- can be done with chemo or stem cell transplantation
chemo maintenance phase
-lower doses of treatment for prolonged periods of time to improve chances of cure
what is chronic leukemia
- no blasts
- slow progression and could go diagnosed for long time
- some of these cancers produce too many cells and some produce too little cells
- involves more mature blood cells that replicate or accumulate more slowly and can function normal for some time
- if white count is increased thats okay until see blasts
CLL symptoms
- b symptoms
- early satiety (getting full)
- increased risk of infection
- hyperkalemia (wbc blow up while drawing blood so now k+ is outside the wbc and in plasma so the sample you drew has high k+ but your actual blood is not)
CLL treatment
- BTK- inhibitors like ibrutinib or acalabrutinib
- BCL-2 inhibitors like venetoclax
CML symptoms
-weakness, fatigue, SOB, fevers, bone pain
treatment of CML
-tyrosine kinase inhibitors like ponatinib, imatinib, nilotinib
what is lymphoma
- arises infection fighting cells of the immune system (lymphocytes-a type of WBC made in the bone marrow)
- when bacteria and other invaders are found in the lymph fluid, lymphocytes will multiply within the lymph nodes including b, t and natural killer cells
- lymphomas develop when these lymphocytes transform from healthy to malignant cells
how do lymphocytes normally circulate the body
-via the lymphatic system
function of lymph nodes
-key structure of lymphatic system found throughout the body and help filter lymph fluid to remove foreign particles
hodgkin lymphoma
- presence of reed stern-berg cells (large cancerous B cell derived cells with distinct appearance)
- one of most treatment responsive cancers that most pt can be cured
Non-hodgkin lymphoma
- diverse group of diseases distinguished by characteristics of the cancer cells associated with each disease type
- most people with NHL have b cell type others will have t cell type or NK cell type lymphoma
- more aggressive but still may be completely cured for fast growing
- slow growing tx effective in stabilizing disease for long time
symptoms of lymphoma
-b symptoms: night sweats, early statiety= weight loss, painless lymphadenopathy, fever
DX for lymphoma
- lymph node biopsy
- Imaging: PET/CT: hot spots may appear
- peripheral labs
- bone marrow biopsy
tx for lymphoma
- immunotherapy
- chemo
- radiation
- stem cell transplant
- CAR-T therapy
multiple myeloma (MM)
- cancerous plasma cells accumulate in bone marrow and crowd out the healthy cells and make abnormal proteins (antibodies)
- forms in the WBC (the plasma cell)
- normally healthy plasma cells would help fight infection by making antibodies that recognize and attack germs but with MM cant
symptoms of MM
- CRAB
- c= high calcium
- R= renal (kidney) problems- AKI
- A= anemia or low HgB
- B= bone problems
-I= infection
DX if MM
- peripheral labs: serum free light chains, immunoglobulins, M protein
- Bone marrow biopsy
- PET/CT: hot spots
TX for MM
- NOT CURABLE
- want to: have longest deepest remission
- immunotherapy
- chemo
- radiation
- stem cell transplant
- CAR-T therapy
Stem cell transplant
- process of administering CD 34 (STEM CELLS) into the host after preparative chemo regimen
- essentially eradicate disease via high dose chemo that people cant survive without stem cell transplant then rescue them with stem cells and or initiating graft vs disease effect
- now new healthy immune system can function and you have functional bone marrow that can provide hematopoiesis
Autologous stem cell source
- patients own stem cell
- collected after mobilization with high dose neupogen
Allogenic stem cell source
- donor stem cell
- matched related donor (sibling)
- matched unrelated donor
- cord (fetal umbilical cord) donor
- syngenic (identical twin)
- Haplo-identical (1/2 matched donor)
major complications of stem cell transplant
- Sinusoidal Obstructive Syndrome
- Graft Versus Host Disease
Sinusoidal Obstructive Syndrome
- rare
- gumming up of the liver
- actegol can help
Graft Versus Host Disease (GVHD)
- donors T cells (graft) view the patients healthy cells (the host) as foreign and attack and damage them
- mild, mod, or severe
- could be threatening
TX of Graft Versus Host Disease (GVHD)
-increased immunosuppression in the form of corticosteroids (medicines such as prednisone, methylprednisolone, dexamethasone, beclomethasone and budesonide)
Chronic GVHD
- syndrome that may involve one organ or many
- leading cause of medical problems and death after allogenic stem cell transplant
hard thing about GVHD
- want some of this to kill of the remaining cancer cells but dont want too much
- very fine balance
cancers that can use autologous stem cell
LETS MAKE CANCER AA TABOO NAME
- Lymphoma
- Multiple Myeloma
- CLL
- Amyloidosis
- Some autoimmunedisorders
- Testicular
- Neuroblastoma
cancers that can use allogenic stem cell transplant
- ALL / AML / MDS
- Some refractoryLymphomas
- PNH
- CML/CLL
- Sickle cell disease
- Some autoimmunedisorders
- Myelofibrosis
- Aplastic Anemia
CAR-T therapy
- type of immunotherapy that genetically modifies a patient’s own T cells to recognize and bind to specific proteins (tumor-associated antigens) on the surface of antigen-expressing cells
- The external targeting domain binds to the antigen, activating the CAR T cell.
