Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med Surg III > Test #3 > Flashcards

Test #3 Flashcards

Respiratory, cancer & Hematology

1
Q

What is cancer?

A

A group of cells that lost its control mechanisms and results in unregulated growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Heart trouble is the 1st cause of death, what is the 2nd?

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cancer

A
  • can develop from any tissue in an organ forming a mass called tumor
  • cancerous cells from the primary site can spread (metastasize) throughout the body
  • cancer cells need more glucose & O2
  • spread through lymphatics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Spreading of cancer (Initiation)

A

(first)

- change in genetic material brought on spontaneously or by a carcinogen (could be a virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Spreading of cancer (Promotion)

A

(second)
-agents in the environment allow the cell that has undergone initiation to become cancerous

-several factors: combo of susceptible cell and carcinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Spreading of cancer (progression)

A

(third)

  • invasion directly
  • through lymphatic system
  • through bloodstream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of cancer

A

Blood & blood forming

Solid tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Blood & blood forming cancers

A
  • leukemias, lymphomas & multiple myelomas
  • these cells remain separate and harm by crowding out normal blood cells in the bone marrow and blood stream.
  • Gradually replace normal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Solid tumor cancers

A

Carcinomas
-epithelial cells that cover inside and outside of body, produce hormones, make up glands
(adeno, basal, squamous, transitional)

-Elders

Sarcomas

  • mesodermal cells that form muscles & connective tissues
  • younger people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Adeno

A

Produced in a place that produces fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

basal

A

lower level of the epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

squamous

A

below outer layer of skin linings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

transitional

A

lining of stretchy things (bladder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors of cancer

A
  • Family history-chromosomal defect passed down
  • Age-77% before age 55
  • Environment-anything causing irritation
  • Geography
  • Diet-obesity, high fat, nitrates
  • Viral infections-puts you at risk (Hep B, mono, HPV)
  • Inflammatory diseases-Chron’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Defenses against cancer

A

Immune system:

  • normally the body recognizes the tumor antigen as foreign & can contain or destroy it before it becomes established.
  • If the cells have reproduced rapidly and formed a mass, the system may be unable to contain/destroy
  • Antibodies are formed but may not be powerful enough to overcome in some cancers
  • Some antigens can be detected with blood test tumor markers (used to screen & evaluate response to treatment)

**Might not have enough T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

S/S of cancer info

A

Some occur with almost all cancers & other are specific to the type of cancer and its location
-growing in large space-minimal S/S

  • s/s due to growing into, thus irritating and destroying tissue
  • putting pressure on tissue
  • producing toxins
  • using nutrients normally available for normal tissue

While growing in primary site may have one set of S/S but different with metz
-complications–paraneoplastic syndrome
(symptoms that occur at sites distant from a tumor or its metastasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

S/S of cancer

A

Pain
-painless > mild discomfort > worsens with time & enlargement
(compression/erosion into nerves & other structures)

Bleeding

  • slight since cells are not well attached to each other and vessels are fragile
  • with better organization, bleeding may be massive
  • site of cancer determines site of bleeding
Weight loss/fatigue 
-increases as cancer progresses
-appetite good > anorexia with nausea
-advanced stage-tired and sleepy
-if anemic, tired and SOB with exertion
(unexplained weight loss, food is nourishing cancer cells)

Swollen lymph nodes

  • swell as the lymph system tries to clear
  • start to become immovable and possibly painful

Depression

  • related to illness, fear of dying & loss of control
  • could be from spread to brain
  • respiratory system
  • due to blockage, pressure, bleeding, anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diagnostics of cancer

A

Physical exams (risk factors looked at-smoker, drinker, obese)

Screeners-not defenitive

  • further testing necessary
  • tumor markers in blood-test further

Staging

  • clinical (labs, x-rays, scans, biopsies, etc.)
  • pathological (excision of tumor and node exam-more precise)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is cytology?

A

biopsy of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is excision?

A

take lump out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Staging of cancer

A
  • Determines size & location and growth into near structures
  • helps determination of treatment and prognosis

Most common is TNM

  • tumor
  • nodes
  • metastasis

Cancer staging number doesn’t change, even if condition does

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TNM system (T)

A

T-Primary tumor
size, how deep into organ, has it grown into surrounding tissue?

