Pulm EXAM 1

State the four functions of the lungs

1. Exchange gases (“arteriolize” pulmonary venous blood)

2. Metabolize select compounds 

   a. Peptides (angiotensin I, bradykinin)

   b. Amines (serotonin, norepinephrine)

   c. Arachidonic acids (prostaglandins, leukotrienes) 

3. Filter the circulation

4. Serve as a blood reservoir for left ventricle

   1. ~70-100 ml in pulmonary capillaries

   2. ~500 ml in bronchial circulation

2.  Given a diagram of the human body, identify each of the following:

The five airway wall layers and their function

1. Epithelial - Pseudostratified ciliated epithelial cells 

2. Basement membrane - Structural (support) function

3. Submucosal- contains submucosal glands that produce mucus and blood vessels 

4. Smooth muscle

5. Cartilage - larger airways only; provides airway support with flexibility

Conducting Zone

 The pathway for airflow, but not gas exchange

Respiratory Zone

 Where the magic happens, gas exchange begins and occurs

principal muscles of inspiration

1. Accessory

   1. Sternocleidomastoid

   2. Scalene Groups

   3. Pectoralis minor

2. Principal

   1. External intercostals

   2. Diaphragm

principal muscles of expiration

1. Quiet breathing 

   1. expiration results from passive, elastic recoil of the lungs, dip cage and diaphragm 

2. Active breathing

   1. Internal intercostals

   2. Abdominals

   3. Quadratus Lumborum

Epithelium type I pneumocytes function

Support

Epithelium type II pneumocytes function

metabolically active; secrete surfactant

Alveolar macrophage function

• Clear the alveolar space of mucus and debris

• Alert immune system

Lymphatics

• Helps clear fluid, protects lungs from issues (particles)

• Fluid balance

Phrenic Nerves

Motor innervation to the diagram, our principal muscle of respiration

6.  State why ventilation and perfusion are greatest at the base of the lung.  

gravity (closer to the earth)

7.  State the role of the medullary respiratory control center, cortex and pons in the control of ventilation.

• Medullary respiratory control center - “on/off” system 

• Cortex (voluntary)

• Pons (controls the rate of involuntary respiration)

• There are many sensors in this system to tell the control center how to regulate respiration

Describe the effect of changing area, thickness and diffusion capacity on the diffusion of oxygen and  carbon dioxide.

• Increase in area = Lower Vgas, Decrease in area = Higher Vgas

• Increase in thickness = Lower Vgas, Decrease in thickness = Higher Vgas

• Increase in diffusion capacity = Higher Vgas, Decrease in diffusion capacity = Lower Vgas

Cardiopulmonary circulation

1. Deoxygenated blood enters the right atrium from:

   1. Superior vena cava (from upper body)

   2. Inferior vena cava (from lower body)

2. Flows into the right ventricle

   1. Pumped through the pulmonary artery → lungs

3. In the lungs:

   1. CO₂ is exhaled

   2. O₂ is absorbed into blood

   3. Oxygenated blood returns to the left atrium via the pulmonary veins

   4. Flows into the left ventricle, then pumped to the rest of the body via the aorta

Systemic circulation:

The pathway of blood from the left side of the heart to the body tissues and back to the right side of the heart

PaCO2

Respiratory alkalosis/acidosis

Bicarbonate

Metabolic Acidosis/Alkalosis

Hemoglobin Right Shift

CADET

C: CO2 increase

A: Acid increase (low pH)
D: DPG increase (2,3-BPG)

E: Exercise
T: Temperature increase

(hemoglobin less affinity for O2 release oxygen more quickly)

Hemoglobin left shift

- Body does not need as much oxygen, curve shifts to the left. (O2 conservation)

1. oral candidiasis - THRUSH

1. White slough on tongue  

2. Looks like cottage cheese or milk curds

3. When the patches are wiped away, area underneath is red and may bleed

Edema

1. Swelling of throat and structures in mouth

1. Pharyngitis

1. “Group A Streptococcus”

   1. White and Red splotches

   2. Swollen Uvula

Viral

Redness in throat

1. Xerostomia

dry mouth bumpy tongue

Leukoplakia

white spilled paint

State the mechanism of action of antihistamine drugs.

H1 inverse agonist

Block the immediate hypersensitivity reaction: Anaphylaxis and Allergic reactions:

H1 antihistamines block the increased capillary permeability and formation of edema and swelling caused by histamine.

