Smc Pa Medicine Exam 1 B

Front 1

What is cancer?

Back 1

Malignant neoplasia marked by uncontrolled cell growth and the tendency to invade healthy tissues locally or throughout the body

Front 2

malignant

Back 2

Growing worse, resistant to treatment, harmful, tending to or threatening to produce death

Front 3

neoplasia

Back 3

The development of new tissue which serves no useful function and grows at the expense of the healthy organism

Front 4

solid tumors

Back 4

Carcinoma
Sarcoma

Front 5

carcinoma

Back 5

A cancer that arises from epithelial cells: skin, glandular cells, mucosa

Front 6

Squamous cell carcinoma

Back 6

Most common kind of cancer.

Lung, pharynx and larynx, anorectal, skin;

HARD TO TREAT – NEED SURGERY

Front 7

adenocarcinoma

Back 7

Cancer of glandular cells: breast, thyroid, ovary, mucus glands, pancreas, testis. Usually within the duct; responds well to chemo

Front 8

sarcoma

Back 8

A cancer arising from mesenchymal tissue: muscle, bone, connective tissue

Front 9

rhabdomyosarcoma

Back 9

A cancer made from skeletal muscle cells (red muscle cells)

Front 10

Non-solid (hematogenous) malignancies

Back 10

Leukemia: cancer of blood-forming cells;

Lymphoma: cancer of lymphocytes

Front 11

How does cancer kill?

Back 11

KILL PC HOMeS:
Pulmonary embolism;
Complications of treatment.

Hemorrhage;
Organ failure due to tumor invasion; Metabolic overwhelm/ starvation; Sepsis

Front 12

How does cancer cause symptoms?

Back 12

Pain;
Weight loss;
Hemorrhage;
Compression of normal organs by tumor;
Release of abnormal hormones;
Seizures;
Pathological fractures;
Hypercoagulability;

Front 13

Worrisome features in skin lesions

Back 13

Firm or hard to the touch;
Nontender;
Irregular borders;
Irregular elevation;
Irregular pigmentation;
Growing or changing shape;

Front 14

Biopsy

Back 14

To obtain tissue for microscopic analysis.

All methods of biopsy look for the same things:

Excessive cell multiplication;
Chaotic tissue structure;
Poor cell differentiation;

Front 15

Histologic Grading

Back 15

Cancer cells are described as being “low grade” or “high grade” microscopically (preferred current terminology).
Older literature describes grades 1-4
(1 = lowest grade)
Both systems rank a higher grade when the cells are MORE ABNORMAL in appearance, or differentiation, so high grade is WORSE.
** The higher the grade, the worse, the less differentiated it is

Front 16

mammography

Back 16

Detailed xray with breast tissue compressed between plates of machine.
Irregular lesions, calcium deposits suggestive of malignancy.
May miss small tumors, non-calcified tumors.
Risks of radiation: secondary cancers?

Front 17

Diagnosis of cancer - labs

Back 17

Biopsy.
Tumor marker analysis.
Staging workup.

Front 18

FNA

Back 18

Fine need aspiraton, variation of needle biopsy. Tries to suck out any tissue they can get in the area of the tumor

Front 19

Staging cancer

Back 19

Different cancers are staged differently into stages I-IV depending on severity.

Stages I-IV correlate almost linearly with mortality rate

Front 20

Cancer
Stages I-IV

Back 20

based on TNM score:

TNM classification: Tumor size, Nodes positive, Metastases

Front 21

How does cancer spread?

Back 21

Direct extension/invasion.
Hematogenous metastasis.
Lymphatic metastasis.

Front 22

Staging workup of cancer

Back 22

Identify cell type and histologic grade of tumor.
Measure baseline tumor markers.
Determine local invasion.
Image brain, lungs, liver with CT/MRI.
Bone scan.
Bone marrow biopsy.

Front 23

Surgical Treatment of Cancer

Back 23

Curative surgery = large operations.

Palliative surgery = stent placements, curettage to stop bleeding, diverting ostomies

Front 24

chemotherapy

Back 24

50% of cancers can be cured with chemotherapy.

Particularly chemo-sensitive:
lymphomas, acute leukemias, choriocarcinoma, testicular carcinoma, small cell (oat cell) lung cancer.

Adjuvant chemotherapy useful for other cancers.

Drugs designed to interfere with chromosomal replication and cell division.

Nonspecifically kills all actively multiplying cells

Front 25

What cells divide rapidly?

Back 25

ROB's SHIVering:
rectal mucosa, Oral, Blood cells.
skin cells, hair, intestinal, vaginal.

*Complications of chemo is that it kills these cells

Front 26

Complications of chemotherapy

Back 26

Mucosal ulcerations.
Bone marrow suppression:
Anemia,
Thrombocytopenia,
Leukopenia.
Alopecia.
Anorexia and weight loss.
Menopause.
Sterility.

Hypercalcemia.
Abnormal hormone production (PTH, ADH, estrogen, etc).
Hypercoagulability.
Immunocompromise.
Coagulopathy.
Hemorrhage.

Front 27

When should you think of cancer?

Back 27

CAUTION!

C hange in bowel/bladder habits.
A sore that doesn’t heal.
U nusual discharge or bleeding.
T hickening or lump in breast.
I ndigestion or difficulty. swallowing
O bvious change in a wart or mole.
N agging cough or hoarseness.

Front 28

Differential diagnosis of cancer

Back 28

Benign growth.
Inflammation.
Chronic (fungal, TB) infection.
Sarcoidosis.

Front 29

Serum cancer markers

Back 29

PSA – used for routine screening;
CEA – cancer of the colon;
Alpha – fetoprotein – primary liver cancer;
CA-125 – ovarian cancer (not a good screening test);
HCG – human corionogonadotropin – tells maternal immune system she’s pregnant. Tumors also producde HCG (one of the ways they get the immune system to not kill them)

Front 30

Cancer Emergencies

Back 30

1. Superior vena cava syndrome. 2.
Spinal cord compression.
3. Massive hemorrhage

Front 31

Treatment of cancer emergencies

Back 31

SVC syndrome, spinal cord compression: emergency radiation therapy.

Massive hemorrhage: surgery, angiographic embolization

Front 32

CAM in cancer

Back 32

88% of cancer patients admit to using some form of CAM.

Most do not discuss this with their clinicians.

Many herbal treatments and supplements can interfere with Western treatment

Front 33

CAM: pharmacological treatments

Back 33

Herbs;
Chelation therapy;
Pyrogenic therapy;
Laetrile;
Non-Western experimental drugs;
Clinical trials

*these things are not well controlled

Front 34

Asthma

Back 34

Disease characterized by paroxysmal narrowing of the bronchial airways due to inflammation of the bronchi and contraction of the bronchial smooth muscle.
Bronchoconstriction and airway hyper-responsiveness lead to dyspnea and wheezing.
Reversible phenomenon; no destruction of lung parenchyma.
No associated structural change.

Front 35

Prevalence of asthma

Back 35

8-11% of the population – about 30 million Americans:
Half of these are children; higher in African Americans;
<10 yrs of age, male to female ratio is 2:1;
18-54 yrs of age, female to male ratio is 2:1.
Childhood asthma persists into adulthood in 30%.
Those with sx into second decade usually have asthma throughout adulthood.
Severity varies widely among patients.

Front 36

Extrinsic Asthma

Back 36

Pts who are predisposed to respond to certain allergens by producing IgE antibody.
Termed atopy: may manifest as allergic rhinitis or eczema in childhood.
Characterized by family hx, onset age < 30 yrs, elevated serum IgE, seasonal symptoms, frequent remission later in life.
More common in males.

Front 37

Intrinsic Asthma

Back 37

Absence of atopy or specific external triggers.
Exacerbations frequently accompany URIs.
Older onset, no family hx, normal serum IgE, no bronchial responsiveness to allergen challenges.
Less responsive to therapy; persistent and progressive disease.

Front 38

Pathophysiology of asthma

Back 38

Basic functional abnormality is narrowing of the airway.
Pathophysiologic process is inflammatory.
Numerous inflammatory mediators involved: mast cells, basophils, eosinophils, alveolar macrophages.
Inflammatory mediators cause bronchial smooth muscle contraction resulting in airway edema, inflammation and narrowing.
Mediators also increase mucus production; mucosal edema and mucus plugging leads to narrowing of peripheral airways causing increased resistance to inspiratory and expiratory air flow and trapping of air.
The patient must breathe at high volumes to keep the airway open causing hyperinflation.

Front 39

Factors causing Bronchoconstriction

Back 39

Allergens (extrinsic),
Upper respiratory infections,
Atmospheric pollutants (extrinsic), Hypertonic aerosols,
Gastroesophageal reflux,
Food preservatives,
Aspirin, NSAIDs,
Dry or cold air

Vigorous exercise

Front 40

Clinical Characteristics of asthma

Back 40

Intermittent paroxysms of cough, wheezing, and dyspnea.
May or may not have associated provoking factors.
Onset of symptoms slowly progressive over a period of hours or days.

Front 41

PE of asthma

Back 41

Tachypnea, SOB, diffuse inspiratory and/or expiratory wheezes.
Use of accessory muscles for respiration.
Hyperinflation.
Hyper-resonance.
Tachycardia.
Positions: mild - supine; moderate - sitting; severe – tripod.

Front 42

Arterial blood gas

Back 42

Required in any pt where pulse oximetry not restored to ≥ 90% after tx.
Most patients with acute asthma will have hypoxemia; arterial pO2 < 80.
Most are hypocapneic as a result of reflex hyperventilation.
Typical ABG in moderately ill pt:
pO2=67, pCO2=32, pH =7.47.
Severe asthma: hypoxemia worsens and pCO2 increases.

Front 43

Diagnostics of asthma

Back 43

WBCs may be elevated if pt taking prednisone, infection, received epinephrine, or under stress.
Eosinophilia: useful in diagnosing asthma in a new onset wheezing reversible by β-2 agonists.
Serum theophylline: monitor compliance/toxicity.
Pulse oximetry: measure desaturation with exertion.
Peak Expiratory Flow Rate (PEFR) -
serial measurements document response to tx.

Front 44

Pulmonary Function Tests

Back 44

Spirometry,
Measurement of lung volumes,
Quantitation of diffusing, capacity of CO,
Pulse oximetry

Front 45

Spirometry

Back 45

Closed box, hooked up to machine, plug pt’s nose; pt takes a deep breath and then blows out air as fast as they can, as quickly as they can

Front 46

Forced Vital Capacity: FVC

Back 46

Volume of gas that can be forcefully expelled from the lungs after maximal inspiration

Front 47

Forced Expiratory Volume: FEV1

Back 47

Volume expelled in the first second of the FVC

Front 48

PEFR (peak flow)

Back 48

Maximal flow rate achieved in the FVC

Front 49

Total Lung Capacity: TLC

Back 49

Volume of gas in lungs after a maximal inspiration

Front 50

Residual Volume: RV

Back 50

Volume remaining after maximal expiration

Front 51

restrictive lung dz

Back 51

decreased lung volume

Front 52

obstructive lung dx

Back 52

decreased flow rate

Front 53

Bronchoprovocation Test

Back 53

Performed in PFT laboratory.
Inhaled methacholine is the most common stimulus used.
Indicated in patients with unusual presentation of asthma or unclear diagnosis.
Baseline spirometry; repeat after inhaled saline; repeat after inhalation of methacholine.

Front 54

CXR of asthma

Back 54

Normal or hyperinflation.
R/O pneumonia in pts with fever.
If pleuritic chest pain or subcutaneous emphysema, r/o pneumothorax or pneumomediastinum.
Sinus films may be useful to r/o sinusitis.

Front 55

Classification of Asthma Severity

Back 55

Step 1: Mild Intermittent.
Step 2: Mild Persistent.
Step 3: Moderate Persistent.
Step 4: Severe Persistent.

Front 56

asthma Rule of 2s

Back 56

Rule of 2s – more than 2 days a week, 2x waking up/week, exacerbations >2x mo, or 2 albuterol inhalers/yr, etc – not well controlled. If pt exceeds rule of 2s – change control mechanisms - give them multiple rescue inhalers

Front 57

Management of asthma

Back 57

Stepwise approach: Short term vs long term management;
Rescue vs controller medications.

Supplemental O2 if pulse oximetry < 93%.
Cardiac monitoring in acutely ill patients

Front 58

β-adrenergic (β2) Agonists

Back 58

Smooth muscle relaxant.
Bronchodilation for short term treatment:
Blocks muscular contraction,
Increases ciliary motion,
Decreases mediator release from basophils and mast cells.
Side effects include tremor, tachycardia, headache.
Short acting and long acting β-agonists -
Rescue medication vs controller medication.
Albuterol, levalbuterol are examples of short acting drugs; treatment of choice for exacerbations of asthma.
Salmeterol, formoterol are examples of long acting drugs; recommended only as add-on therapy to inhaled corticosteroids as controller medications

Front 59

Anti-Cholinergic Agents

Back 59

Cholinergic receptor blockade promotes bronchodilation by removing tonic vagal input to the smooth muscle of the airway:
Atropine: effective anticholinergic but numerous side effects (HA, flushing, palpitations, delerium).
Ipratropium bromide (Atrovent): same anticholinergic activity with less side effects; added therapeutic effect when combined with β2 agonists.

Front 60

Corticosteroids

Back 60

Anti-inflammatory therapy with inhaled corticosteroids.
Topical use of inhaled corticosteroids exhibit local while minimizing systemic effects.
Systemic steroids:
Frequent ER visits,
Hx of admissions for recurrent asthma exacerbations,
Hx of intubation for acute asthma,
Currently on inhaled steroids,
Experiencing symptoms > 3 days per week

Front 61

Leukotriene Receptor Antagonists

Back 61

Long term controller medication; oral.
Anti-inflammatory and bronchodilatory effects by blocking leukotrienes in bronchial smooth muscle cells, macrophages, and eosinophils.
Also useful in some patients with allergic disease.
Montelukast and Zafirlukast are examples

Front 62

Methylzanthines (Theophylline)

Back 62

Widely decreased use due to side effects and potential toxicity; best used only by specialists; oral medication.
Alternative to inhaled corticosteroids.
Bronchodilator effect.
Decrease respiratory muscle fatigue.
Increased ventilatory response to hypoxia.
Toxicity: GI upset, seizures, dysrhythmias.

Front 63

Cromolyn Sodium

Back 63

Inhaled anti-inflammatory mast cell stabilizers.
No bronchodilator effect.
Prevents mast cell degranulation by interfering with intracellular calcium influx.
May be an effective prophylactic med for some pts, not for use in young children.

Front 64

MDI Technique

Back 64

Shake vigorously,
Keep tongue from obstructing mouthpiece,
Place canister between lips,
Breathe out normally,
Breathe in slowly; actuate MDI at beginning of inspiration.
Inhale to full lung capacity,
Hold breath for 4-10 seconds and slowly exhale

Front 65

Emergency Management of asthma

Back 65

Pt appears frightened and fatigued.
Respiratory pattern deep and slow with progression to rapid shallow breathing; expiratory grunting heralds the onset of respiratory failure.
Coughing is ineffective.
Absent breath sounds in one hemithorax with wheezing in another suggests possible pneumothorax.

Front 66

Allergen Avoidance

Back 66

Pollens: keep windows and doors closed, use AC, stay indoors during high pollen count days.
Cockroaches: keep food and trash in closed containers, don’t keep paper products or boxes, use boric acid traps.
Cats: avoid cats in the home, especially on bedding and clothing.

Front 67

CODP

Back 67

Chronic obstructive pulmonary disease (COPD) is an umbrella term used to describe airflow obstruction that is associated mainly with emphysema and chronic bronchitis; CD8. 4th leading cause of death in the US.
Kills more than 100,000 people per year.
Appropriate diagnosis and management can prevent most of the complications and significantly improve quality of life of patients.

Front 68

Etiology - CODP

Back 68

Long-term smoking is the most frequent cause of COPD.
80-90% of all cases due to smoking.
Smoker is 10 times more likely than a non-smoker to die of COPD.
Other risk factors include:
Heredity,
Second-hand smoke ,
Exposure to air pollution at work and in the environment ,
A history of childhood respiratory infections

Front 69

Clinical Characteristics - CODP

Back 69

Chronic cough, chronic sputum production, dyspnea at rest or on exertion, and/or history of inhalational exposure.
Persistent, progressive and exacerbated by respiratory infection.
Irreversible inflammatory damage to airways and destruction of alveoli. Breath sounds diminished in COPD due to hyperinflation.
Increased anteroposterior thoracic diameter and low diaphragms.
Impairment of expiratory airflow – “air trapping”
Destruction of lung parenchyma.
Advanced: accessory muscles, cor pulmonale (JVD, hepatomegaly, peripheral edema).

Front 70

Pulmonary Function Tests - COPD

Back 70

Reduced FEV1.
Decreased FEV1/FVC ratio.
FVC may be normal with mild obstruction but becomes reduced with progressive disease secondary to air trapping.
Increased residual lung volume to total lung capacity; hyperinflation.

Front 71

Differential Diagnosis of COPD

Back 71

Asthma,
Heart failure,
Bronchiectasis,
Tuberculosis,
Obliterative bronchiolitis,
Diffuse panbronchiolitis.

Front 72

Diagnostics of COPD

Back 72

CXR: lung volumes normal but often with hyperinflation and air trapping.
Decreased FEV1.
Decreased peak flow rate.
Pulsus paradoxus:
inspiratory fall in systolic blood pressure,
present in severe attacks

Front 73

Emphysema

Back 73

Characterized by destruction of alveolar septa with enlargement of the distal air spaces.
Loss of alveolar capillary surface area reflected in elevated CO2.
Increased lung compliance due to loss of elastic fibers within alveolar walls causing air trapping.
Varying degrees of dyspnea, hyperinflation, and irreversible airflow abnormalities.

Front 74

Chronic Bronchitis

Back 74

Chronic, productive cough for three months over two consecutive years.
Smooth muscle hypertrophy, inflammation, and plugging of small airways with mucus.
Obstruction somewhat but not completely reversible with β-agonists.
May be accompanied by significant hemoptysis.
Must r/o neoplasm.

Front 75

COPD - diffusion

Back 75

Reduced diffusion capacity for carbon monoxide due to loss of pulmonary vasculature and disruption of the alveolar-capillary interface

Front 76

Diagnosing COPD

Back 76

Chronic cough -
Present intermittently or every day;
Often present throughout the day;
Seldom only nocturnal.
Chronic Sputum Production -
Any pattern of chronic sputum production may indicate COPD.
Dyspnea -
Progressively worsening over time.
Persistent (present every day).
Described as “increased effort to breath,” “heaviness,” “air hunger,” or “gasping”.
Worsens with exercise or exertion.
Worsens during respiratory infections.
History of exposure to:
Tobacco smoke,
Occupational dusts/chemicals,
Smoke from home heating or cooking fuels.

Front 77

Diagnosing COPD - Labs

Back 77

Labs -
Polycythemia in pts with chronic hypoxia,
ABG: respiratory acidosis with hypoxemia.
Determination of FEV1 and FVC to detect degree of airflow obstruction.
Use of staging system for classification of severity of airflow limitation -
May be used as a guide to management and for assessing the presence of significant hypoxia.

Front 78

COPD Stage 0

Back 78

At risk,
Normal spirometry,
Chronic symptoms,
Cough,
Sputum production

Front 79

COPD Stage 1

Back 79

Mild COPD,
FEV1/FVC < 70% of predicted,
FEV1 ≥ 80% of predicted,
Mild airflow limitation,
Minimal symptoms,
Not at increased risk for mortality,

Front 80

COPD Stage 2

Back 80

Moderate COPD,
FEV1/FVC < 70% of predicted,
FEV1 < 50% of predicted,
Moderate symptoms of chronic cough, sputum production,
Mild hypoxia.
Obtain pulmonary consultation

Front 81

COPD Stage 3

Back 81

Severe COPD,
FEV1/FVC < 70% of predicted,
FEV1 < 30% of predicted,
Symptoms of right heart failure,
More likely to have severe hypoxemia,
Increased mortality,
Obtain pulmonary consultation

Front 82

COPD Stage 4

Back 82

Very severe COPD,
FEV1/FVC < 70% of predicted,
FEV1 < 30% of predicted or FEV1 < 50% of predicted and symptoms of chronic respiratory failure -
PaO2 < 60mmHg +/- PaCO2 > 50mmHg.
* these pts show R heart failure

Front 83

BODE Index for COPD

Back 83

provides better prognostic information than the FEV1 alone and can be used to assess therapeutic response.

Includes BMI

Front 84

CXR of COPD

Back 84

Hyperinflation,
Flattened diaphragms,
Reduction in vascular markings,
Bullae.

Front 85

Management of COPD

Back 85

BASS:
Bronchodilators for reversible airflow obstruction,
Antibiotic tx for exacerbations of purulent chronic bronchitis; superinfection is common with H. influenza, S. pneumoniae, M. catarrhalis, Mycoplasma,
Supplemental oxygen: more benefit from continuous rather than intermittent use.
Smoking cessation,

Front 86

Bronchodilators - COPD

Back 86

Mainstay of treatment for stable COPD,
Inhaled β-adrenergic agonists, short and long term, primary medications used,
Anticholinergic bronchodilators may be used in combo to provide synergistic effect,
Theophylline – oral bronchodilator:
Many adverse effects, interactions,
Used primarily by Pulmonologists.

Front 87

Corticosteroids - COPD

Back 87

Chronic steroid administration may have adverse side effects and have not been shown to benefit most COPD patients.
Studies on the regular use of inhaled steroids have not shown any significant long term improvement in lung function.
Proven beneficial if given for up to 2 weeks in acute exacerbations of chronic bronchitis.

Front 88

Antibiotics - COPD

Back 88

Recommended in cases of acute exacerbation characterized by increased volume and purulence of sputum production.
Antibiotics accelerate improvement in peak expiratory flow rates and lessen the rate of relapse.

Front 89

Oxygen therapy - COPD

Back 89

Acute hypoxemia is one of the defining features in acute exacerbations of COPD.
Supplemental O2 is a critical component of acute therapy.
Target PAO2 of 60-65.
Target O2 saturation > 90%.

Front 90

Supplemental Therapy - COPD

Back 90

Pulmonary Rehabilitation -
Increase exercise capacity, improve QOL.
Nutrition -
Correct calorie-protein deficiencies.
Surgery -
LVRS or lung transplant.
Prevention -
Pneumovax (q 5 yrs), Influenza vaccine (annually).
Patient education.