TX-cannot be measured
T0-cannot be found
T1, T2, T3, T4-size of tumor and/or the more spread to surrounding tissue

Higher the number, larger the tumor or more it has spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TNM System (N)

A

N-Nodes
Number of nearby lymph nodes that have cancer

NX-cannot be measured
N0-do not contain cancer
N1, N2, N3-describes size, location and/or number affected

Higher the number, greater the spread`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TNM system (M)

A

M-Metastasis
has the cancer spread or not?

MX-cannot be measured
M0-no distant cancer spread found
M1-cancer has spread to other parts of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Grouping of cancer

A

Once these values have been achieved, they can be grouped into stages I-IV.

Stage 0 is very early and Stage I is next least advanced and has good prognosis.

Higher the stage, poorer the outlook.

Stage I-cells slightly different, not differentiated
Stage II-slight differentiated
Stage III-severe, differentiated
Stage IV-immature, primary, totally differentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

In situ

A

abnormal cells are present but have not spread to other tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Localized

A

cancer is limited to the starting place with no sign of spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Regional

A

cancer has not spread to nearby nodes, tissue or organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Distant

A

Cancer has spread to distant part of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Unknown

A

there isn’t enough info to figure out stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Primary prevention of cancer

A

clean eating
stop smoking
limit drinking
exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Secondary prevention of cancer

A

screening (mammogram, etc)

health promotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Treatment of cancer

A

-Surgery (includes portacath)
-Radiation (destroys cells-directly on tumor)
(also brachial therapy)
-chemo
-immunotherapy
-combo
-alternative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where is bone marrow found?

A
  • long bones
  • sternum
  • vertabrae
  • ribs
  • hip bone/pelvis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is hematology?

A

study of blood and blood forming tissues

includes blood, bone marrow, spleen and lymph system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is blood?

A

**a unique organ because it’s fluid

  • composed of plasma, various cells, proteins, clotting factors, electrolytes, nutrients, to include O2 & waste products
  • kidneys are stimulated to produce erythropoietin when oxygen levels are low.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Hematopoiesis

A

Occurs in 5 days

low O2 level > stimulates kidney to secrete erythropoietin > increases erythroblast formation > forms reticulocytes (immature RBCs)

If rapid erythropoiesis is necessary, may release reticulocytes and nucleated RBCs

  • After maturity, cells live about 120 days
  • when destroyed, causes increased billi > liver filters out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

RBC function

A
  • 95% of cell mass is hemoglobin
  • No nucleus
  • flexible & disk shaped to facilitate absorption and release of gases
  • transport gases through diffusion
  • main function–transport O2 between lungs
  • aids in buffer system (tries to keep us from going into acidosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is epogen?

A

Used to treat anemia

-creates RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is neupogen?

A

Used to treat neutropenia

  • bone marrow stimulant
  • creates WBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

RBC needs

A
  • Iron stores & metabolism
  • Vitamin B12 & folic acid metabolism
  • destruction
42
Q

WBC

A

Total amount=5,000-10,000

  • 60-70% granulocytes
  • 30-40% lymphocytes (fights germs)
  • agranulocytes
43
Q

WBC function

A

Protects against bacterial invasion and other foreign entities

  • neutrophils
  • monocytes
  • lymphocytes
  • eosinophils
  • basophils
44
Q

Neutrophils

A

fast arrival for short lived phagocytosis

45
Q

monocytes

A

long term phagocytosis as macrophages, also digest old RBC (spleen)

46
Q

Lymphocytes

A

produces substances that attack foreign material that kill directly or that enhance phagocytic cells (T cells)

B cells differentiate into plasma cells which produce immunoglobulins

47
Q

Eosinophils

A

allergic reactions (neutralizes histamine) and phagocytosis of parasites

48
Q

Basophils

A

produce and store histamine which when released provokes an allergic reaction

49
Q

Platelets (thrombocytes)–granular fragments

A
  • produced in marrow
  • regulated by the hormone thrombopoitin
  • controls bleeding (initiates clotting process)
  • -collects & activates at the site of injury forming a plug
  • -releases substances that activate coagulation factors

-Nurture and maintain the lining of the vessels

50
Q

Plasma & plasma protein

A

90%=water rest=plasma proteins, clotting factors, nutrients enzymes, waste and gases

  • serum
  • protein–albumin, globulins

alpha & beta (transport)
gamma (immune system)

51
Q

Reticuloendothelial system

A
  • monocytes derived cells live within the tissues
  • liver, spleen, lymph nodes, & lungs
  • protect against foreign invaders
  • stimulate inflammatory process
52
Q

Hemostasis

A

Primary
-formation of platelet plug (vessels constrict)

Secondary

  • inactivated coagulation factors are activated on the surface of the plug
  • end result is fibrin anchoring to plug forming a clot
53
Q

What is ecchymosis?