- Once activated, CAR T cells release cytokines and other soluble mediators that may play a role in the killing of antigen-expressing target cells.
benefit of CAR-t therapy
- manufactured for each individual patient using their own T cells.
- After a one-time treatment, CAR T cells can continue to multiply in a patient’s body (cell expansion) and have the potential to remain in the blood for up to 1 year following administration
What is CAR T currently used in
- Multiple Myeloma
- Lymphoma
- ALL (Acute Lymphocytic Leukemia)
CAR-T therapy toxicity
- Cytokine Release Syndrome (CRS)
2. Immune Effector Cell-Associated Neurotoxicity
Cytokine release syndrome (CRS)
-response to the over-activation of the immune system response with a supraphysiological release of inflammatory cytokines
symptoms of CRS
- MIMIC SEPSIS
- can be quickly progressive
- fever
- hypotension
- hypoxia
- organ dysfunction
*occur rapidly and without warning within the first 8 weeks (average at 5-7 days) after CAR T-cell infusion
life threatening complications of CRS
- cardiac dysfunction
- ARDS from capillary leak
- renal or hepatic failure
- DIC
- HLH
Immune effector cell associated neurotoxcicty (ICANS)
-diverse adverse event associated with immune effector cells (IEC) and may involve blood-brain barrier disruption, elevated levels of excitatory neurotransmitters as well as pro-inflammatory cytokines and activated lymphocytes in the CNS
symptoms of ICANS
-aphasia (expressive), altered mental status, impaired cognition, motor weakness, seizures or cerebral edema, encephalopathy
non specific symptoms of ICANS
headache, tremor, myoclonus (quick, involuntary muscle jerk), asterixis (loses motor control), hallucinations, weakness, and intracranial hemorrhage
Stages of CRS
- grade 1: fever
- Grade 2: hypotension, hypoxia
- grade 3: requires one pressor for hypotension and at least 6 L of O2
- stage 4: requires at least 2 pressers and ventilator
TX for CRS grade 2 or higher
- tociluzumab
- if the symptoms then dont resolve add steroids
- if have neuro toxcicity add anakinra
Neurotoxcicity scoring questions to ask
- who
- where
- year (anything for time)
- one more orientation
- name 3 objects
- follow a command
- count backwards from 100 by 10’s
- write a sentance
grades for neurotoxcicity
- GR 1: score of 7-9
- GR 2: 5-7
- GR 3: 3-5
- GR 4: 3-0
what is an oncologic emergency
- Any acute, potentially life-threatening event in the oncology patient
- Directly or indirectly related to cancer or treatment
- May develop at any stage of treatment
- Immediate intervention is required `
Onc emergency category: Metabolic
-TLS, Hypercalcemia, SIADH, Hyper/hypoglycemia
categories of onc emergencies
- metabolic
- structural
- hematologic
- infusional
Onc emergency: structural
-SVC obstruction, Airway obstruction, Cord compression, Effusion, increase ICP, Seizure
Onc emergency: hematologic
-Fever, Leukostasis/Viscosity, Bleeding, Thrombosis, DIC, CRS/ICANS
Onc emergencies: infusional
-Extravasation, Anaphylaxis, Reactions
Tumor lysis syndrome (TLS)
- Life threatening condition occurring after cellular destruction of rapidly growing tumors
- Release of intracellular components of tumor cells causing hyperkalemia, hyperuricemia, hyperphosphatemia, secondary hypocalcemia, renal failure
- Typically during first several days of chemotherapy but can occur spontaneously prior to chemotherapy
Complications of tumor lysis syndrome
-rapidly progressing renal failure, seizure and cardiac dysrhythmia leading to death
Tumor lysis syndrome is most common in…
- high grade, high bulk lymphomas
- acute leukemias
- low to intermediate grade heme malig such as myeloma, CLL, etc..
