PATH 370 WEEK 4 Chap 22, 23, 24, 25

A set of vocabulary flashcards covering obstructive and restrictive pulmonary disorders, fluid and electrolyte imbalances, and acid-base homeostasis principles directly from the lecture notes.

Obstructive Respiratory Disorder

A condition manifested by increased resistance to airflow due to an airway problem, primarily described as an exhalation problem where air does not reach the respiratory zone; ex Asthma, COPD (Chronic Bronchitis and Emphysema)

Pathogenesis of Obstructive Respiratory Disorder

hyperplasia of glands -> hypersecretion; smooth muscle contraction -> bronchospasm; inflammation RESISTANCE TO AIRFLOW

Diagnosis of Obstructive Disorders

Decreased FEV1; Low FEV1/FVC ratio (<70%); Improvement in FEV1 after use of bronchodilator (asthma); Increased residual volume; Increased functional residual capacity; Inhaled bronchodilator given, repeat test in 15-20 minutes

Restrictive Respiratory Disorder

A lung disorder resulting from decreased lung expansion that impacts gas exchange and lung capacity, primarily characterized as an inhalation problem.

Diagnosis of Restrictive Disorders

FEV1/FVC ratio could be normal to high since both of them are reduced; Decrease in vital capacity (VC), Decrease in total lung capacity (TLC), Decrease in functional residual capacity (FRC), Decrease in residual volume (RV)

Chronic Bronchitis

Also known as Type B COPD (blue bloater), it involves a chronic or productive cough with hypersecretion of bronchial mucus and persistent scarring of the bronchi.

Cor pulmonale

Right-sided heart failure resulting from increased pulmonary vascular resistance, which is a common complication of chronic bronchitis.

COPD

consists of chronic bronchitis and emphysema; leads to a barrel chest due to air trapping

Chronic Bronchitis

aka Type B COPD (blue bloater); chronic or productive cough with hypersecretion of bronchial mucus, it is irreversible when paired with emphysema. 1:2 male-to-female ratio.

Pathogenesis of chronic bronchitis

Chronic inflammation (usually smoking) causes persistent scarring of the bronchi.

The IL-8 and CD8 T cells recruit inflammatory cells that lead to swelling and scarring of the bronchial walls.

Goblet cells and mucus glands enlarge (hyperplasia) and produce excess mucus that forms a mucus plug.

All the scar tissue and mucus will cause the airway walls to thicken and swell, which results in increased airflow resistance and difficulty breathing.

Pulmonary hypertension (COR PULMONLE) causes further hypoxemia

and vasoconstriction of the pulmonary vessels; leads to cor pulmonale due to increased pulmonary vascular resistance

The last stage is destruction of the bronchial walls, where there is dead space (emphysema).

Low Dose O2 Therapy for Chronic Bronchitis

They often have chronically high CO₂ levels and rely more on low oxygen levels to stimulate breathing. Giving too much oxygen can reduce their respiratory drive and worsen CO₂ retention (hypercapnia).

Emphysema

Also known as Type A COPD (pink puffer), it involves the destruction of alveolar walls through the release of proteolytic enzymes from immune cells, leading to loss of elastic tissue and air trapping; destruction of alveolar walls without fibrosis; damage is irreversible and often caused by smoking or air pollution.

Pathogenesis of Emphysema

Release of proteolytic enzymes from neutrophils and macrophages leading to alveolar damage; Smoking causes alveolar damage

Inflammation leads to release of proteolytic enzymes; Inactivates α 1 -antitrypsin (normally protects surfactant, which protects lung parenchyma)

Loss of elastic tissue in lung; Results in loss of radial traction (normally holds airway open); Air becomes trapped in distal alveoli

Loss of alveolar wall and air trapping leads to bullae (large, thin-walled cysts in the lung) formation

Bullae

Large, thin-walled cysts in the lung formed by the loss of alveolar walls and air trapping in cases of emphysema.

Barrel Chest

An increased total lung volume observed in emphysema patients to compensate for lost lung capacity due to dead space and air trapping; this results in a rounded, barrel-like shape of the chest (increased anterior and posterior diameter) as the ribs become more horizontal.

Asthma

an allergic reaction (hypersensitivity type 1- IgE); IgE is associated with inhaled allergens in asthma; reversible airway obstruction -> same pathogenesis as COPD; airway inflammation and increased airway responsiveness to a variety of stimuli. Asthma occurs in 5% to 12% of the U.S. population and is the most common chronic disease of children.