A

bruising without a cause

54
Q

Acquired coagulation disorders

A

Liver disease-prolonged pt

Vit K deficiency-gut isn’t helping reduce

Complications of anticoag therapy-warfarin

Disseminated intravascular coagulation (DIC)-mini clots
-give heparin!

55
Q

Hemostasis disorders

Clinical manifestations

A

Occasionally, none

Bleeding

  • mucosa/skin
  • hemorrhage
  • prolonged bleeding for venipuncture sites
  • with TTP, increased range of PCs due to clots in systems
56
Q

Hemostasis Disorders

Diagnostics

A

Labs

  • platelet counts
  • peripheral smears
  • pt
  • ptt
  • RBC morphology (size, shape)
  • bone marrow exams
57
Q

Hemostasis Disorders

A

Thrombocytopenia-platelets below 150,000

  • decreased production of platelets within the bone marrow (aplasticanemia)
  • increased destruction of platelets (septicemia, certain drugs, cancer)
  • increased construction of platelets (large bleed)

Inherited
Acquired
-immune-(ITP) Immune thrombocytopenia purpura (most common)
-non-immune-due to shortened circulation, turbulent blood flow (causes damage), decreased production

**avoid rough activity. Pt needs to be aware of any bruising or bleeding

58
Q

Acquired Immune: Immune thrombocytopenic purpura (ITP)

A

Normal function of platelets-shortened life

  • coated with antibodies
  • recognized by spleen as foreign material & destroyed by macrophages
  • marrow cannot keep supply to demand

Acute-most common in kids. Usually 1-6 weeks after viral infection (measles or chicken pox, or immunizations to either), self limiting

Chronic-due to autoimmune problems, or a drug reaction

59
Q

Acquired Non-immune: Thrombotic thrombocytopenia purpura (TTP)

A

RARE!!!

Absence of anti-clotting plasma enzyme leads to enhanced agglutination of platelets form micro-clots that deposit in capillaries, decreasing # in system.

***Medical emergency-clotting/bleeding at the same time

micro-clots will form and go to the brain, heart, kidney; may have headache, confusion, coma, disrrhythmias, kidney failure.

Special, shorter tubing when giving platelets!

60
Q

Acquired Non-immune: Heparin Induced Thrombocytopenia and Thrombosis Syndrome (HITTS)

A
  • Microclotting with reduction of circulating platelets
  • Immune-mediated response to heparin=antibodies=removal=decreased platelets & platelet/fibrin clots
  • Heparin neutralized–NO HEPARIN!!!

Special, shorter tubing when giving platelets!

61
Q

Other Acquired-Non-immune

A
  • end stage renal disease
  • multiple myeloma (bone cancer)-will have abnormal proteins that interfere with platelet function
  • cardiopulmonary bypass-destroys platelets
62
Q

Disseminated Intravascular Coagulation (DIC)

A

Starts with small clots in blood stream, blocking vessels.

  • stimulated by infection, toxins, complication of child birth or dead fetus.
  • Hemorrhage
  • Severe head injury

Increased clotting depletes platelets and clotting factors needed to control bleeding

63
Q

DIC treatment

A

Correct underlying cause

Heparin therapy to slow clotting

Platelet transfusion and clotting factors to replace those depleted

Temporary fix-steroids or IV immune globulin

Spenectomy

64
Q

Marrow aspiration

A

Purpose

  • hematopoiesis evaluation
  • cytopathology
  • chromosomal study

site-anterior/posterior iliac crest, sternum

MD under local anesthesia

Needle inserted, stylet removed, 0.2-0.5 mL removed, needle removed and pressure applied 10 min to avoid bleeding!

65
Q

Graft vs Host rejection

A

Fatal in 20% of patients

S/S- peeling of hands and feet

Call Dr STAT!

66
Q

Bone marrow transplant

A

Kill off bone marrow with drug (chemo)

Increase doses so patient doesn’t reject immune cells

Wait 2-3 days, keep in reverse isolation

Give stem cells IV and they will repopulate marrow and will start to put out healthy cells

Monitor: fluids, infections, toxicity, small meals-high protein, low calories.