- Solid Tumor patients with high bulk disease
what causes hyperkalemia in TLS
-release of intracellular potassium from tumor and can also be exacerbated by AKI
what causes hyperuricemia in TLS
-released from tumor, exacerbated by AKI and contributes to AKI crystal obstructive nephropathy
What causes hyperphosphatemia in TLS
Tumor cells contain up to 4X the inorganic phos than normal cells and this is released with cell death, again exacerbated by AKI, and contributes to AKI when Calcium and phosphate combine forming Ca/phos crystals and an obstructive nephropathy
What causes hypocalcemia in TLS
-secondary to increased phosphate binding, exacerbated by AKI and contributes to direct tubular injury.
Signs of hyperkalemia
Muscle cramps Paresthesias ECG changes Bradycardia Dysrhythmias Cardiac arrest
signs of hyperphosphatemia
Nausea/Vomiting/Diarrhea
Lethargy
Seizure
AKI
signs of hypocalcemia
Muscle cramps Tetany Hypotension Dysrhythmia AKI
signs of hyperuricemia
AKI
TX of hyperkalemia
- avoid potassium supplementation
- NS infusion
- cardiac monitoring
- Stabilize heart
- calcium gluconate - Shift potassium
- sodium bicarbonate
- insulin/D50
- albuterol - Remove potassium
- sodium polystyrene resin (kayexalate)
- dialysis
TX for HYPERURICEMIA
- allopurinol
- rasburicase
- NS infusion
- dialysis
TX for HYPERPHOSPHATEMIA
- avoid phos and calcium supplementation
- NS infusion
- phosphate binder *ONLY OF EATING(sevelamer; aluminum hydroxide, calcium acetate)
- dialysis
TX for Hypocalcemia
- if asymptomatic, no intervention
- if symptomatic, calcium gluconate
if you give rasburicase…
walk labs down on ice for 48 hours
Hypercalcemia of malignancy (HCM)
- HCM is a complex metabolic disorder occurring in approx. 25% of cancer patients
- Most common in (breast, lung, squamous, myeloma)
mild HCM level
-10.5-11.9mg/dL
moderate HCM level
12-13.9
severe HCM level
> 24
how is calcium homeostasis maintained normally
- intestinal absorption, bone resorption and renal excretion.
- In certain cancers this homeostasis can get out of whack due to renal dysfunction or hormonal dysregulation.
Acronym for HCM
Stones, Groans, Bones, and Moans
- stones: ca stones =renal dys and gum up of the kidneys = renal failure
- Groans: abdominal pain, anorexia, ulcers
- Bones: Fractures
- Moans: neuro symptoms: Drowsiness, lethargy, weakness, depression, confusion, delirium
other renal symptoms of HCM
Polyuria, polydipsia, e-lyte wasting, dehydration, nephrolithiasis (kidney stones), renal insufficiency
other GI symptoms of HCM
Anorexia, N/V, constipation, abdominal pain, ulcers, pancreatitis
other cardiovascular symptoms of HCM
ECG changes (prolonged PR/QRS, shortened QT/ST, bradycardia, arrhythmia)
other MSK symptoms of HCM
Muscle weakness, fatigue, reduced muscle tone, bone pain
Interventions for mild HCM
- Close monitoring
- Oral hydration
- Ambulation
- Limit nephrotoxins
- Limit drugs that inc. Calcium
- Treat underlying malignancy
- Treat as “severe” if symptomatic
interventions for moderate HCM
- Hospitalization often required
* Typically treat as “severe”
interventions for severe HCM
- Hospitalization required
- Baseline ECG and Telemetry
- Close electrolyte monitoring
- IV Fluids
- Diuresis
- Administration of Calcitonin +/- Bisphosphonates and Steroids
- May need emergent Dialysis
- TREAT DISEASE
Superior Vena cava obstruction syndrome
- Compression or invasion of the SVC by tumor, thrombosis or infection causing obstruction of blood flow to the heart from the head, neck, arms and upper thorax
- 80% caused by cancer (Lung cancers, lymphoma, thyroid, head and neck cancer, other metastases)
early signs of Superior Vena cava obstruction syndrome
- Edema of face, neck, arms, thorax
- Dilated veins (spider veins)
