Brainscape's Knowledge GenomeTM

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


See full index

patho > patho final > Flashcards

patho final Flashcards

1
Q

atrophy

A

decreased workload

decreased cell size

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

hyperplasia

A

increased number of cells

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

hypertrophy

A

increased workload

increased cell size

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

benign

A
  • usually harmless
  • almost always encapsulated
  • prevents the release of cells, restricting the spread
  • problems are related to compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

malignant

A
  • rapid, uncontrolled and disorganized growth
  • metastasis
  • starve normal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hypersensitivty reactions

A
  • inappropriate response to antigen
  • occurs immediately or within minutes to hours
  • classified by pathogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

type 1 hypersensitivty

A

immediate reaction
- had to have been previously exposed (sensitization)

1st exposure: IgE: antibodies are made and attach to mast cells through the body

2nd exposure: antigen causes IgE to trigger T cells and histamine

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

type 11 hypersensitivity

A

cytotoxic and cytolytic reaction
- igG and igM antibodies bind with antigen on cell surface

  • cell destruction occurs
  • resulting in: Lysis, phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

type 3 hypersensitivity

A
  • immune complex reactions: antigen-antibody complexes
  • ineffectively removed by phagocytosis
  • autoimmune diseases
  • sites: kidneys, skin, joints, blood vessels. and lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

type 4 hypersensitivity

A
  • cell-mediated or delayed hypersensitivity reactions. mediated by t cells as opposed to antibodies
  • occurs in two phases
  • sensitization phase
  • effector phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

neutropenia

A
  • decrease neutrophil- leads to more infections
  • normal: 2,000-7,500 cells/ml
  • causes: increase use infection, decrease production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

thrombocytopenia

A

low platelets

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

anemia

A
  • decrease in rbc
  • decrease in hemoglobin content
  • abnormal Hgb

results from:

  • impaired production
  • increased destructing
  • blood loss

leading to
- decreased oxygen-carrying capacity

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

anemia cm

A
  • weakness
  • fatigue
  • pallor
  • syncope
  • dyspenea
  • tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

iron deficiency anemia

A
  • low iron
  • decrease hgb production
  • decrease absorption (upper gi tract)
  • increase bleeding (menstruation)

prevalence

  • women of childbearing age
  • children under 2
  • elderly

diagnosis

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

pernicious anemia

A
  • b12 deficency or megaloblastic anemia
  • decrease cyancobalmin b12
  • lack on intristic factor
  • acquired: portion of stomach/intestines

autoimmune

  • destruction of pareital cells
  • results in immature rbcs

diagnosis

  • cbc
  • vitamin b12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

aplastic anemia

A
  • destruction of bone marrow
  • resulting from variety of factors

autoimmune conditions

  • medications
  • viruses
  • toxins
  • genetic abnormalities
  • pancytopenia: low rbc, wbcs, plts
  • increase clinical manifestations

diagnosis

  • cbc
  • bone marrow biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hemolytic anemia

A
  • destruction (hemolysis of rbc

multiple types

  • sickle anemia
  • thalassemia- rare
  • erthryoblastosis- children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

sickle cell anemia

A
  • inherited autosomal recessive
  • hgb becomes sensitive to changes in 02
    • changes from disk shape to crescent shape
  • not able to flow through vessels leading to clumping
  • only live for 20 days instead of 120 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

signs and symptoms of sickle cell anemia

A
  • severe pain and swelling
  • abdominal pain
  • tachypnea
  • dilute urine and blood in the urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

sickle cell diagnosis

A
  • sickledex test

- hemoglobin electrophoresis

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

neutropenia diagnosis and treatment

A
  • complete blood count
  • bone marrow biopsy

treatment
- causative in nature: need to know underlying cause treatment

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

neutropenia

A
  • decrease neutrophil- leads to more infections
  • normal: 2,000-7,500 cells/ml
  • causes: increase use infection, decrease production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

clinical manifestations of neutropenia

A

fever
chills
fatigue

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

regurgitation

A
  • valve does not close completely

- blood flow backs up

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

stenosis

A
  • narrowed, valve does not open completely
  • forward blood flow hindered
  • decreases cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

right- sided heart failure

A
  • left-sided heart failure major cause must continually pump blood against increased fluid in the pulmonary artery and lungs
  • cor pulmonale: right ventricle hypertrophies and fails due to increased pulmonary pressures
  • a backward buildup of blood systematic blood vessels
  • peripheral edema results
  • backs into body= edema, jugular vein distension
  • body can attain a liter of fluid before showing signs: weigh pt.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

left- sided heart failure

A
  • afterload: force generated by left ventricle to eject blood to the aorta through aortic valve
  • peripheral vascular resistance: pressure within aorta/arteries
  • pvr influences afterload
  • hypertension major cause
  • blood backs up from left ventricle into lungs into pulmonary circulation= flooded capillaries
  • avelora edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

atherosclerosis

A

thickening/ hardening of arterial walls from plaque formation
- may begin in childhood

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

coronary artery disease (CAD)

A

obstruction of blood flow through coronary arteries typically caused by atherosclerosis

can cause:

  • angina
  • myocardial infarction
  • sudden death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

myocardial infarction

A

death of heart muscle

types

  • non-st segment elevation myocardial infarction (NSTEMI)
  • st segment elevation myocardial infarction (STEMI)

etiology

  • atherosclerosis: narrowing of coronary arteries
  • thrombus: embolism
  • vasospasm: constriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hypertension

A

persistently high blood pressure

  • systolic BP > 130 mmhg
  • diastolic bp > 80 mmhg
  • average of two or more readings on different dates: two weeks apart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

patho of mi

A
  • coronary artery blockage

- decreased cardiac blood supply

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

signs and symptoms of mi

A
  • crushing viselike pain arm, shoulder, neck, jaw, back
  • shortness of breath
  • restlessness
  • dizziness, fainting
  • nauesea
  • sweating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

atypical signs of MI

A
  • abscne of classic pain
  • dyspena
  • fatigue
  • anxiety
  • impending doom
  • chest cramps
  • abdominal pain
  • indigestion
  • restlessness
  • falling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

prehospital MI

A

“time is muscle”

  • asprin
  • call 911 of 5 min of chest pain
  • do not drive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

hospital MI

A

Morphine
Oxygen
Nitroglycerin
Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CAD prevention

A
  • non-modifiable risk factors: age and family

modify risk factors

  • tabacco use
  • obesity
  • inactivity
  • stress
  • dm
  • hld
  • htn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

patho of atherosclerosis

A
  • injury to artery–> inflammation–> accumulation of lipids, platelets and clotting factors
  • scar tissue replaces normal endothelial lining
  • plaque leads to narrowing (stenosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

non-modifiable risk factors of ac

A
  • age: 50+
  • gender: male
  • ethnicity: African Americans
  • genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

modifiable risk factors of ca

A 
diabetes
hypertension
smoking
obesity
sedentary lifestyle
increased serum homocysteine
increased serum iron levels
infection
depression
hyperlipidemia
excessive alcohol intake stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

hypertension

A

persistently high blood pressure

  • systolic BP > 130 mmhg
  • diastolic bp > 80 mmhg
  • average of two or more readings on different dates: two weeks apart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

etiology of hypertension

A

unkown

two types:
- primary- essential hypertension which is a chronic elevation of bp from an unknown cause

- secondary
known cause
- acute stress
- excessive alcohol intake
- sickle cell disease
- renal disorders
- endocrine disorders
- neurologic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

risk of hypertension

A

non modifiable

  • age
  • gender
  • ethnicity
  • family history

modifiable

  • alcohol
  • cigarette smoking
  • diabetes
  • obesity
  • stress
  • elevated serum lipids
  • excess dietary sodim
  • decreased kidney function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

signs/ symptoms of HTN

A

silent killer

rare:

  • headache
  • dizziness
  • blurred vision
  • angina
  • fatigue
  • dyspena
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

hypertensive urgency

A
  • sever bp elevation without target organ dysfunction progression
  • relatively asymptomatic
  • oral medication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

hypertensive emergency

A
  • sbp> 180 mm hg systolic
  • dbp > 120 mm hg systolic
  • risk for progression for target organ dysfunction
  • immediate gradual reduction of bp to protect target organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is pneumonia

A
  • an infection that inflamed the lungs and impairs gas exchange
  • air sacs fill with fluid causing cough and difficulty breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

patho of pneumonia

A

development occurs when a pathogen reaches the alveoli and host defesnes are overwhelmed by microorganisms or by the inoculum size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

pneumonia diagnosis symtoms

A
  • ineffective airway clearance
  • impaired gas exchange
  • ineffective breathing pattern
  • risk for infection
  • acute pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

pneumonia etiology

A
  1. infectious agents
    A: bacteria and viruses that are usually inhaled
    - infection gets into lungs causing inflammation
    - steptococcus pneumoniaw is responsible for most cases of pneumonia
    B: fungi
2. injurious agents
A: aspiration
- gastric contents
B: endotracheal intubation
C: smoke
- inhalation of smoke or chemicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

clinical manifestations pneumonia

A
  • hypoxemia
  • cough
  • fever
  • rapid and shallow breathing
  • loss of appetite
  • abnormal lung sounds
  • fatigue
  • chest pain
  • dehydration
  • clammy skin
  • difficult or labored breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

pt. teaching pneumonia

A
  • what exactly pneumonia is
  • different stages of pnemonia
  • when/how to take medications
  • what the medications are used for
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

pneumonia prevention

A
  • many different pneumonia vaccines
  • flu vaccines
  • quit smoking
  • wash hands often
  • maintain healthy lifestyles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

medications/treatment pneumonia

A
  • macrolide medications
  • oral antibiotics
  • antiviral medications
  • over the counter meds
  • hospitalization
  • oxygen therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

asthma clinical manifestations

A
  • Shortness of breath.
  • Chest tightness or pain.
  • Wheezing when exhaling, which is also a common sign of asthma in kids.
  • Trouble sleeping caused by shortness of breath, coughing or wheezing.
  • Coughing or wheezing attacks that are worsened by a respiratory virus, such as a cold or
    the flu.
  • being too breathless to eat, speak or sleep.
  • breathing faster.
  • a fast heartbeat.
  • drowsiness, confusion, exhaustion or dizziness.
  • blue lips or fingers.
  • fainting.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

patho of asthma

A
  • inflammed airways react to environmental triggers such as smoke, dust, pollen
  • airway epithelial cells, which are the first line of defense against inhaled pathogens are partiles, initiate airway inflammation and produce muscous
  • leads to coughing and breathign dificulties
  • airway narrows
  • result of immune response in the bronchial airways
  • in response bronchi contract into spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