1. Explain two major pharmacological differences between 1^st and 2^nd  generation antihistamines.

1st generation crosses BBB (causes sleepiness), while 2nd generation doesn’t

1st generation interacts with multiple other receptors causing a variety of unwanted effects, while 2nd generation specifically interact with peripheral H1 receptors

Polar groups

Do not cross BBB - 2nd gen

Allergic Rhinitis

1. Disease caused by an IgE-mediated inflammatory response of the nasal mucous membranes after exposure to inhaled allergens

seasonal allergic rhinitis

Occurs during different seasons

perennial allergic rhinitis:

Occurs from year round exposure (dust mites, mold, etc.)

intermittent allergic rhinitis:

1. Symptoms or exposure < 4 days per week OR < 4 weeks 

persistent allergic rhinitis

1. Symptoms present >4 days per week AND >4 weeks

episodic allergic rhinitis

1. Not normally encountered in the individual’s usual environment (Episodic exposure, cat allergy)

rhinitis medicamentosa

Nasal mucosal inflammation caused by topical nasal decongestant overuse (greater than 7-10 days) 

AR

allergic rhinitis

PAR

perennial allergic rhinitis

SAR

seasonal allergic rhinitis

OAH2G

oral antihistamines 2nd gen

INAH

intranasal antihistamine

PSE

pseudoephedrine

INCS

intranasal corticosteroid

IND

intranasal decongestant

INAC

intranasal anticholinergic

INC

intranasal cromolyn sodium

SLIT

sublingual immunotherapy

SCIT

subcutaneous immunotherapy

Describe the immune response to allergens.

1. Sensitization

2. IgE production

3. Arming of mast cells

4. Release of mediators

5. Clinical effects

6. Immediate vs. Delayed Reaction

   1. Onset

   2. Cellular involvement

   3. Symptoms

Histamine action

Stimulates irritant receptors

Pruritis

Increased Vascular and mucosal permeability

Smooth muscle Contraction

Neutrophil Chemotactic factor Action

Inflammatory cell influx

Eosinophil Chemotactic factor Action

Inflammatory cell influx

Kinins

Increased vascular permeability

N-a-tosyl -arginine methylesterase action

Increased vascular permeability

Leukotrienes

Smooth muscle contraction

Increased vascular permeability

Thromboxanes

Smooth muscle spasm

Platelet Activation factor

Mucus Secretion

Increased Airway and vascular permeability

Chemotaxis

Heparin

Anti-inflammatory

Tryptase and kallikrien

Protein Hydrolysis

Allergic rhinitis

Bilateral

Frequent (Paroxysmal) Sneezing

Rhinorrhea Anterior and Watery

Frequent pruritis

Nasal obstruction variable

Non Allergic rhinitis

Unilateral

Infrequent Sneezing

Rhinorrhea Posterior and Watery and thick

Nasal obstruction usually present

Allergic shiners

swelling and darkening of circles under the eye due to nasal obstruction and venous congestion

Dennies lines

1.  fold or crease of skin below the lower eyelid

Allergic crease/ allergic salute

1. visible line across the bridge of the nose due to repeated rubbing or pushing upwards of the nose

Allergic Gape

open mouth breathing due to allergic rhinitis and its long-term complications

1.  Identify drugs that cause nonallergic rhinitis.

1. Local inflammatory

   1. Acetyl salicylic acid

   2. NSAIDs

2. Neurogenic

   1. Alpha- and beta- adrenergic blockers (clonidine risperidone, methyldopa)

   2. Ganglion blockers (trimethaphan)

   3. Phosphodiesterase-5 inhibitors (sildenafil)

   4. Calcium channel blockers

   5. Angiotensin converting enzyme inhibitors (ACEi)

   6. Gabapentin

   7. Psychotropics

3. Rhinitis medicamentosa

   1. Intranasal decongestant

Identify the medications that must be held prior to skin prick/puncture or intradermal allergy skin testing.

1. First generation antihistamines - at least 3 to 5 days before testing

2. Second generation antihistamines - at least 7 days before testing

3. Medications that interact with epinephrine (tricyclic antidepressants, beta-blockers)

Identify exclusions to self-care of allergic rhinitis.

1. Children ≤ 12 years old

2. Pregnant or lactating women

3. Symptoms of nonallergic rhinitis

4. Symptoms of otitis media, sinusitis, bronchitis, or other infection

5. Symptoms of undiagnosed or uncontrolled asthma (wheezing or shortness of breath)

6. Severe or unacceptable side effects of treatment

Identify adverse effects associated with antihistamines, decongestants, intranasal corticosteroids, cromolyn sodium and antileukotrienes.

1. Antihistamines: Drowsiness, anticholinergic, epigastric distress

2. Decongestants: Rhinitis medicamentosa (caused by intranasal decongestants), Contraindicated in pregnancy – risk of birth defects

3. Intranasal corticosteroids: sneezing, stinging, headache, epistaxis

4. Cromolyn sodium: Local irritation (sneezing and nasal stinging)

5. Antileukotrienes: BBW: behavioral changes and serious neuropsychiatric events

State the place in therapy of allergic rhinitis for nasal saline (nasal spray and nasal irrigation) and immunotherapy.

1. Nasal saline: removing mucus from the nose and clearing blocked nasal passages

2. Immunotherapy: considered for patients whose symptoms are not relieved with pharmacologic management and for those who are experiencing undesirable adverse effects

Differentiate between the advantages and disadvantages of subcutaneous and sublingual immunotherapy.

1. Subcutaneous immunotherapy

   1. Earlier and more pronounced response

   2. Local: redness and induration at site of injection

   3. Systemic: urticaria, GI upset and wheezing 

   4. Provider administered

2. Sublingual immunotherapy 

   1. Safer 

   2. Self-administered tablet

   3. Local: oral itching and discomfort

Nasal spray administration:

1. Clear nasal passages gently before administration

2. Wash hands before and after

3. Gently depress the other side of the nose with finger to close off the nostril not receiving medication

4. Aim tip of delivery device away from nasal septum to avoid accidental damage to the nasal septum

5. Activate the spray. Do not sniff

6. Breath through the mouth and wait a few minutes after using the medication before blowing the nose

1. Immunotherapy administration:

1. First dose to be given in providers office; monitor for 30 min at least

2. Always have epi-pen available

3. Instructions: 

   1. Handle with clean, dry hands

   2. Remove from blister pack

   3. Place under tongue

   4. Hold under tongue and allow to dissolve completely

   5. Wash hands after handling

   6. Do not ingest food or beverages for 5 minutes after dose

1. State the black box warning for subcutaneous (SCIT) and sublingual immunotherapie (SLIT)

1. SCIT: uncontrolled asthma

2. SLIT: anaphylaxis (good for self administration)

1. Describe the management of rhinitis medicamentosa.

1. Discontinue nasal decongestant

2. May require intranasal corticosteroids or short course of oral corticosteroids

Mild Intermittent Allergic Rhinitis

1st- Oral Antihistamine (2ng gen) or INAH

Mild Persistent Allergic Rhinitis

INCS

Moderate/Severe Intermittent Allergic Rhinitis

1st- Oral Antihistamine (2ng gen) or INAH

Moderate/Severe Persistent

INAH and INCS

Mild Intermittent non allergic rhinitis

INAH

Mild Persistent non allergic rhinitis

INAH

Moderate/Severe Persistent non allergic rhinitis

INAH + INCS

Moderate/Severe Intermittent non allergic rhinitis

INAH

Common cold mechanism role of ICAM

• cell surface protein involved in cell adhesion and inflammation of the airway that lead to symptoms like cough

•  Describe the mechanism of cough production and different types of cough

• A cough is an innate primitive reflex and acts as part of the body’s immune system to protect against foreign materials

• The most common causes of chronic cough are postnasal drip, asthma, and acid reflux from the stomach

•  Other causes of cough include smoking, infections (viral and bacterial), some medications and lung diseases

• Pertussis, also known as whooping cough, is an illness with a classic clinical finding of paroxysmal episodes of intense coughing lasting up to several minutes followed by a loud gasp for air.

• It is an infection of the respiratory tract by Bordetella pertussis, where the bacterium produces a toxin, pertussis toxin (PTx), that affects the cyclic AMP signaling through inhibition of Gi in many cell types including neutrophils and epithelial cells. The infection induces mucopurulent sanguineous exudate formation within the respiratory tract

• PTx is extensively used in signal transduction studies in cell biology

• Smokers cough: A tobacco smoking-induced cough can start off dry and hacky in the early stages and then become more phlegmy and productive as the cough progresses

• Chronic cigarette smoke-induced desensitization of airway cough receptors and paralysis of the ciliated cells in the airway

•  Smoking cannabis also induces chronic cough

• ACEI cough → bradykinin build up 

• Non Productive (Dry Cough):

  • Needs to be suppressed

  • Incessant non-productive cough leads to loss of sleep, rib fractures, pneumothorax, rupture of surgical wounds and syncope

• Productive Cough (Wet Cough)

  • Needed to clear airways; dangerous to suppress

  • Beneficial as it expels irritating substances such as dust, pollen, fluids and inflammatory cells from the upper respiratory airways

• Recall and describe the mechanism of cough suppression

• General Mechanism of Cough Suppressants (Antitussives)

  • Via the CNS, by raising the threshold of cough centers

  • Via the periphery to reduce cough impulse

• CNS acting cough suppressants 

  • Opioids (cross BBB) 

    • Suppress cough reflex on cough center (medulla)