Intrinsic Asthma

Non-allergic, adult-onset asthma where there are no known allergens; often triggered by internal factors like respiratory infections or psychological factors. Prognosis is not as favorable because allergen-specific immunotherapy or environmental control won’t help.

Extrinsic Asthma

allergic, pediatric-onset, makes up a third to half of asthma cases. IgE- mediated response due to hypersensitivity type I. Mast cell activation and inflammatory cell infiltration; inflammation, mucosal edema, and bronchoconstriction are associated with the allergic form of asthma.

Clinical Manifestations of Asthma

wheezing during EXHALATION; feeling tightness of chest, dyspnea, cough, increased sputum production (hypersecretion), hyperinflated chest, bronchospasm, and decreased breath sounds.

Status Asthmaticus

A severe, life-threatening complication of asthma characterized by continuous exacerbations without relaxation, potentially leading to tetanic lung fatigue and death.

Clinical Manifestations of Status Asthmaticus

use of accessory muscles for respiration (intercostal retraction), orthopnea (trouble breathing while sitting), agitation (irritable), tachypnea (>30 breaths per min), and tachycardia (>120 beats per min). Distant breath sounds with expiratory wheezing;

Bronchoconstriction, bronchial mucosal edema, hypersecretion of mucus, and hypoxemia are associated with an acute asthma attack.

Use of accessory muscles, expiratory wheezing, coughing, and feeling of chest tightness are all part of an acute asthma episode.

Diagnosis of Asthma

radiographic findings (hyperinflation with flattening of diaphragm), physical findings, pulmonary function tests (expiratory volume decrease, FEV/JFVC < 70% after use of short-acting bronchodilator), ABG (respiratory alkalosis). Sputum examination should show Charcot-Leyden crystals formed from eosinophilic membranes. CBC would show elevated WBCs and eosinophils; RBCs would be normal.

Charcot-Leyden crystals

Specific crystals formed from eosinophilic membranes found during a sputum examination in asthma patients.

ABG Diagnostic testing

Arterial blood gas measures are useful to determine the acid-base status of extracellular fluids. Includes pH, PaCO2, and HCO3.

Normal Values for an ABG *** IMPORTANT

NORMAL PH (7.35-7.45) → BLOOD

NORMAL PaCO2 (35-45 mmHg) → LUNG (Respiratory)

NORMAL HCO3 (22-26 mEq/L) → KIDNEY (Metabolic)

PaCO2

Normal (35-45 mmHg) l measures how much CO2 is in arterial blood; CO2 is ACIDIC. More CO2 = Respiratory Acidosis VICE VERSA

HCO3

Normal (22-26 mEq/L) measures how much bicarbonate is in arterial blood, which is a BASE/BUFFER. Low HCO3 = Metabolic Acidosis, high HCO3 = Metabolic Alkalosis.

Pulmonary Function Test

Forced expiratory volumes decrease; Peak expiratory flow rate (PEFR); Ratio of FEV1/FVC before and after administration of short-acting bronchodilator (>15% change); Obstructive would decrease FEV1/FVC ratio while restrictive would increase FEV1/FVC ratio.

Treatment of Asthma

corticosteroids, anticholinergics (prevent ACh from causing bronchocontriction and mucus production), B-2 agonists (bronchodilators), Leukotriene modifiers (reduce bronchocontriction)

Restrictive Pulmonary Disorders

result from decreased lung expansion; INHALATION issue. EX: Pneumothorax and ARDS

Occupational Lung Disease

lung disorders caused by long-term exposure to harmful dust, chemicals, fumes, or fibers in the workplace.

Clinical Manifestations of Occupational Lung Disease:

progressive productive cough, dyspnea w/ exercise, Late Clinical Features: chronic hypoxemia, cor pulmonale, and respiratory failure.

ARDS (Acute Respiratory Distress Syndrome)

Damage to the alveoli leading to flooding with proteinaceous fluid (hyaline membrane/fibrosis), characterized by hypoxemia refractory to supplemental oxygen. Hypoxemia is the hallmark for acute respiratory distress syndrome.

Etiology of ARDS

severe trauma, sepsis (>40%), aspiration of gastric acid (>30%), and shock. Atelectasis and a decrease in lung compliance from lack of surfactant (type II alveolar cells).

