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Complex care final > Oncology > Flashcards

Oncology Flashcards

1
Q

type of blood cancers

A
  • leukemias
  • lymphomas
  • plasma cell disorder
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2
Q

solid tumor types

A
  • diff. by type (breast, prostate, colon, lung-most common)
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3
Q

types of cancer treatments

A
  • chemo
  • immunotherapy
  • radiation
  • surgery (solid only)
  • stem cell transplant
  • CAR-T therapy
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4
Q

what are blood cancers

A
  • malignancy originating from hematopoietic (blood producing) cells in the bone marrow
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5
Q

types of myeloid blood cancer

A

-MDS, AA, AML, CML

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6
Q

Types of lymphoid blood cancer

A

-acute lymphocytic leukemia, MM, lymphomas

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7
Q

acute leukemia

A

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

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8
Q

DX of acute leukemia

A
  • peripheral blood tests (blasts)
  • bone marrow biopsy
  • lumbar puncture
  • imaging
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9
Q

systemic symptoms of acute leukemia

A
  • weight loss
  • fever
  • lots of infections
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10
Q

lung symptoms of acute leukemia

A

-sob

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11
Q

Muscular symptoms of acute leukemia

A

-WEAKNESS

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12
Q

bone and joint symptoms of acute leukemia

A

-pain and tenderness

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13
Q

psychological symptoms of acute leukemia

A
  • fatigue

- loss of appetite

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14
Q

lymph node symptoms of acute leukemia

A

-swelling

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15
Q

spleen and liver symptoms of acute leukemia

A

-enlargement

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16
Q

skin symptoms of acute leukemia

A
  • night sweats
  • easy bleeding and bruising
  • purplish patches or spots
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17
Q

difference between AML and ALL

A
  • AML: fatigue, DIC, Bleeding (sicker on presentation)

- ALL: hepatosplenomegaly

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18
Q

B-symptoms

A
  • will be seen with lymphoid lineage cancers (ALL, lymphomas, CLL)
  • unintentional weight loss
  • drenching night sweats
  • fever (unknown why)
  • painless lymphadenopathy
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19
Q

chemo induction phase

A
  • initial chemo treatment
  • meant to induce remission
  • response to induction can predict outcomes/response to future treatment
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20
Q

chemo consolidation phase

A
  • goal to eradicate disease that is below the level of detection
  • can be done with chemo or stem cell transplantation
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21
Q

chemo maintenance phase

A

-lower doses of treatment for prolonged periods of time to improve chances of cure

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22
Q

what is chronic leukemia

A
  • 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
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23
Q

CLL symptoms

A
  • 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)
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24
Q

CLL treatment

A
  • BTK- inhibitors like ibrutinib or acalabrutinib

- BCL-2 inhibitors like venetoclax

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25
Q

CML symptoms

A

-weakness, fatigue, SOB, fevers, bone pain

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26
Q

treatment of CML

A

-tyrosine kinase inhibitors like ponatinib, imatinib, nilotinib

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27
Q

what is lymphoma

A
  • 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
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28
Q

how do lymphocytes normally circulate the body

A

-via the lymphatic system

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29
Q

function of lymph nodes

A

-key structure of lymphatic system found throughout the body and help filter lymph fluid to remove foreign particles

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30
Q

hodgkin lymphoma

A
  • 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
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31
Q

Non-hodgkin lymphoma

A
  • 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
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32
Q

symptoms of lymphoma

A

-b symptoms: night sweats, early statiety= weight loss, painless lymphadenopathy, fever

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33
Q

DX for lymphoma

A
  • lymph node biopsy
  • Imaging: PET/CT: hot spots may appear
  • peripheral labs
  • bone marrow biopsy
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34
Q

tx for lymphoma

A
  • immunotherapy
  • chemo
  • radiation
  • stem cell transplant
  • CAR-T therapy
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35
Q

multiple myeloma (MM)

A
  • 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
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36
Q

symptoms of MM

A
  • CRAB
  • c= high calcium
  • R= renal (kidney) problems- AKI
  • A= anemia or low HgB
  • B= bone problems

-I= infection

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37
Q

DX if MM

A
  • peripheral labs: serum free light chains, immunoglobulins, M protein
  • Bone marrow biopsy
  • PET/CT: hot spots
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38
Q

TX for MM

A
  • NOT CURABLE
  • want to: have longest deepest remission
  • immunotherapy
  • chemo
  • radiation
  • stem cell transplant
  • CAR-T therapy
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39
Q

Stem cell transplant

A
  • 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
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40
Q