67
Q

The anemias

A

Deficiency in the number of RBCs

Quantity of hemoglobin

Decreased volume packed RBCs (hematocrit)

**Decreased RBC means decreased O2 (SOB) means increased H&H

68
Q

Anemia

A

Decreased production of RBC (hypoproliferative)

Blood loss

Increased RBC destruction (hemolytic)

69
Q

Clinical manifestations of anemia

A

Depends on severity

Weakness, fatigue, malaise, pallor are common

Bone pain, yellow sclera, hemorrhage of eyes, blurred vision, enlarged liver & spleen, sore mouth, difficulty swallowing, coffee ground emesis, jaundice, and puritis

Cardiac-high B/P, HF, PAD, heart enlarged

GI-dark stool, red/smooth tongue

Neuro-headache, vertigo, ataxia

70
Q

Angular cheilitis

A

cracked corners of mouth

71
Q

Management of anemia

A

correcting/controlling cause

replacement of RBCs (epogen, blood transfusion or marrow)

  • *B12=problem with vegetarians
  • give iron with OJ, sticks with them better
72
Q

Types of anemia

A
  • Iron deficiency (d/t inadequate intake, but mostly blood loss)
  • Anemias or renal/chronic disease
  • Aplastic
  • Megaloblastic
  • Myelodysplastic syndromes
  • Sickle cell
  • Thalassemia
  • Glucose-6-Phosphate Dehydrogenase deficiency
  • Hereditary Spherocytosis
  • Immune Hemolytic
73
Q

Sickle Cell Anemia

A

**Short life!

Genetic defect-hemolytic (may be born with trait, mostly in Mediterranean area)

Low O2 causes crystal-like formations–rigid sickle shape

Tangle causing ischemia/infarctions

Sickling takes time so can fix itself when passes through well oxygenated areas

Cold aggravates condition, so does increased viscosity

74
Q

Sickle cell anemia S/S

A

tachycardia
murmurs
cardiomegaly

Hgb 7-9

jaundice
enlarged face/head if severe as child

*most of the time, begins in feet, see scars where clots are that get into capillaries and kill skin cells.

75
Q

Sickle cell crisis

A

Can be deadly!

Sickle crisis-painful d/t death to tissue

Aplastic crisis-infection (parvovirus) yields rapid fall in hemoglobin

Sequestration crisis-pooled sickle cells.

Acute chest syndrome

  • S/S-rapid fall in Hgb, tachycardia, fever, bilateral infiltrates of lungs
  • Potentially lethal
76
Q

Priapism

A

erection that won’t go away

77
Q

Hereditary Hemochromatosis

A

Iron is excessively absorbed in GI tract

  • deposited in organs causing dysfunction
  • can be secondary to other anemias, liver disease and multiple transfusions

**Mostly in men, because women have periods.

S/S-fatigue, arthralgia, impotence, abdominal pain, weight loss

  • liver enlargement (Cirrhosis, cancer)
  • other organ involvement

Removal of excess iron-therapeutic phlebotomy
Genetic counseling
Dietary-low iron
Manage organ involvement-treat organ involved

78
Q

Polycythemias

A

Polycythemia Vera-overproduction of RBCs, RBCs, platelets

  • increased viscosity/volume
  • congested organs/tissues (enlarged spleen/liver)

Secondary Polycythemia-caused by excessive production of erythropoietin
-may occur as response to hypoxia or neoplasms (tumors)

NO cure.

PCs-clots, CVA, DVT, bleeding, MI

79
Q

Leukopenia & Neutropenia

A

1 thing to remember-wash hands!!

Leukopenia-fewer WBCs than normal
-could be neutropenia or lymphopenia

Neutropenia-fewer neutrophils than normal

  • results from decreased production/increased destruction
  • increased risk for infection

Reverse isolation because decreased WBCs at risk for infection, sepsis and septic shock!

80
Q

Leukocytosis & leukemia

A

Leukocytosis-increased level of WBCs
-occurs in infection, injury, inflammatory disorders, some drugs
Evaluation-look for immature cells indicating disorder in the marrow

Cause could be malignancy/leukemia
-DIAGNOSTIC: bone marrow biopsy

Treatment: start on antibiotics to reduce need for WBC so body will stop manufacturing them

81
Q

Therapies for blood disorders

A

Splenectomy

  • may be necessary after trauma
  • possible treatment for some hematologic disorders

Therapeutic Apheresis
-removes certain cells from blood

Therapeutic phlebotomy
-removal of certain amount of blood under controlled conditions

82
Q

Leukemia-what is it? And how does it happen?