genetic predisposition of asthma

A
  • more than 100 genes associated with allergic asthma
  • offspirng of asthmatic parents
  • ORMDL3 gene associated with childhood onset
  • HLA-DQ gene was related to later onset asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

treatment of asthma

A
  • symptoms controlled
  • inhaled and systemic corticosteroids: supress airway inflammation
  • bronchiodilators
  • leukitriene
  • mast cell stabilizer
  • anticholinergics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

diagnosis of asthma

A
  • lung function test

- chest or sinus x ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

pt teaching of asthma

A
  • properly teach pt. how to use inhaler
  • take asthma medication directly as your provider tells u
  • be sure to always have a quick- relief inhaler
  • watch for early changes of symptoms getting worse by using a peak flow meter
  • use dust proof covers
  • dont smoke
  • try to keep window closed during pollen seasons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

COPD risk factors

A
  • exposure to tobacco smoke
  • exposure to dust and chemicals
  • exposure to fumes from burning fuel
  • people with ashma
  • genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

COPD treatment

A
  • bronchodilators

- steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

diagonsis of COPD

A
  • pulmonary function test
  • spirometry
  • chest x-rays and ct scans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

patho of COPD

A
  • combined process of narrowing airways- limitd airflow and causes loss and destruction of aveloi, bronchioles, and surrounding capillary vessels
  • lung capacity further decreases
  • reduced airflow
  • dyspnea
  • hypercapina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

etiology of COPD

A

smoking and people exposed to fumes, like carbon monoxide or chemicals
- alpha-1 antitrypsin genetic link to copd

two causes:

  • emphysema
  • chronic bronchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

prevention of copd

A
  • no prevention
  • getting flu vac
  • quit smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

clinical manifestations of copd

A
  • shortness of breath
  • wheezing
  • chest tightness
  • lack of energy
  • weight loss
  • chronic cough
  • edema
  • anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

pleural effusion

A

accumulation of excess fluid in the plerual space or pleura (membranous linning of the lungs and chest cavity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

normal fluid in lungs

A
  • 10-20ml of fluid
  • lubricates lungs
  • decreases friction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

patho of pleural effusion

A
  • excessive fluid in small space
  • compresses lungs
  • limits expansion during inhalation
  • can affect one or both lungs
  • various types of fluid can accumulate in a variety of locations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what can accumulate in pleural effusion

A
  • exudative: protein- rich fluid
  • transudative: watery
  • hemothorax: blood
  • pneumothorax: air
  • empyema: pus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

etiology pleural effusion

A
  • heart failure
  • pulmonary embolism
  • cirrhosis
  • pneuminia
  • kidney disease
  • cancer
  • bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

diagnosis pleural effusion

A

xray
ct scan
ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

clinical mafiestations pleural effusion

A
  • dyspnea
  • pleuritic chest pain
  • tachypnea
  • tracheal deviation
  • pleural friction rub
  • tachycardia
  • dminished/absent lung sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

pleural effusion treatments

A
  • depends on s/s
  • some resolve w/o tx
  • correct underlying cause
  • remove excess fluid: thoracentesis, chest tube
  • antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

atelectasis

A

incomplete alveolar expansion or collapse of the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

normal for alveolo

A
  • alveoli expand
  • has exchange
  • o2 is brought in during inhalation
  • co2 is expelled during exhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

patho of atelectasis

A
  • walls of alveoli stick together

- prevents adequate gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

etiology atelectasis

A
  • surfactanr deficiency- prevents aveloi from sticking together
  • bronchus obstruction
  • compression of lung tissue
  • lung fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

risk factors atelectasis

A
  • surgery

- inmmobility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

clinical manifestations atelectasis

A
  • tachypnea
  • decrease breath sounds
  • dyspnea
  • anxiety
  • restlessness
  • tachycardia
  • asymmestrical chest expansion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

prevention of atelectasis

A
  • increase mobility
  • breathing exercises
  • cough and deep breaths
  • inventive spirometry
  • pain management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

treatment of atelectasis

A
  • antibiotics
  • thoracentesis
  • incentive spirometry
  • bronchodilator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

hypervolemia

A

excess fluid in the intravascular space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

water intoxication

A

excess fluid in the intracellular space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

causes for excess fluid

A

excessive sodium or water intake

  • high sodium diet
  • psychogenic polydipsia
  • hypertonic fluid administration
  • free water
  • enteral feedings

inadequate sodium or water elimination

  • system/ organ failure (renal, liver, heart)
  • endocrine disorders (hyperaldosteronism, crushing syndrome, syndrome of inappropriate antidiuretic hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

clinical manifestations for excess fluid

A
  • edema( peripheral, perorbital, cerebral)
  • dyspnea
  • bounding pulse
  • tachycardia
  • jvd
  • htn
  • polyuria
  • weight gain
  • crackles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

diagnosis for excess fluid

A
  • H&P
  • daily weights
  • I&O
  • labtest (CBC, chemistry)
  • urinary analysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

treatment for excess fluid

A
  • compression socks
  • diuretics
  • restricting NA
  • fluid restriction
  • hypertonic solutions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Fluid imbalance- deficit

A
  • dehydration
  • hypovolemia or fluid volume deficit
  • decreased fluid in the intracellular space
  • can occur independently without electrolyte defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

fluid imbalance deficit reasoning

A

inadequate fluid intake

  • poor oral intake
  • inadequate iv fluid replacement

excessive fluid or sodium losses

  • gastrointestinal losses
  • excessive diaphoresis
  • prolonged hyperventilation
  • hemorrhage
  • nephrosis
  • diabetes mellitus
  • diabetes insipidus
  • burns
  • open wounds
  • ascites
  • effusions
  • excessive use of diuretics
  • osmotic diuresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

fluid imbalance deficit clinical manifestations

A
  • thirst
  • altered LOC
  • hypotension
  • tachycardia
  • weak/thready pulse
  • dry mucous membranes
  • tenting skin turgor
  • oliguria
  • weight loss
  • sunken fontanelles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

fluid imbalance deficit diagnosis

A
  • h&p
  • daily weights
  • I&Os
  • lab test (cbc & chemistry)
  • U/A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

deficit treatment

A
  • identifying/ managing underlying cause

- replacement fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

hyponatremia

A

sodium < 135 mEq/l

- serium osmolarity decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

hyponatremia causes

A

deficient sodium

  • too much: diuretics, Gi loss (V/d), diaphoresis
  • not enough in: Na restricting

excessive water

  • too much in: hypotonic solutions, oral hydration
  • not enough out: renal failure, heart failure, SIADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

hyponatremia clinical maifestations

A
  • GI upset
  • lethargy
  • confusion
  • decrease deep tendon reflexes
  • muscle weakness
  • seizures
  • coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

hyponatremia diagnosis

A
  • serum Na level

- urinalysis

100
Q

hyponatremia treatment

A
  • fluid restriction

- increase dietary Na

101
Q

hyperkalemia

A

potassium > 5 mEq/l

102
Q

hyperkalemia causes

A
  • deficient excretion: renal/ liver failure, medications
  • excessive intake: oral K supplements, rapid IV administration
  • lot of older adults defficent
  • check inf they are on a diuretic
103
Q

hyperkalemia clinical manifestations

A
  • paraesthesia
  • muscle weakness
  • respiratory depression
  • EKG CHANGES ( dysrthmias) need to shock them
  • cardiac arrest
  • abdominal cramping
104
Q

hyperkalemia diagnosis

A
  • serum k levels

- EKG

105
Q

hyperkalemia treatment

A
  • decrease intake
  • hold supplements
  • medications: diruects, kayexalate, insulin
  • telemetry monitoring (continuous way to monitor EKG)
106
Q

Incontinence

A

loss of urinary control

- affects 25-35% of population

107
Q

types of incontinecne

A

children

  • enuresis
  • nocturnal enuresis

adults

  • stress
  • urge
  • reflex
  • overflow
  • functional
  • treatment
108
Q

incontinence children enuresis

A

involuntary urination by a child after 4-5 years of age

109
Q

incontinence children nocturnal enuresis

A
  • bed wetting

types

  • primary: child never developed normal bladder control @ night. might bc bladder too small
  • secondary: normal urinary control. physiological causes changes it

causes:

  • psychological
  • structural
  • underlying condition
110
Q

incontinence adulthood stress

A
  • combined process of weakening of bladder sphincter and intra-abdominal pressure

contributing factors:

  • pregnancy
  • child birth
  • menopause
  • prostate removal and obesity
111
Q

incontinence adulthood urge

A
  • sudden, intense urge to urinate and involuntary loss of urine
  • overacting bladder
  • few second warning

causes

  • parkinson
  • alzheimer disease
  • stroke
  • injury to nervous system
  • frequent uti
112
Q

incontinence adulthood reflex

A

trauma or damage to nervous system

  • detrusor hyperreflexiaxia
  • increased detrusor muscle contractility
  • urine is released bladder cant relax and fill
113
Q

incontinence adulthood overflow

A
  • inabilty to empty bladde ror retention
  • chronic distention
  • “nursing/teaching bladder”

causes:

  • bladder damage
  • urethral blockage
  • nerve damage
  • prostate conditons
114
Q

incontinence adulthood functional

A
  • physical or mental impairment that prevents toileting in time
115
Q

incontinence transient

A
  • resulting from underlying cause
  • temporary

causes

  • delirium
  • infection
  • use of diuretics and sedatives
  • high urine output
  • alcohol and caffeine consumption
116
Q

risk factors for incontinence

A
  • female gender- pelvic floor muscle and vaginal wall weakening
  • advancing age- both muscle weaken and urine storage
  • obesity
  • smoking
117
Q

complications innocence

A
  • impaired skin integrity
  • recurrent utis
  • impaired body image/ sexual disfunction
  • interruption of usual activities
118
Q

benign prostatic hyperplasia (BPH)

A

nonmalignant enlargement of the prostate gland

119
Q

benign prostatic hyperplasia (BPH) etiology

A
  • unknown –> decreased testosterone

- common over age 50

120
Q

benign prostatic hyperplasia (BPH) patho

A
  • abnormal proliferation –> enlargement of prostate
  • compression of urethra –> obstruction of urine flow
  • urine collects in bladder causing uti and thickening of bladder
121
Q

benign prostatic hyperplasia (BPH) risk factors

o-dice

A 
obesity
cardiovascular disease
DM2
inactivity
ED
122
Q

acute kidney injury

A

sudden loss of renal function

  • days to weeks
  • generally reversible
123
Q

acute kidney injury etiology

A

inadequate renal perfusion

  • prerenal (before kidney)- decrease bp, HF
  • intrarenal (within kidney)- inflammation of glomerulus/ compression on internal structures
  • postrenal (after kidney)- urethral/ bladder obstruction- interfere with the ability to secrete urine
124
Q

acute kidney injury patho

A
  • abrupt onset

- 4 phase process

125
Q

acute kidney injury lab values

A

creatinine increase

  • decreased urinary excretion
  • waste product produced by muscle

BUN increase
- decreased urinary excretion

126
Q

acute kidney injury phases

A
  • prodromal
  • oliguric
  • diuretic
  • recovery
127
Q

acute kidney injury phases: prodromal

A
  • damage occurs

- pt. asyomptomatic

128
Q

acute kidney injury phases: oliguric

A
  • nephrons are damaged
  • decreased glomerular filtration
  • decreased urine output
  • less than 400 ml/day
129
Q

acute kidney injury phases: diuretic

A
  • renal function begins to improve
  • tubular damage continues to impair ability to concentrate urine appropriately
  • leads to diuresis- excess urine output (depletes fluids and electrolytes)
  • up to 5l
130
Q

acute kidney injury phases: recovery

A
  • can take 3-12 months

- glomerular filtration returns to normal

131
Q

chronic kidney disease

A

gradual, irreversible loss of renal function

  • nephrons become injured
  • replacement by scar tissue
  • affects 30 million adults
132
Q

chronic kidney disease etiology

A
  • DM- diabetes #1 cause
  • HTN- affects glomelura
  • urinary obstruction- increase pressure on kidneys
  • renal artery stenosis- not good blood flow
  • nephrotoxic medications- kidney toxic (NSAIDS)
  • sickle cell disease
  • SLE- sickle cell attacks cells in nephron
  • smoking- harden Bu- small Bu in kidneys
  • aging- less effective
133
Q

chronic kidney disease patho

A

damaged nephrons –> impaired kidney function

  • decrease regulation and ability to eliminate waste products and drug exretion
  • increase bp
134
Q

chronic kidney disease stage 1

A

kidney damage present by GFR > 90

135
Q

chronic kidney disease stage 2

A

kidney damage worsens as the GFR falls (60-89)

136
Q

chronic kidney disease stage 3

A

kidney function is signficantly impaired as GFR is between 30 and 59

137
Q

chronic kidney disease stage 4

A

kidney function is barley present with GFR dropping between 15 and 29

138
Q

chronic kidney disease stage 5

A

kidney failure as the GFR drops to less than 15

139
Q

gastroesophageal reflux disease

A

chyme or bile periodically backs up from the stomach into the esophagus

140
Q

patho gastroesophageal reflux

A
  • gastic secretions reflux into esophagus
  • esophaguses damaged
  • lower esophageal spincter does not close tightly
141
Q

gastroesophageal reflux risk factors

A
  • foods (chocolate, citrus fruit, spicy or fatty foods)
  • beverages (caffeine, carbonated beverages, alcohol)
  • medical conditions (hiatal hernia, obesity, pregnancy)
142
Q

gastroesophageal reflux clinical manifestations

A
  • heartburn or epigastric pain
  • dysphagia
  • sensation of a lump in throat
143
Q

cholecystitis

A

inflammation of galbladder

144
Q

cholelithiasis

A

stones

145
Q

choledocholithiasis

A

stones in CBD- common bile duct

first two happen independtly

146
Q

gallbladder disorders risk factors

A
  • age
  • obesity
  • diet (increase fat, increase cholesterol, decrease fiber)
  • pregnancy: after delivery= change in nutritional status
  • chronic diseases (of hypatbillary system)
147
Q

gallbladder disorders clinical manifestations

A
  • biliary colic- specific pain in RUQ radiates to shoulders and back after fatty meal
  • RUQ pain
  • n/v

when stone lodged:

  • jaundice
  • chronic disease
148
Q

hepatitis

A

inflammation of liver

etiology

  • viral or bacterial infections
  • drugs
  • alcohol
  • hepatotoxic drugs
  • metabolic/ vascular disorders
149
Q

hepatitis types

A
  • HAV- most common transmitted tru frcal oral route
  • HBC- transited thru blood, sexually transmited fluids: blood, stool, urine, saliva
  • HCV- transmitted thru blood, Iv drug use (not really seen anymore) use to associated with blood tranfusions
  • HDV- extremely rare
  • HEV- extremely rare
150
Q

hepatitis prevention

A
  • hand hygiene

- vaccines: hav, hbc

151
Q

cirrhosis

A

progressive, irreversible replacement of healthy tissue with scar tissue
- 12th leading cause of death in US

152
Q

cirrhosis etiology

A
  • chronic alcohol use- most common
  • hepatotoxins drugs
  • hepatitis- left untreated
  • gallbladder obstruction- prolonged
  • heart failure
153
Q

cirrhosis patho

A
  • inflammation of liver cells
  • infiltration with fat and wbc
  • fibrotic scar tissue replacements liver tissue
  • abnormal regeneration
  • impaired liver blood flow and function
154
Q

cirrhosis complication

A
  • clotting defects
  • encephalopathy: elevation of ammonia
    portal hypertension
  • varices: enlarged vessels- risk for rapture: coughing/ vomitting can cause repture
  • ascites: fluid accumulation in addomen: fluid not being held in vascular system
155
Q

appendicitis

A

inflammation of appendix

patho

  • infection triggers localized edema
  • fluid builds inside the appendix
  • appendix fills with purulent exudate
  • pressure inside the appendix escalates causing reputure
156
Q

appendicitis’s clinical manifestations

A
  • fever
  • pain
  • n/v
  • anorexia
  • pressure make it better
  • check for rebound tenderness
157
Q

ascites

A

fluid accumulation in abdomen: fluid not being held in vascular system

158
Q

encephalopathy:

A

elevation of ammonia

159
Q

varices

A

enlarged vessels- risk for rapture: coughing/ vomitting can cause repture

160
Q

diabetes mellitus

A

glucose intolerance

  • faulty production of insulin
  • tissue insensitivey to insulin
161
Q

type 1 diabetes

A
  • IDDM, juvenile
  • 5% id diabetes cases

etiology:

  • some genetic component (10%)
  • autoimmune responses to virus

patho:

  • destruction of beta cells
  • pancreas secretes no insulin
  • more common in young, thin pt.
  • life long insulin given
162
Q

type 2 diabetes

A
  • NIDDM, adult onset
  • 95% of diabetes cases

etiology

  • large genetic component (90%)
  • obesity: have pt. loose weight and monitor diet

patho:
- decreased beta cells responsiveness to glucose

  • can be put on oral hypoglycemias
  • regulate/ keep sugars in balance
163
Q

prediabetics

A
  • glucose intolerance

- blood sugars elevated but not diabetic

164
Q

secondary diabetes

A
  • drugs
  • pancreatic trauma
  • some other chronic illness that damages beta cells
165
Q

clinical manifestations for diabestes

A

3 P’s:

  • polyuria
  • polydispia: increased thirst
  • polyphagia: increased hunger
  • fatigue
  • blurred vision
  • infection prone
  • abdominal pain
  • headache
  • ketosis/acidosis blood sugars above 100
166
Q

diagnosing diabetes

A

glucose tests

  • fasting plasma glucose > 126 mg/dl
  • casual plasma glucose > 200 mg/dl
  • glucose tolerance test > 200 mg/dl after 2 Hr

additional test:
glychomoglobin: normal 4% to 6%

167
Q

hyperthyroidism patho

A
  • increased metabolic rate
  • increased beta receptors
  • primary: too much TH
  • secondary: too much TSH
168
Q

hyperthyroidism causes

A
  • autoimmune (graves disease)
  • goiter
  • pituitary tumor (secondary)
  • thyroid CA
  • overuse of thyroid hormones
169
Q

hyperthyroidism clinical manifestations

A

Hypermetabolic state

  • heat intolerance
  • increased appetite
  • weight loss
  • frequent stools
  • nervousness
  • tachycardia, palpitations
  • tremor
  • heart failure
  • warm smooth skin
  • exophthalmos (GRAVES DISEASE)
170
Q

hypoparathyroidism patho

A
  • decrease in PTH
  • calcium stays in bones
  • hyperphosphatemia
171
Q

hypoparathyroidism causes

A
  • heredity

- accidental removal of parathyroid during thyroidectomy

172
Q

hypoparathyroidism clinical manifestations

A

tenany

  • neruomucular irritability
  • numbness and tinging of fingers and peri-oral area
  • muscle spasms
  • cardiac dysrthythmias
  • troussa sign
  • trasric sign
173
Q

SIADH patho

A
  • too much ADH
  • water retention
  • hyponatremia
  • decreased serum osmolality
174
Q

SIADH causes

A
  • tumors
  • severe stress/ trauma
  • cerebral hemorrhage
  • diabetes insidious tx complications
175
Q

SIADH signs and symptoms

A
  • weight gain without edema
  • dilution hyponatremia
  • concentrated urine
  • muscle cramps and weakness
  • brain swelling, seizures, death
176
Q

traumatic brain injuries (TBI)

A
  • usually caused by sudden and violent blow or just to the head (closed injury) or a penetrating (open injury) head wound that disrupts the normal brain function
177
Q

traumatic brain injuries (TBI) can

A

bruise the brain
damage nerve fibers
cause hemorrhaging

178
Q

traumatic brain injuries (TBI) causes

A 
falls
being struct by against an object
motor vehicle accidents
sports acitvies
intestinal self harm
179
Q

traumatic brain injuries (TBI) conditions associated with closed tbi

A

concussion: momentary interruption of brain function
- usually results from a mild blow to the head that causes sudden movement of the brain, disrupting neurologic functioning
- may or may not lead to a loss of consciousness
- amnesia, confusion, sleep disturbances, and headaches may occur for weeks or months

cerebral contusion: bruising of the brain

  • most often results from a blunt blow that causes the brain to make a sudden impact with the skull
    coup: initial area where the brain the skull
    contrecoup: opposite side of brain where it rebounds and impacts the skull
  • varies in severity depending on the extent of damage and the amount of bleeding
  • residual effects depend on severity
180
Q

transient ischemic attack

A
  • temporary episode of cerebral ischemia that results in the symptoms of neurologic deficits
  • also called ministries because these neurologic deficits mimic a cerebrovascuale accident (CVA) or stroke except that these deficits resolve within 24 hours (1-2 hours in most cases)
  • may occur singly or in a series
181
Q

transient ischemic attack warning signs

A

warning sign that a cva may be impending; however, not all cvas are preceded by tia
- 1&3 people experienceing a tia eventually have a stroke hold occur within the year