Diagnosis of ARDS + PFTs:

ABG (hypoxia, acidosis, hypercapnia), Chest X-ray (normal with progression to diffuse “whiteout”). Open-lung biopsy shows hyaline membranes. Decrease in FVC, decreased lung volumes, decreased lung compliance; V A/Q mismatch with large right-to-left shunt

Treatment of ARDS

Inhaled nitric oxide: reduces oxygen usage in the heart; vasodilation-increase tissue oxygenation until inflammation resolves. Mechanical ventilation with positive end-expiratory pressure (PEEP). Supplemental O2.

Mechanisms of ARDS

increased permeability of the pulmonary vasculature, flooding of the alveoli with protein and fluid-> protein-rich pulmonary edema (hyaline membrane), severe hypoxemia, diffuse, fluffy alveolar infiltrates, and lack of surfactant (type II) cells.

Pneumothorax

The accumulation of air in the pleural space may cause symptoms such as tracheal shift to the contralateral side and respiratory distress.

Primary Pneumothorax:

Spontaneous; Occurs in tall, thin men 20 to 40 years; No underlying disease factors; Cigarette smoking increases risk

Secondary Pneumothorax

Result of complications from preexisting pulmonary disease

Clinical Manifestations of Pneumothorax

Hypotension---shock; Tracheal shift contralateral (opposite) side; Neck vein distention; Hyperresonance

Diagnosis of Pneumothorax:

Decreased PaO2, acute respiratory alkalosis (due to tachypenia); Depression of hemidiaphragm on side of pneumothorax

Tension Pneumothorax

A medical emergency of traumatic origin resulting from a penetrating or nonpenetrating injury, leading to a decrease in vital capacity ($VC$) and total lung capacity ($TLC$); May also be from iatrogenic causes; Medical emergency

Know about restrictive lung disease and its relationship with lung function tests

Decrease in vital capacity (VC), total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV); Decreased PaO2, Normal or decreased PaCO2, Increased pH (alkalosis)

IRDS (Infant Respiratory Distress Syndrome)

Also known as hyaline membrane disease, it affects premature neonates and is associated with a lack of surfactant and a1-antitrypsin deficiency.

Pleural Effusion

A pathologic collection of fluid or pus in the pleural cavity; different types include transudates, exudates, empyema, hemothorax, and chylothorax.

Transudate

A type of pleural effusion low in protein (ratio < 0.5), often associated with severe heart failure or edematous states.

Exudate

A type of pleural effusion high in protein (> 0.5 \text{ mg/dl}), typically caused by malignancies, infections, or pulmonary embolism.

Empyema

A high-protein exudative pleural effusion caused specifically by an infection in the pleural space.

Hemothorax

(hemorrhagic shock); Presence of blood in pleural space; Result of chest trauma; Contains blood and pleural fluid: hemorrhagic

Chlothorax/Lymphatic

Exudative process that develops from trauma

Pleural Effusion Clinical Manifestations

Pleuritic pain (sharp, worsens with inspiration); Absence of breath sounds; Contralateral tracheal shift (massive effusion)

Pleural Effusion Diagnosis

Signs of CHF, CT or ultrasonographic tests

S/S of Pneumonia

Crackles (rales) and bronchial breath sounds over affected lung tissue; Chills, Fever, Cough, purulent sputum.

S/S of Viral Pneumonia

Fever, nonproductive cough, hoarseness, coryza accompanied by wheezing/rales

S/S of Bacterial Pneumonia

Productive cough and parenchymal infiltrates on X-ray

Legionnaires' disease

Organism lives in H2O; Transmitted by portable H2O, condensers, cooling towers; Fever, diarrhea, abdominal pain, liver and kidney failure, pulmonary infiltrates

Intracellular Fluid

Fluid making up $\frac{2}{3}$ of total body water, containing high concentrations of $K^+$, $Mg^{2+}$, and $PO_{4}^{3-}$ INSIDE cell.

Extracellular Fluid

Fluid making up $\frac{1}{3}$ of total body water, containing high concentrations of $Na^+$, $Ca^{2+}$, and $Cl^-$ / $HCO_{3}^{-}$ OUTSIDE cell; subdivided into interstitial and vascular components. Infants have more extracellular fluid than intracellular fluid.

Total Body Water

Percentage of body weight that is water; Adult males (60%), Adult Females (50%), and infants (75%) ~ weight is best indicator of fluid changes.

Fluid Homeostasis

intake (drinking), absorption, distribution, and excretion (peeing)

Thirst is triggered by

Increased concentration of extracellular fluid (osmolality); decreased circulating blood volume

Which primary stimulus for the sensation of thirst declines with aging? Why?