Autologous stem cell source

A
  • patients own stem cell

- collected after mobilization with high dose neupogen

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41
Q

Allogenic stem cell source

A
  • donor stem cell
  • matched related donor (sibling)
  • matched unrelated donor
  • cord (fetal umbilical cord) donor
  • syngenic (identical twin)
  • Haplo-identical (1/2 matched donor)
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42
Q

major complications of stem cell transplant

A
  • Sinusoidal Obstructive Syndrome

- Graft Versus Host Disease

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43
Q

Sinusoidal Obstructive Syndrome

A
  • rare
  • gumming up of the liver
  • actegol can help
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44
Q

Graft Versus Host Disease (GVHD)

A
  • 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
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45
Q

TX of Graft Versus Host Disease (GVHD)

A

-increased immunosuppression in the form of corticosteroids (medicines such as prednisone, methylprednisolone, dexamethasone, beclomethasone and budesonide)

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46
Q

Chronic GVHD

A
  • syndrome that may involve one organ or many

- leading cause of medical problems and death after allogenic stem cell transplant

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47
Q

hard thing about GVHD

A
  • want some of this to kill of the remaining cancer cells but dont want too much
  • very fine balance
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48
Q

cancers that can use autologous stem cell

LETS MAKE CANCER AA TABOO NAME

A
  • Lymphoma​
  • Multiple Myeloma​
  • CLL​
  • Amyloidosis​
  • Some autoimmunedisorders​
  • Testicular
  • Neuroblastoma
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49
Q

cancers that can use allogenic stem cell transplant

A
  • ALL / AML / MDS​
  • Some refractoryLymphomas​
  • PNH​
  • CML/CLL​
  • Sickle cell disease​
  • Some autoimmunedisorders​
  • Myelofibrosis​
  • Aplastic Anemia​
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50
Q

CAR-T therapy

A
  • 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.
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51
Q

benefit of CAR-t therapy

A
  • 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
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52
Q

What is CAR T currently used in

A
  • Multiple Myeloma
  • Lymphoma
  • ALL (Acute Lymphocytic Leukemia)
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53
Q

CAR-T therapy toxicity

A
  1. Cytokine Release Syndrome (CRS)

2. Immune Effector Cell-Associated Neurotoxicity

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54
Q

Cytokine release syndrome (CRS)

A

-response to the over-activation of the immune system response with a supraphysiological release of inflammatory cytokines

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55
Q

symptoms of CRS

A
  • 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

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56
Q

life threatening complications of CRS

A
  • cardiac dysfunction
  • ARDS from capillary leak
  • renal or hepatic failure
  • DIC
  • HLH
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57
Q

Immune effector cell associated neurotoxcicty (ICANS)

A

-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

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58
Q

symptoms of ICANS

A

-aphasia (expressive), altered mental status, impaired cognition, motor weakness, seizures or cerebral edema, encephalopathy

59
Q

non specific symptoms of ICANS

A

headache, tremor, myoclonus (quick, involuntary muscle jerk), asterixis (loses motor control), hallucinations, weakness, and intracranial hemorrhage

60
Q

Stages of CRS

A
  • 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
61
Q

TX for CRS grade 2 or higher

A
  • tociluzumab
  • if the symptoms then dont resolve add steroids
  • if have neuro toxcicity add anakinra
62
Q

Neurotoxcicity scoring questions to ask

A
  • 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
63
Q

grades for neurotoxcicity

A
  • GR 1: score of 7-9
  • GR 2: 5-7
  • GR 3: 3-5
  • GR 4: 3-0
64
Q

what is an oncologic emergency

A
  • 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 `
65
Q

Onc emergency category: Metabolic

A

-TLS, Hypercalcemia, SIADH, Hyper/hypoglycemia

66
Q

categories of onc emergencies

A
  • metabolic
  • structural
  • hematologic
  • infusional
67
Q

Onc emergency: structural

A

-SVC obstruction, Airway obstruction, Cord compression, Effusion, increase ICP, Seizure

68
Q

Onc emergency: hematologic

A

-Fever, Leukostasis/Viscosity, Bleeding, Thrombosis, DIC, CRS/ICANS

69
Q

Onc emergencies: infusional

A

-Extravasation, Anaphylaxis, Reactions

70
Q

Tumor lysis syndrome (TLS)

A
  • 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
71
Q

Complications of tumor lysis syndrome

A

-rapidly progressing renal failure, seizure and cardiac dysrhythmia leading to death

72
Q

Tumor lysis syndrome is most common in…

A
  • 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
73
Q

what causes hyperkalemia in TLS

A

-release of intracellular potassium from tumor and can also be exacerbated by AKI

74
Q

what causes hyperuricemia in TLS

A

-released from tumor, exacerbated by AKI and contributes to AKI crystal obstructive nephropathy

75
Q

What causes hyperphosphatemia in TLS

A

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

76
Q

What causes hypocalcemia in TLS

A

-secondary to increased phosphate binding, exacerbated by AKI and contributes to direct tubular injury.