- Facial plethora: red and ruddy
- Horner syndrome: spider veins from pressure on the cervical nerves
late signs of Superior Vena cava obstruction syndrome
-Cyanosis
-Absent peripheral pulses
CHF, decreased BP, syncope
-Chest pain/SOB/resp. distress
-Hoarseness, stridor
-Mental status changes, seizure, coma
DX of Superior Vena cava obstruction syndrome
- CT
- Tissue Biopsy
- Radiation +/- Chemotherapy
tx of Superior Vena cava obstruction syndrome
- Steroids
- Surgery/Vascular stenting
- Thrombolysis/anticoagulation
- Frequent VS, Tele Monitoring
Malignant spinal cord compression
- Occurs when malignant disease or pathologic vertebral fracture compresses spinal cord or cauda equina
- Second most common neurologic complication in cancer
- May cause devastating neurologic disability and death
- New pain is the most common presenting symptom
-commonly caused by: head and neck cancer affecting the cervical spine and prostate, bladder, colon, renals affecting lower spine or breast and lung affecting thoracic
cervical injury
-Occipital headache and neck stiffness
Radicular pain in neck, shoulder, arm
thoracic injury
Localized and/or radicular pain in chest and back
lumbosacral injury
Localized and/or radicular pain in groin or sciatic distribution in legs, pain with straight leg raise
Cauda equina
Cauda equina
Localized, radicular or referred pain in back and legs(s)
acute management of malignant spinal cord compression
- Diagnostic Imaging Evaluation (MRI entire spine)
- Neurosurgical and Rad Onc consultation
- Dexamethasone
- Radiation
- Surgery (laminectomy, vertebral resection, kypho/vertebroplasty)
- Chemotherapy
malignant pleural effusion
-Malignancy associated collection of fluid in the pleural space
-Life threatening emergency affecting respiratory function through restriction of lung expansion, decreased lung volume and altered gas exchange
-Most commonly in lung, breast, lymphoma
Associated with advanced disease and poor outcomes
subjective signs of malignant pleural effusion
Dyspnea Dry cough Pleuritic chest pain Orthopnea/PND Hemoptysis, tracheal deviation Anxiety/fear of suffocation Fever Malaise Weight loss
objective signs of malignant pleural effusion
Tachypnea Dullness to percussion Decreased/absent lung sounds Tracheal deviation (away) Egophony, tactile fremitus Bronchial breath sounds Friction rub diaphragmatic excursion Cyanosis, accessory muscle use
dx of malignant pleural effusion
- CXR-lateral and decubitus
- CT-detect smaller effusions; differential diagnoses
- Thoracentesis
TX of malignant pleural effusion
- Treat underlying cause of effusion: Chemo, XRT, antibx, diuresis, steroids, NSAIDs
- Therapeutic thoracentesis
- Chest tube drainage
- Pleurodesis/talc
- Pleuroperitoneal shunt
- Pleurex catheter
- Pleurectomy and pleural abrasion
hypersensitivity reaction
- Reaction of variable severity occurring in response to the administration of chemotherapy, biotherapy or supportive care therapies in cancer treatment
- Can be allergic (immunogenic) or nonallergic (nonimmunogenic)
- Hypersensitivity reactions, despite the cause, are treated similarly
Grade one hypersensitivity reaction
urticaria, pruritis, rash, mild upper resp. symptoms
grade two hypersensitivity reaction
1+ wheezing, N/V, SOB
grade 3 hypersensitivity reaction
grade 1/2+ serious cardiopulmonary or neurologic compromise
hypersensitivity reaction Prevention
- pre-medication
- H1/H2
- Acetaminophen
- Corticosteroids
Hypersensitivity reaction tx Cutaneous/Mild reaction
slow or stop infusion
H1/H2 blockers; +/- corticosteroids
Demerol/dilaudid for rigors
Hypersensitivity reaction tx Anaphylactoid reactions
STOP infusion Epinephrine Corticosteroids H1/H2 Blockers Resuscitation (O2, fluids, nebs, intubation, pressors, etc.)