Increased serum osmolarity because as we age, our hypothalamic osmoreceptors become less sensitive to increases in serum osmolarity, so older adults won’t feel as thirsty.

Electrolyte Composition

Too much (Hypertonic/hyperosmolar); Too little (hypotonic/hyposmolar)

Antidiuretic Hormone (ADH)

A hormone from the posterior pituitary that helps the body reabsorb water, decreasing urine output and increasing blood volume.

Aldosterone

A hormone from the adrenal cortex that promotes sodium retention in the blood and the excretion of $K^+$ in the urine.

ANP/BNP

Hormones from the heart that promote the excretion of $Na^+$ and water to increase urine volume and decrease blood volume.

Plasma Magnesium Normal Range + Impacts?

normal 1.5-2.5; impacts neuromuscular relaxation and cardiac stabilty

Hypomagnesemia

A serum magnesium level below $1.5 \text{ mEq/L}$ caused by decreased magnesium intake or absorption; chronic alcoholism, malnutrition, ileal resection; Increased magnesium excretion: usually renal; Loss of magnesium by an abnormal route: emesis

Clinical Manifestations od Hypomagnesemia

Increased neuromuscular excitability from excessive amounts of acetylcholine; Insomnia, Hyperactive reflexes, Muscle cramps, Muscle twitching, grimacing, Positive Chvostek sign, Positive Trousseau sign, Cardiac dysrhythmias

Hypermagnesemia

A serum magnesium level above $2.5 \text{ mEq/L}$ caused by Increased magnesium intake or absorption: laxatives, antacids; Decreased magnesium excretion: oliguric renal failure, adrenal insufficiency

Clinical Manifestation of Hypermagnesium

Depression of neuromuscular function; related to decreased release of acetylcholine at neuromuscular junctions; Decreased deep tendon reflexes, Lethargy, Hypotension, Flushing, Diaphoresis, Drowsiness, Flaccid paralysis, Respiratory depression, Bradycardia, Cardiac dysrhythmias, Cardiac arrest

Plasma Phosphate Normal Range + Impacts?

normal 2.5-4.5; impacts energy (ATP), bones/teeth, and cell function

Hypophosphatemia

Decreased phosphate intake or absorption, Chronic alcoholism, chronic diarrhea, malabsorption syndromes, antacids that bind phosphate; Alcohol withdrawal, diuretic phase after extensive burns, emesis, hemodialysis.

Clinical Manifestations of Hypophosphatemia

Due in part to decreased ATP within the cells, anorexia, Malaise, Hemolysis, Paresthesias, Diminished reflexes, Muscle aches, weakness, and respiratory failure

Hyperphosphatemia

Overzealous phosphate therapy, excessive use of phosphate-containing enemas or laxatives; Tumor lysis syndrome, crushing injuries, rhabdomyolysis

Clinical Manifestations of Hyperphosphatemia

Increased neuromuscular excitability; Depends on area where salts precipitate; May cause aching and stiffness of joints, Itching, and conjunctivitis

Hypovolemia

(Volume Deficit) A loss of extracellular fluid characterized by weight loss, decreased skin turgor, dry mouth, and orthostatic blood pressure shifts, while sodium levels remain normal.

Hypervolemia

excess of extracellular fluid (heart failure, increased aldosterone & ADH secretion); sodium normal/high/low. Caused by addition or retention of isotonic saline; excessive secretion of aldosterone causes kidneys to retain saline, excessive IV infusion, or renal retention of sodium and water.

Clinical Manifestations of Hypervolemia

Bounding pulse, Neck vein distention in upright position, crackles in dependent portions of lungs, dyspnea, orthopnea. Sudden weight gain, edema, frothy sputum of pulmonary edema. IN INFANTS, BULGING FONTANEL.

Edema + Mechanism

An accumulation of excess fluid in the interstitial compartment; Increased hydrostatic pressure, capillary permeability, decreased lymphatic drainage, and oncotic pressure. Increased fluid causes hydrostatic pressure causing water to be pushed out of the capillaries, capillary permeability causes more fluid to leak, while decreased lymphatic drainage cannot drain water and decreased oncotic pressure because there is not enough protein (albumin) to pull fluid back into blood vessel.