A

**Leading cause of death for kids

Cancer of the WBCs or cells that develop into WBCs
(usually takes place in bone marrow)

WBCs develop into stem cells

  • if development goes awry, chromosomes get rearranged, interfering with normal cell division
  • multiply uncontrollably
83
Q

Leukemia types

A

Types define how quickly the progress and kind of cells affected

Myeloid leukemia (MORE RARE)
-Acute/Chronic (AML/CML)

Lymphocytic (MORE COMMON)
-Acute/chronic (ALL/CLL)

Acute and chronic-depends on time it takes for S/S to appear and the phase at which the cell stopped development
-in acute form can infiltrate other organs

84
Q

Etiology of leukemia

A

connected to possible genetics, viruses, chemical and radiation exposures

85
Q

Leukemia cell information

A

Unregulated rapid production of WBCs in the marrow leaving little room for normal cell production
(Although there is overproduction of WBCs, it will still cause you to have a decreased leaukocyte number because they’re IMMATURE)

  • decreased RBCs/platelets=anemia/bleeding
  • increased IMMATURE WBCs=increased R/F infection

-can also grow in liver

86
Q

Clinical manifestations of Acute Leukemia

A
  • Abrupt onset
  • WBCs undifferentiated or “blasts”
  • progresses rapidly

Without aggressive treatment, death occurs in weeks-months

87
Q

Clinical manifestations of chronic leukemia

A

S/S occur in months-years

  • majority of WBCs are mature
  • progresses slowly
88
Q

What are lymphomas?

A

Neoplasms of lymphoid cells

-Can be cured but may lead to other malignancies like acute myeloid leukemia

89
Q

What are the types of lymphomas?

A

Hodgkin’s disease

Non-Hodgkin’s disease

Multiple myeloma

90
Q

Hodgkin’s disease cause

A

Cause unknown-virus or familial pattern

*Nodes upper body

15-24 years of age

91
Q

Symptoms of Hodgkin’s disease

A

Painless enlargement of neck nodes on 1 side
Mediastinal mass

  • jaundice, itching, shingles, bone & abdominal pain, cough, pulmonary effusion, night sweats
  • Aggravated by alcohol
92
Q

What is Non-Hodgkin’s disease?

A

Nodes infiltrated by malignant cells

Prevalent in immuno compromised clients

in ages 60+

93
Q

Non-Hodgkin’s disease survival info

A

in mild early cases is over 10 years

94
Q

Treatment for Hodgkin’s disease

A

chemo
then radiation
followed by BMT or stem cell transplant

95
Q

Non-Hodgkin’s disease symptoms

A

No S/S until late
-lymphadenopathy

upper body
rash
can impact different organs

96
Q

Treatment of Non-Hodgkin’s disease

A

**Most treatable

Non aggressive type: localized radiation

Aggressive type: radiation and chem

May be followed by BMT and stem cell transplant

97
Q

S/S of multiple myeloma

A

Bone pain

  • increased with movement
  • decreased with rest
  • better in AM

Bone breakdown

Hypercalemia (thirst, dehydration, constipation, confusion, coma)

Renal failure

Bleeding, HA, blurred vision, HF

Anemia

98
Q

Is multiple myeloma curable?

A

NO, not curable

99
Q

Clinical manifestations of Multiple myeloma

A

Bone breakdown-due to osteoclast activating factor and other substances secreted from plasma cells

Due to destruction, excessive ionized Ca++ enters serum (hypercalemia)

Excessive excretion of immunoglobins-renal failure, hyper viscosity of serum

Due to less space for RBC production-anemiWhat is a in late stages and decreased WBC and platelets

100
Q

What is a lymphogram?

A
  • Insert dye between toes
  • Do scan after 30 min
  • Scan q24hrs
  • then daily for several days to watch lymphatic system
101
Q

Treatment of multiple myeloma

A

NOT CURABLE
-survivors develop leukemia

  • Pain management
  • Teach S/S hypercalemia
  • maintain mobility and hydration
  • Dialysis
  • Infection precautions
  • Chemo slows progression
102
Q

Chemo/Radiation

A

ChemotherapyYields systemic side effects

  • Myelosuppression
  • Nausea
  • Hair loss
  • Infection

Radiation is specific to area being treated
-N/D

  • Watch platelets
  • Keep moving

Med Surg III (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions