Education Project Review

Lauren Dinkelacker

ASTHMA

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Pathogenesis


  • Asthma is caused by bronchial hyperresponsiveness
  • Triggers: cold air, cigarette smoke, exercise, upper respiratory infection, and respiratory allergies.
  • The pathology of the airways of asthma are lung hyperinflation, smooth muscle hypertrophy, mucosal edema, epithelial cell sloughing, and mucous gland hypersecretion.
  • Asthma attacks are caused by an increase in leukocytes from the bloodstream to the airway, which then activates inflammatory response.

Risk Factors

  • Family History
  • Allergies
  • Overweight
  • Smoking
  • Secondhand smoke
  • Exposure to pollution and fumes
  • Occupational hazards

Diagnostics


  • A Physical Exam can be Performed to rule out other disorders/diseases such as COPD or respiratory infection.
  • Tests can be done for lung function.
  • Spirometry
  • Peak flow can be measured by measuring how the strength of the exhale.

Treatment

  • Short Acting Beta Agonist, these are quickly inhaled and are bronchodilators that act within minutes to ease symptoms. These are medications such as ProAir HFA and Ventolin HFA.
  • There are also Long Acting Beta Agonist these are inhaled and use to control persistent bronchospasms. These are medications such as Serevent and Foradil.
  • There are also Inhaled Corticosteroids and these are anti-inflammatory drugs used to treat persistent asthma and are medications such as Flonase and Qvar.
  • Aother treatment is theophylline which is a daily pill that is used to keep the airway open by relaxing muscles around the airway.
  • Bronchial Thermoplasty is used for severe asthma cases that does not improve with inhaled corticosteroids or long term medications. Works by heating the airway in the lungs with an electrode, which reduces smooth muscle in the airway. This limits the ability of the airway to tighten.
  • Finally omalizumab can be used and it is an allergy medication that acts by altering the immune system of a person. Medication is injected every 2 to 4 weeks and used on those with a lot of allergies.

Clinical Manifestations

  • Exercise induced asthma- cold or dry air
  • Occupational induced asthma- workplace irritants such as chemical fumes, gases or dust
  • Allergy Induced asthma- Symptoms triggered by particular allergens, such as pet dander, cockroaches or pollen
  • shortness of breath
  • chest pain
  • chest tightness
  • trouble sleeping caused by shortness of breath
  • whistling or wheezing exhale
  • coughing or wheezing attacks

SMALL CELL LUNG CARCINOMA

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Pathogenesis

  • Complex and not completely understood.
  • They most commonly arise in peribrochial locations and infiltrate into the submucosa of the bronchioles.
  • They are fast spreading and quick to metastasizs, usually to the lymph nodes, liver, bones, adrenal glands, and brain.
  • The cancer first originates as the cells and begin to rapidly reproduce, eventually affecting nearby cells, spreading the cancer and creating more systemic problems that can lead to a diagnosis.
  • Lung cancer starts in the cells lining the bronchi, bronchioles, alveoli, or other parts of the lung. Cells may start growing faster and seem abnormal. Over time, abnormal cells may acquire other gene changes and may progress to be cancerous.

Risk Factors

  • Smoking
  • Radon
  • Asbestos
  • Air pollution
  • Personal or family history

Dianostics

  • Medical History and Physical Exam
  • Imaging Tests (X-rays, magnetic fields, sound waves, or radioactive substances)
  • Chest x-ray
  • Computed Tomography (CT) Scan
  • Magnetic resonance imaging (MRI)
  • Positron emission tomography (PET) scan
  • Sputum cytology
  • Needle biopsy (Observed under microscope for presence of cancer cells)

Treatment

Different treatments and medications are available for Small Cell Carcinomas and are given depending on the stage of cancer. Surgery to remove the mast or tumor is a common treatment.

During this type of cancer, specific drugs and treatments are implemented:

  • Chemotherapy
  • Radiation Therapy
  • Etoposide- along with chemo radiation
  • Cisplatin or Carboplatin- along with Etoposide
  • Prophylactic Cranial Irradiation- To prevent metastasis to the brain

Clinical Manifestations

Symptoms for small cell lung carcinoma are presented 8-12 weeks before an individual sees his/her physician. These symptoms can be a result of tumors that have metastasized.