182
Q

transient ischemic attack can occur

A

because of a cerebral artery occlusion, cerebral artery narrowing, cerebral artery injury

183
Q

transient ischemic attack additional risk factors

A
  • migranes
  • smoking
  • diabestes mellitus
  • advancing age
  • inadequate nutrition, hypercholesterolemia, oral contraceptive usage, excessive alcohol combustion, illicit drug use
184
Q

transient ischemic attack complications

A

permanent brain damage
injury from falls
cva`

185
Q

cerebrovascular accident

A

stroke

  • an interruption of cerebral blood supply
  • ischemic damage is permanent
186
Q

cerebrovascular accident causes

A

total vessel occlusion

cerebral vessel rupture

187
Q

cerebrovascular accident major types

A
  • ischemic strokes are most common

- hemorrhagic stroke are most fatal

188
Q

cerebrovascular accident complications

A

neurologic deficits and death

189
Q

cerebrovascular accident most common in

A

african americans and those living in the south east region

190
Q

cerebrovascular accident additional risk factors

A 
physical inactivity
phychosocial stress
obesity
hypertension
smoking
dyslipidemia
diabetes mellitus
atherosclerosis
oral contraceptive usage
excessive alcohol combustion
illicit drug use
advancing age
191
Q

cerebrovascular accident treatment

A
  • requires prompt treatment to minimize brain damage
  • determining whether the cva ischemic or hemorrhagic on origin prior to treatment
  • treatment should be delivered within 3 hours of symptom onset
192
Q

osteoporosis

A

hip/ vertebral fractures

  • reduced quality o lie
  • increased liability
  • risk of death (during year after fracture)
193
Q

osteoporosis prevention

A
  • build bone through age 30
  • obtain adequate calcium and vitamin d
  • exercise (especially childhood)
  • avoid alcohol and smoking
  • fractures can be life treating
  • increased rate of death in first year over age 50
194
Q

osteoporosis risk factors

A
  • female gender
  • aging
  • causcasins
  • asian
  • smal boned, petite
  • postmenopausal status
  • low testosterone and estrogen in men
  • family history
  • history of fractures
  • low calcium intake
  • low vitamin d
  • excessive caffein, protein, sodium
  • sedentary lifestyle
  • excessive alcohol use
  • cigarette smoking
195
Q

fractures

A

breaks in bones

  • open- break skin
  • closed- does not break skin
  • complete: done divided into 2 or more pieces
  • incomplete: no degree of separation
196
Q

fracture cause

A

trauma

pathological

197
Q

simple fracture

A

clean break

maintain of alignment

198
Q

communuted fracture

A

multiple fractures

199
Q

spiral fracture

A

twist around bone shaft

200
Q

fracture healing process

A
  1. clot formation at fracture site
  2. fibroblast and osteoblast arrive, fibrocartilage callus forms
  3. new bone forms
  4. bone remodeling continues until bone intact, repair and healing completed

takes up to 4-6 weeks

201
Q

pressure injuries

A
  • soft tissue injuries that result of unrelieved mechanical pressure
  • results in areas of necorsis and ulceration where the tissue is compressed between bony prominences and extrernal hard surfaces
  • can develop in 1-2 hours if pressure is not relieved
  • classification using a stagng system but not all injuries follow a linear progression
202
Q

pressure injuries common sites

A 
sacrum
ischial tuberosities
trochanters
malleoli
heels
can develop anywhere
203
Q

pressure injuries risk factors

A 
advancing age
impaired circulation
tissue perfusion
immobilization
malnutriton
decreased sensation
incontinence
204
Q

stage 1

A

skin is intact, nonblanchable erthema is present

205
Q

stage 2

A

erosion or blister with or without true ulcerations, no exposed sub c tissue

206
Q

stage 3

A

full thickness skin loss with damage to sub q tissue down to the underlying fascia

207
Q

stage 4

A

full thickness skin loss with extensive destruction, tissue necrosis, and damage to exposed supporting structures

208
Q

deep tissue injury

A

skin may or may not be intact

underlying tissue is damaged

209
Q

unstageable

A

full thickness skin tissue loss in which the extent of damage cannot be determined because it is hidden by slough or eschar

210
Q

pressure injuries complications

A

challenging mitigating factors

  • ulcers can become infected with hospital acquired
  • antibitoic resistant organism
  • sinus tracts
  • osteomyelitis
  • cellutitis
  • tissue calcifcation
  • bactermia
  • meningitis
  • endocaridits
  • squamous cell carcinoma
211
Q

pressure injuries diagnosis

A

physical examination

additional test depending upon the stage

212
Q

pressure injuries treatment

A 
reduce pressure
care for wound
minimize infection
support nutritional needs
pain management
antibiotics
negative pressure therapy
topical recombinant growth factors
electrical stimulation therapy
therapeutic ultrasonography
surgical closure
skin grafts
213
Q

pressure injuries healing

A

take weeks, prevention is critical
several scales developed to assess risk:
- norton scale
- braden scale

214
Q

viral infectons: herpes zoster (shingles)