extravasation
- Infiltration of a vesicant agent into surrounding tissue with potential to cause tissue destruction, nerve and tendon damage and functional impairment
- Vesicants classified as DNA binding (worse) or Non-DNA binding
- Vesicant extravasation is an emergency requiring immediate intervention and specialty consultation
acute management of extravasation
- Stop the infusion (including chemotherapy and any other fluids)
- Do NOT remove the catheter/needle (disconnect IV tubing, but leave IV catheter/needle)
- Aspirate fluid (attempt to aspirate any fluid from the subcutaneous tissue through the IV catheter/needle)
- Do NOT flush the IV line/catheter
- If indicated, Sodium thiosulfate is the only antidote
- Elevate and immobilize the affected extremity (for 24-48 hrs.)
- Monitor the site closely (outline the extravasation area)
- Consultation/evaluation by plastic surgery team
Disseminated intravascular coagulation
- Hematologic oncologic emergency that develops secondary to an underlying pathologic condition
- Coagulation disorder characterized by widespread intravascular thrombosis causing tissue ischemia and organ dysfunction (clotting and bleeding at the same time)
- depletion of coagulant factors and platelets contributing to hemorrhage
common causes of DIC
sepsis, trauma, obstetric conditions and malignancy
how DIC works
- result of the destruction of leukemic blast cells that release procoagulant substances from the leukemia cells causing systematic activation of coagulation
- can cause microvascular clots and, in pts whose platelets are already low due to the pathophysiology of the disease as we already discussed, increased platelet consumption, which can lead to bleeding
- need to transfuse products so that the patient can keep up with her consumption demands until we can treat the underlying leukemia
DIC manifestations
- Thrombosis is most common in solid tumors
- Bleeding occurs more often in Heme Malignancy
- Oozing from multiple sites, ecchymosis, petechiae, uncontrolled hemorrhage
- Microvascular thrombosis with hypoperfusion, ischemia, necrosis, organ failure
- Mental status changes, irritability, confusion
- Cardiopulm decompensation, shock, MODS, death
general management of DIC
- Treat underlying cause of DIC (cancer, infection, trauma)
- Monitor DIC panel every 6-12hrs (cbc, dimer, fib, INR, PTT)
- Heparin anticoagulation if thrombosis predominates or for VTE prophylaxis if not contraindicated
- Blood product replacement
management of DIC if plt are <10-20 or <30 if heme malignancy and <50 if active bleeding
1 unit of plt
management of DIC if INR is >2
2 u FFP
management of DIC if fibrinogen is <100
2 u FFP or CRYO
management of DIC if HGB is <8
1-2 u PRBC’s
iMMUNO COMPROMISED FEVER most common causes
- gram negative or positive bacteria
- yeast/fungal organisms
- viral
fever is…
- FEVER is a sign of INFECTION
- FEVER is a sign of SEPSIS
- FEVER may be the ONLY sign of INFECTION and impending SEPSIS
- SEPSIS may progress to SHOCK and DEATH
Immuno-compromised Fever: Timeliness of interventions makes a difference
reduces morbidity reduces mortality reduces hospital LOS reduces ICU interventions reduces healthcare cost
management of Immunocompromised fever
- Vital signs
- Volume resuscitation
- Oxygen support - Labs
- CBCd, CMP, PT/INR, fibrinogen, lactate - Cultures
- Blood (line/peripheral), urine, sputum, wound/lesions, abscess, etc. - ANTIBIOTICS
* DO NOT DELAY antibiotics for labs, diagnostic testing or any cultures OTHER THAN blood cultures - Diagnostic testing
- CXR, CT, US, Bronchoscopy, etc.
normal WBC
4,500 to 11,000
normal HGB
For men, 13 to 16
for women, 11 to 15
normal Hct
For men, 38 to 48 percent. For women, 35 to 44 percent
normal plt
150,000 to 450,000
normal sodium
135 and 145
normal K+
3.6 to 5.2
normal BUN
6 to 24
normal Creatinine
around 1 or less