Localized tumor growth symptoms:

  • Cough
  • Hemoptysis
  • Shortness of breath
  • Chest pain

Spread of cancer to nearby areas symptoms:

  • Hoarse voice due to compression of the nerve that supplies the vocal cords
  • Shortness of breath due to compression of nerve that supplies muscles of the diaphragm or fluid-filled lungs
  • Stridor due to compression of the trachea or larger bronchi
  • Dysphagia due to compression of esophagus
  • Swelling of face and hands due to compression of superior vena cava

Distant spread of cancer symptoms:

  • Spreading to the brain: headache, vision loss, nausea, vomitting, weakness, seizures
  • Spreading to the vertebral column: back pain
  • Spreading to spinal cord: paralysis, loss of bowel or bladder function
  • Spreading to bones: bone pain
  • Spreading to liver: pain in right upper abdomen

Alzheimer's

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Pathogenesis


  • The pathogenesis of Alzheimer’s Disease is typically driven by 2 processes: extracellular deposition of beta amyloid- α-βand intracellular accumulation of tau protein.
  • Beta amyloid is the main component of senile plaques which are more commonly known as Alzheimer’s plaques. It is made by an amino acid protein which is part of a larger protein called the Amyloid Precursor Protein, made by neurons and other brain cells. Defective clearance of this results in accumulation in the brain, resulting in α-β plaques. Buildup of these Amino acid plaques is toxic to neurons and can cause long term potency, damage to synapses and eventual death of neurons.
  • Tau protein is the main component of neurofibrillary tangles. Is it also known as over-phosphorylated microtubule associated protein tau.
  • Neurofibrillary tangles occur when pairs of tau protein filaments twist around one another which ultimately interferes with cellular functions by displacing organelles and distorting placement of microtubules The end result is impaired axon transport which further disrupts nutrition of axons and dendrites.Most cases of Alzheimer’s show a combination of the 2 but there are variations where one is seen more than the other.

Risk Factors

Age

  • Risk increases greatly after age 65 and even more after age 85
  • Family history and genetics
  • If a first degree relative (parent or sibling) have AD your risk of developing it increases
  • If there is a mutation in one of the three genes associated with AD that person is basically guaranteed to inherit AD

· Sex

  • Women live longer so seem to be more likely to develop AD

· Mild cognitive impairment

· Past head trauma

  • Severe or repeated head trauma

· Lifestyle and heart health

  • Evidence suggests that the same factors that put you at risk for heart disease increase your risk for AD
  • Lack of exercise, smoking, high blood pressure, high blood cholesterol, elevated homocysteine levels, poorly controlled diabetes, diet lacking in fruits and vegetables

· Reduce risks

  • Lifelong learning and social engagement
  • Higher levels of formal education, stimulating job, mentally challenging leisure activities such as reading/playing games/playing a musical instrument, frequent social interactions

Diagnostics


  • MRI
  • CT scans
  • PET scans
  • Doctors also try to detect the function of the blood-brain barrier

Treatment

Currently scientists have no found a cure for Alzheimer’s disease. Most patients are prescribed a drug to help maintain a clear cognitive mindset and memory and help with symptoms. Two popular medications used for memory loss are cholinesterase inhibitors and memantine.

Clinical Manifestations

Mild Alzheimer disease

· Memory loss

· Confusion about the location of familiar places

· Taking longer to accomplish normal activities of daily living

· Trouble managing handling money and paying bills

· Weakened judgment, often resulting in poor decision making

· Loss of impulsiveness and sense of drive

· Mood and personality changes

· Increased anxiety


Moderate Alzheimer disease

· Increasing memory loss and confusion

· Shortened attention span

· Problems recognizing friends and family members

· Difficulty with language

· Problems with reading, writing, working with numbers

· Difficulty organizing thoughts and thinking logically

· Inability to learn new things or to handle new or unexpected situations

· Restlessness, agitation, irritability, anxiety, tearfulness

· Wandering, especially in the late afternoon or at night

· Repetitive statements or movement; occasional muscle twitches

· Hallucinations, delusions, suspiciousness or paranoia

· Loss of impulse control: Shown through behavior such as undressing at inappropriate times or places or vulgar language

· Perceptual-motor problems: Such as trouble getting out of a chair or setting the table


Severe Alzheimer disease

· Weight loss

· Seizures, skin infections, difficulty swallowing

· Groaning, moaning, or grunting

· Increased sleeping

· In bed all or almost all the time

· Lack of bladder and bowel control

· Unable to recognize loved ones

· Unable to communicate

· Dependent on others to do all care for them


· Identity disappears

Rheumatoid Arthritis

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Pathogenesis

It is not known what the exact cause of Rheumatoid Arthritis is.It is an Immune mediated inflammatory disease, which means the body’s immune system mistakenly attacks the joints.Inflammation, swelling due to leukocytes traveling to the damaged area, and thickening of the synovial membranes cause incurable/irreversible damage to the joint capsule and the joint cartilage.The inflammation causes extra secretion of the synovial fluid, causing joint swelling.This swelling is called joint effusion, which is swelling by excessive fluid and causes deformities.The first tissue to be affected is the synovial membrane, and then travels to the articular cartilage and the fibrous joint capsule.