    • Via mu and kappa opioid receptors 

      • G protein coupled receptors

    • Moderate acting opioid agonist drugs

      • Codeine

      • Hydrocodone

  • Non-opioids (cross BBB)

    • Suppress cough reflex in cough center (medulla)

    • Via sigma receptors (and other receptors)

    • Drugs

      • Dextromethorphan (synthetic) 

        • Sigma 1 receptor

      • Diphenhydramine (antihistamine)

      • Benzonatate 

• Peripheral acting cough suppressants

  • Antitussives & Demulcents

    • A demulcent (cough drop) is a high molecular weight compound that coats the skin surface

    • Peripheral acting agents work either by anesthetizing the local nerve endings or acting as demulcents 

    • Demulcents have a soothing effect on the throat

    • Camphor, menthol, eucalyptus oil

• Expectorants

  • Help thin and loosen mucus so you can cough it up more easily

  • Helps body get rid of excessive mucus more quickly

  • The active ingredient in OTC cough expectorants is guaifenesin

    • Found in mucinex, robitussin cough, and chest congestion DM

  • Used in patients who have thick, tenacious respiratory tract secretions and in sinusitis  

Acute cough

less than 3 weeks

Subacute

Cough between 3-8 weeks

Chronic

more then 8 weeks

2.  State common medical conditions associated with acute cough, subacute cough, and chronic cough.

• Acute: Upper respiratory tract infection (dry), acute bronchitis (dry), pneumonia (dry or wet), GERD, asthma (wet or dry), HF (dry)

• Subacute: Upper respiratory tract infection (dry), upper airway cough syndrome (dry)

• Chronic: Chronic bronchitis (wet), upper airway cough syndrome (dry), GERD, asthma (wet or dry), HF (dry)

3.  Identify the signs and symptoms of common medical conditions associated with cough.

• Upper respiratory tract infection (URTI; “common cold”):  Acute dry cough; rhinorrhea/nasal obstruction, sneezing, sore throat

• Acute bronchitis:  Acute dry cough; often follows viral URTI; ± wheezing, mild dyspnea, chest wall and substernal musculoskeletal pain

• Chronic bronchitis:  Chronic wet cough; COPD signs/symptoms/history

• Pneumonia:  Acute wet or dry cough; abnormal vital signs (fever, tachypnea, tachycardia), mental status changes especially in the elderly

• Upper Airway Cough Syndrome (UACS):  Acute or chronic dry cough; postnasal drip sensation, frequent throat clearing, ± rhinorrhea

• Gastroesophageal reflux syndrome (GERD):  Acute or chronic dry cough; heartburn, regurgitation, dysphagia

• Asthma:  Acute or chronic wet or dry cough; episodic wheezing and shortness of breath

• Heart failure:  Acute or chronic dry cough; cough with exertion or supine; heart failure signs (+S3, displaced apical pulse, increased jugular venous pressure, peripheral edema, weight gain)

• Pulmonary emboli:  Abrupt onset dry cough; dyspnea, pleuritic chest pain, hemoptysis, tachypnea, tachycardia, peripheral edema

• Lung cancer:  Persistent cough/worsening dry cough; acute changes in chronic “smokers cough”, hemoptysis, recurrent pulmonary infections, new onset wheezing

• Common complications cough

• Exhaustion

•  Sleep deprivation

•  Musculoskeletal pain

•  Hoarseness

•  Excessive perspiration

•  Social embarrassment

•  Urinary incontinence

less common

• Syncope

•  Stridor

•  Pneumothorax

•  Rib fractures

•  Cardiac arrhythmias

Dextromethorphan MOA/dosage

1. Acts on the cough center in the brain to reduce the urge to cough, sigma

10-20 mg q4-6. max 120mg

Codeine MOA/ Dosage

Acts centrally on the cough center of the brain, reducing the sensitivity of the cough reflex, kappa mu

10-20mg q4-6h max 120mg

Guaifenisin MOA/ Dosage

1. involves increasing the volume and reducing the viscosity of respiratory tract secretion

2. Unknown; may increase respiratory tract hydration

200-400mg q4h max 2400mg

Benzonotate MOA/ Dosage

1. Anesthetic

2. Tetracaine congener; topical anesthetic action on respiratory stretch receptors (lung airways)

100-200mg TID max 600mg

Dextromethorphan Adverse effects

1. Dizziness, drowsiness, nausea, and gastrointestinal upset

2. Should not be take with monoamine oxidase inhibitors (MAOIs)/ medications that increase serotonin levels (serotonin syndrome)

Codeine Adverse Effects

1. dizziness, constipation, nausea, and respiratory depression, particularly at higher doses