A
  • caused by the varicella-zoster virus
  • appears in adulthood years after primary infection of varicella in childhood
  • virus lies dormant on a cranial nerve or a spinal nerve dermatone untill it is activated years later
  • virus affects this nerve only, giving the condition its typical unilateral manifestations
215
Q

herpes zoster (shingles) manifestations

A
  • pain
  • paresthesia
  • red or silvery vesticaulr rash develops in a line over the area innervated by the affected nerve (may last for weeks or months)
  • extremely sensitive skin
  • pruritis
216
Q

herpes zoster (shingles) complications

A

neuralgia and blindness

217
Q

herpes zoster (shingles) treatment

A

antivirals
antidepressants
anticonvulsants
vaccines

218
Q

abnormalities of urethral meatus

A

epispadias

hypospadias

219
Q

epispadias

A

dorsal (upper) opening

220
Q

hypospadias

A

ventral (underside) opening

221
Q

cryptorchisim

A

one or both testes undescend

  • prior to birth
  • common birth defect
  • right more than left
  • 80% naturally descend
  • after 6 months see a doctor
222
Q

erectile dysfunction

A

known as impotece

etiology:

  • physchological: stress, depression, relationship issues, smoking, obesity, medications
  • neurologic- spinal cord injuries
  • vascular-cardiovascular impairment, HTN, DM, asclerosis
223
Q

priapism

A

prolonged erection > 4 hr typically painful

patho:
- blood cannot drain from penis –> ischemia–> tissue damge

etiology:

  • age: 5-10 20-50
  • blood, circulatory, nervous dysfunction
  • sickle cell, leukemia, trauma, tumors, DM, MS, stroke, medications, alcohol, drug use
224
Q

hydrocele

A
  • fluid in scrotal sac= enlargement of scrotum
  • uncomferable

etiology:

  • congenital
  • inflammation, infection, trauma
225
Q

varicocele

A
  • dilation of a scrotal vein –> painful swelling
  • most commonly affects left testicle

etology

  • congenital
  • obstruction
226
Q

testicular torsion

A

twisting of the testes and spermatic cord

227
Q

prostate cancer

A
  • most common cancer among men
  • minimal metastasis: 90% localized
  • enlargement of prostate: compression of urethra

risk factors:

  • family hx
  • sti
  • inherited genetic conditions
228
Q

testicular cancer

A
  • men 15- 34 years old
  • often asymptomatic
  • usually affects one testicle: hard painless mass, testicle enlargement, gynecomastia
229
Q

testicular cancer risk factors and prevention

A
  • family hx
  • infection
  • trauma
  • alcohol use
  • cryptochidism

prevention:
- early detection –> self testicular exam

230
Q

amenorrhea

A

absense of mestruation

primary:
- females >16 have yet to start menstruation

secondary:
- changing hormone levels: tumors, weight loss, chemo, eating disorders

231
Q

dysmenorrhea

A

painful menstruation

- affects the ability to complete daily activites

232
Q

cystocele

A

bladder sags into vaginal space

- urinary freqeuncy and or incontinence

233
Q

rectocele

A

portion of rectum sags into vaginal space

- constipation, soiling, or painful defecation

234
Q

uterine prolapse

A

uterus sags into vaginal space

- fullness within the pelvis, backaches, and stress incontinence

235
Q

patho of pelvic organ prolapse

A

heavy lifting, constipation and obesity

236
Q

endometriosis

A

functioning tissue cyclically sloughs off

patho:

  • functioning tissue thickens, slough and bleeds like normal endometrial tissue
  • blood becomes trapped –>irritation, pain, scaring, and adhesions

etiology:
- unclear

237
Q

endometriosis risk factors

A
  • early onset mestruation
  • late onset menopause
  • delayed childbearing or nulligravida
238
Q

breast cancer

A
  • cancer in glandular tissue of the breast

risk factors

  • early menses
  • nulligravida
  • last menopause
  • familt hx
  • genetic predisposition: brca gene

prevention
- monthly breast self exam

239
Q

cervical cancer

A
  • cancer of the cervix
  • 100% survial rate w/early detection

etiology: HPV
screening: pap spear
prevention: HPV vaccine

240
Q

endometrial cancer

A

cancer of endometrial tissue: uterine linning

  • 83% 5 year survial rate
  • etology unknown

risk factors:

  • excessive estrogen
  • obesity
  • inactivity
  • htn
241
Q

ovarian cancer

A

cancer of one or both ovaries
- 47% 5 year survival rate: no screening tool

risk factors:

  • genetic predisposition: BCRA
  • early menses
  • late menopause
  • excessive estrogen
  • obesity
242
Q

STI

A

transmission

  • sexual contact
  • mother to child: preg/childbirth
  • blood

incidence rate
- 20 million new STI in 2019 15-24 years

mandated reporting:

  • chlamydia
  • gonorrhea
  • syphillis
243
Q

chlamydia

A

etilogy: chlamydia trachomatis

transmission

  • sexual contact
  • mother to child during childbirth

incubation
- 1-3 weeks

treatment
- antibiotics: 7 days

244
Q

genital herpes

A

etiology:
herpes simplex virus (HSV)
1. type 1- above wait cold sores
2. type 2- below waist

transmission

  • sexual contact
  • oral- genital contact
  • mother to child (type 2 only)

incubation

  • 4 phases
  • lifelong recurrence

treatment
- antivirals

245
Q

genital warts

A

etiology

  • human papillomavirus
  • affects 79 million

transmission

  • skin to skin contact
  • mother to fetus

prevention
- hpv vaccine

patho (24 decks)

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