• Cartilage damage occurs by 3 processes

1. Neutrophils and cells in the synovial fluid become activated, breaking down the top layer of articular cartilage

2. Inflammatory cytokines start enzyme breakdown of cartilage and bone

3. T cells and synovial fibroblasts change synovium into thick layer of tissue called pannus.

*This formation causes immobilization of the joint*

Risk Factors

  • Obesity
  • Smoking
  • Blood Transfusion
  • Oral contraceptives. Early studies showed a decrease risk for RA, new studies have not shown a decrease in these women.
  • Live Birth History
  • Breastfeeding

Diagnostics

  • Feel the joints for warmth, swelling, or redness. Range of motion is also assessed.
  • RA is seen symmetrically and can also reveal rheumatoid nodules or even a low-grade fever.
  • Blood tests to indicate presence of the inflammatory response in the body and presence or rheumatoid factor
  • X-rays can be done to monitor the RA progression in your joints

Treatment

  • Anti-Inflammatory
  • Steroids
  • Biological agents
  • DMARDS
  • NSAIDs
  • Physical Therapy
  • Stretching
  • Heating pads
  • Joint replacement
  • Arthroplasty
  • Arthrocentesis

Clinical Manifestations

  • Tender, swollen joints most commonly seen in the fingers
  • Stiffness in the morning that can last for hours
  • Redness and warmth in joints
  • Rheumatoid nodules, firm bumps, under the skin of the arms
  • Fatigue
  • Fever
  • Weight loss
  • Eventual loss of function of the affected joint

GUILLAIN-BARRE SYNDROME

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Pathogenesis

  • No known reasoning behind Guillain-Barré syndrome
  • What scientists do know is when an infection or virus enters the body in an individual with Guillain-Barré syndrome, the body’s immune system is tricked into thinking that its own nerve cells are foreign cells.
  • This autoimmune disease occurs when the body’s immune system begins to destroy the myelin sheath of axons of peripheral nerves.
  • When these myelin sheaths are destroyed, the speed of conduction along the nerves is disrupted. When these nerves can’t fire correctly, the muscles lose their ability to function properly.
  • The conduction between the brain and muscles is usually disrupted and can cause inappropriate senses for that individual because there is not proper translation through the nerve network.
  • This is why individuals with Guillain-Barré syndrome experience weakness and a tingling sensation in their lower extremities moving to the upper body.

Risk Factors

  • Usually triggered by a benign gastrointestinal or respiratory infection; may be triggered by improper immune response to illness
    INFECTIONS ASSOCIATED WITH GUILLAIN-BARRE
  • Campylobacter jejuni- most common cause of diarrhea in the United States, often found in undercooked foods (especially poultry); axons are attacked by antibodies against Campylobacter, reacting with proteins of the peripheral nerves and causing damages
  • Influenza
  • Cytomegalovirus- strain of the Herpes virus
  • Epstein-Barr virus infection (mononucleosis)
  • Mycoplasma pneumonia- caused by bacteria-like organisms
  • HIV/AIDS
  • Hodgkin disease
  • Systemic lupus erythomatosus
    OTHER FACTORS
  • Recent surgery (due to weakened immune system)
  • Slightly increased risk for men and older adults
  • Associated with influenza vaccinations and childhood vaccinations, but this is rare

Diagnostics

  • Can be difficult to diagnose in early stages and can be different for each person
  • Medical history and physical exam
  • Spinal tap/ lumbar puncture: small amount of fluid is withdrawn from the spinal canal in the lower back. It is then tested for a type of change that occurs in people who have the disease
  • Electromyography
  • Nerve conduction studies
  • Doctor will assess if symptoms appear on both sides of body which is common in disease, reflexes in knees are often lost, symptoms appear slower and over time

Treatment

  • No cure, but treatments can help with recovery and reducing severity
  • Plasma exchange
  • Immunoglobin therapy
  • Use of steroid hormones
  • Most critical treatment is placing patient on ventilator and heart monitor to assist body functions since their nervous system is recovering.

Clinical Manifestations

  • Presents 2-4 weeks after a benign respiratory or gastrointestinal illness
  • Finger dysesthesias (abnormal sensation, burning/painful sensation under skin with extreme sensitivity to touch)
  • Proximal muscle weakness of the lower extremities, may involve arms, truncal muscles, cranial nerves, muscles of respiration
  • May present as pure motor dysfunction or acute dysautonomia
  • Loss of tendon reflexes in upper and lower extremities
  • Uncoordinated movement
  • Hypotension
  • Abnormal heart rate
  • Blurred/double vision
  • Symptoms can increase in intensity until certain muscles cannot be used at all, in severe cases leads to paralysis