77
Q

Signs of hyperkalemia

A 
Muscle cramps
Paresthesias
ECG changes
Bradycardia
Dysrhythmias
Cardiac arrest
78
Q

signs of hyperphosphatemia

A

Nausea/Vomiting/Diarrhea
Lethargy
Seizure
AKI

79
Q

signs of hypocalcemia

A 
Muscle cramps
Tetany
Hypotension
Dysrhythmia
AKI
80
Q

signs of hyperuricemia

A

AKI

81
Q

TX of hyperkalemia

A
  1. avoid potassium supplementation
  2. NS infusion
  3. cardiac monitoring
  4. Stabilize heart
    - calcium gluconate
  5. Shift potassium
    - sodium bicarbonate
    - insulin/D50
    - albuterol
  6. Remove potassium
    - sodium polystyrene resin (kayexalate)
    - dialysis
82
Q

TX for HYPERURICEMIA

A
  • allopurinol
  • rasburicase
  • NS infusion
  • dialysis
83
Q

TX for HYPERPHOSPHATEMIA

A
  • avoid phos and calcium supplementation
  • NS infusion
  • phosphate binder *ONLY OF EATING(sevelamer; aluminum hydroxide, calcium acetate)
  • dialysis
84
Q

TX for Hypocalcemia

A
  • if asymptomatic, no intervention

- if symptomatic, calcium gluconate

85
Q

if you give rasburicase…

A

walk labs down on ice for 48 hours

86
Q

Hypercalcemia of malignancy (HCM)

A
  • HCM is a complex metabolic disorder occurring in approx. 25% of cancer patients
  • Most common in (breast, lung, squamous, myeloma)
87
Q

mild HCM level

A

-10.5-11.9mg/dL

88
Q

moderate HCM level

A

12-13.9

89
Q

severe HCM level

A

> 24

90
Q

how is calcium homeostasis maintained normally

A
  • intestinal absorption, bone resorption and renal excretion.
  • In certain cancers this homeostasis can get out of whack due to renal dysfunction or hormonal dysregulation.
91
Q

Acronym for HCM

A

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
92
Q

other renal symptoms of HCM

A

Polyuria, polydipsia, e-lyte wasting, dehydration, nephrolithiasis (kidney stones), renal insufficiency

93
Q

other GI symptoms of HCM

A

Anorexia, N/V, constipation, abdominal pain, ulcers, pancreatitis

94
Q

other cardiovascular symptoms of HCM

A

ECG changes (prolonged PR/QRS, shortened QT/ST, bradycardia, arrhythmia)

95
Q

other MSK symptoms of HCM

A

Muscle weakness, fatigue, reduced muscle tone, bone pain

96
Q

Interventions for mild HCM

A
  • Close monitoring
  • Oral hydration
  • Ambulation
  • Limit nephrotoxins
  • Limit drugs that inc. Calcium
  • Treat underlying malignancy
  • Treat as “severe” if symptomatic
97
Q

interventions for moderate HCM

A
  • Hospitalization often required

* Typically treat as “severe”

98
Q

interventions for severe HCM

A
  • Hospitalization required
  • Baseline ECG and Telemetry
  • Close electrolyte monitoring
  • IV Fluids
  • Diuresis
  • Administration of Calcitonin +/- Bisphosphonates and Steroids
  • May need emergent Dialysis
  • TREAT DISEASE
99
Q

Superior Vena cava obstruction syndrome

A
  • 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)
100
Q

early signs of Superior Vena cava obstruction syndrome

A
  • 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
101
Q

late signs of Superior Vena cava obstruction syndrome

A

-Cyanosis
-Absent peripheral pulses
CHF, decreased BP, syncope
-Chest pain/SOB/resp. distress
-Hoarseness, stridor
-Mental status changes, seizure, coma

102
Q

DX of Superior Vena cava obstruction syndrome

A
  • CT
  • Tissue Biopsy
  • Radiation +/- Chemotherapy
103
Q

tx of Superior Vena cava obstruction syndrome

A
  • Steroids
  • Surgery/Vascular stenting
  • Thrombolysis/anticoagulation
  • Frequent VS, Tele Monitoring
104
Q

Malignant spinal cord compression

A
  • 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

105
Q

cervical injury

A

-Occipital headache and neck stiffness

Radicular pain in neck, shoulder, arm

106
Q

thoracic injury

A

Localized and/or radicular pain in chest and back

107
Q

lumbosacral injury

A

Localized and/or radicular pain in groin or sciatic distribution in legs, pain with straight leg raise

108
Q

Cauda equina

A

Cauda equina

Localized, radicular or referred pain in back and legs(s)

109
Q

acute management of malignant spinal cord compression

A
  • Diagnostic Imaging Evaluation (MRI entire spine)
  • Neurosurgical and Rad Onc consultation
  • Dexamethasone
  • Radiation
  • Surgery (laminectomy, vertebral resection, kypho/vertebroplasty)
  • Chemotherapy
110
Q

malignant pleural effusion

A

-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

111
Q

subjective signs of malignant pleural effusion

A 
Dyspnea
Dry cough
Pleuritic chest pain
Orthopnea/PND
Hemoptysis, tracheal deviation
Anxiety/fear of suffocation
Fever
Malaise
Weight loss
112
Q

objective signs of malignant pleural effusion

A 
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
113
Q

dx of malignant pleural effusion

A
  • CXR-lateral and decubitus
  • CT-detect smaller effusions; differential diagnoses
  • Thoracentesis
114
Q

TX of malignant pleural effusion

A
  • 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
115
Q

hypersensitivity reaction

A
  • 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
116
Q

Grade one hypersensitivity reaction

A

urticaria, pruritis, rash, mild upper resp. symptoms

117
Q

grade two hypersensitivity reaction

A

1+ wheezing, N/V, SOB

118
Q

grade 3 hypersensitivity reaction

A

grade 1/2+ serious cardiopulmonary or neurologic compromise

119
Q

hypersensitivity reaction Prevention

A
  1. pre-medication
    - H1/H2
    - Acetaminophen
    - Corticosteroids
120
Q

Hypersensitivity reaction tx Cutaneous/Mild reaction

A

slow or stop infusion
H1/H2 blockers; +/- corticosteroids
Demerol/dilaudid for rigors

121
Q

Hypersensitivity reaction tx Anaphylactoid reactions

A 
STOP infusion
Epinephrine
Corticosteroids
H1/H2 Blockers
Resuscitation (O2, fluids, nebs, intubation, pressors, etc.)
122
Q

extravasation

A
  • 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
123
Q

acute management of extravasation

A
  • 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
124
Q

Disseminated intravascular coagulation

A
  • 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
125
Q

common causes of DIC

A

sepsis, trauma, obstetric conditions and malignancy

126
Q

how DIC works

A
  • 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
127
Q

DIC manifestations

A
  • 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
128
Q

general management of DIC

A
  • 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
129
Q

management of DIC if plt are <10-20 or <30 if heme malignancy and <50 if active bleeding

A

1 unit of plt

130
Q

management of DIC if INR is >2

A

2 u FFP

131
Q

management of DIC if fibrinogen is <100

A

2 u FFP or CRYO

132
Q

management of DIC if HGB is <8

A

1-2 u PRBC’s

133
Q

iMMUNO COMPROMISED FEVER most common causes

A
  • gram negative or positive bacteria
  • yeast/fungal organisms
  • viral
134
Q

fever is…

A
  • 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
135
Q

Immuno-compromised Fever: Timeliness of interventions makes a difference

A 
reduces morbidity
reduces mortality
reduces hospital LOS
reduces ICU interventions
reduces healthcare cost
136
Q

management of Immunocompromised fever

A
  1. Vital signs
    - Volume resuscitation
    - Oxygen support
  2. Labs
    - CBCd, CMP, PT/INR, fibrinogen, lactate
  3. Cultures
    - Blood (line/peripheral), urine, sputum, wound/lesions, abscess, etc.
  4. ANTIBIOTICS
    * DO NOT DELAY antibiotics for labs, diagnostic testing or any cultures OTHER THAN blood cultures
  5. Diagnostic testing
    - CXR, CT, US, Bronchoscopy, etc.
137
Q

normal WBC

A

4,500 to 11,000

138
Q

normal HGB

A

For men, 13 to 16

for women, 11 to 15

139
Q

normal Hct

A

For men, 38 to 48 percent. For women, 35 to 44 percent

140
Q

normal plt

A

150,000 to 450,000

141
Q

normal sodium

A

135 and 145

142
Q

normal K+

A

3.6 to 5.2

143
Q

normal BUN

A

6 to 24

144
Q

normal Creatinine

A

around 1 or less

Complex care final (8 decks)

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