Clinical Manifestations of Edema

localized swelling, pale/gray/or red skin color, weight gain, slow, rapid pulse, high BP, lethargy, seizures, pulmonary congestion (cough + rales), LAB (decreased hematocrit, serum sodium, urine = low specific gravity, high volume).

Fluid Deficit S/S + Lab Findings

Dehydration; sunken/soft eyes, decreased skin turgor, dry mucous membrane, thirst + weight loss, low BP, orthostatic hypotension, fatigue, weakness, dizziness, increased body temp, flat neck veins. LAB (Increased hematocrit, increased electrolytes, Urine: high specific gravity, low volume). IN INFANTS, SUNKEN FONTANEL.

Fluid Deficit Etiology

dehydration; vomiting, diarrhea, hypernatremia, extracellular volume deficit

Serum Sodium Normal Range + Impacts?

135–145 mEq/L; impacts fluid balance and nerve conduction

Hyponatremia

also called hypotonic syndrome, hypoosmolarity, or water intoxication (MORE WATER LESS SALT). 2 primary causes is a gain of relatively more water than salt (prolonged or excess release of ADH or water intake that exceeds normal limits) and a loss of relatively more salt than water.

Clinical Manifestations of Hyponatremia

Nervous system dysfunction, malaise, anorexia, nausea, vomiting, headache, confusion, lethargy, seizures, coma, fetal cerebral herniation. LOW BP

Hypernatremia

also called water deficit, hypertonic syndrome, hyperosmolarity (MORE SALT LESS WATER); serum sodium concentration above normal limits, which causes cells to shrivel. Caused by a gain of more salt than water or a loss of more water than salt.

Clinical Manifestations of Hypernatremia

thirst, oliguria, confusion, lethargy, seizures, coma, and death. HIGH BP

Serum Potassium Normal Range + Impacts?

3.5 - 5 mEq/L; impacts cardiac and muscle function

Serum Glucose Normal Range

70–99 mg/dL; Prediabetes: 100–125 mg/dL; Diabetes: ≥126 mg/dL

Hypokalemia

Decreased serum potassium ion concentration in extracellular fluid below 3.5; caused by decreased intake, shift into cells, or increased excretion (usually renal but can be through feces, sweat, GI (emesis/diarrhea), diuretics, during treatment of diabetic ketoacidosis with insulin. Hormonal imbalances can also cause excess aldosterone or glucocorticoids (Cushing's syndrome).

Clinical Manifestations of Hypokalemia:

dysrhythmias, fatigue, lethargy, muscle weakness, paresthesia (pins and needles), constipation, anorexia, polyuria, and nausea; flattened T-waves

Hyperkalemia

Rise of serum potassium above 5 mEq/L; increased potassium intake, rapid/excessive IV infusion, acidosis, crushing injuries, decreased potassium excretion (oliguria, potassium-sparing diuretics (drugs that reduce aldosterone effects or are nephrotoxic)

Clinical Manifestations of Hyperkalemia

cardiac arrest, paralysis, paresthesias, fatigue, and nausea; Intestinal cramping, diarrhea, and muscle weakness: ascending, beginning in lower extremities,

Serum Calcium Normal Range + Impacts?

8.5-10.5 mg/dL; impacts bone, muscle contraction, and clotting

Hypocalcemia

Serum calcium concentration drops below the lower limit of normal; caused by decreased calcium intake or absorption (lack of vitamin D), decreased physiological availability of calcium, increased calcium excretion (steatorrhea and pancreatitis). Also caused by hypoparathyroidism, malabsorption syndrome, deficient serum albumin, and renal failure (inactivates vitamin D).

Clinical Manifestations of Hypocalemia

Decreases the threshold potential, causing hyperexcitability of neuromuscular cells resulting in: Positive Trousseau sign; Positive Chvostek sign; Paresthesias; Muscle twitching and cramping; Hyperactive reflexes; Carpal spasm, Pedal spasm, Tetany, Laryngospasm, Seizures, Cardiac dysrhythmias

Hypercalcemia

Occurs when the serum calcium concentration rises above the upper limit of normal; Increased calcium intake or absorption (Milk-alkali syndrome, vitamin D overdose), shift of calcium from bone to extracellular (Hyperparathyroidism, immobilization, bone tumors), and decreased calcium excretion (thiazide diuretics). Bronchogenic carcinomas secrete PTH.

Clinical Manifestations of Hypercalcemia

decreased neuromuscular excitability caused by elevation of the threshold potential of excitable cells; Muscle weakness; Diminished reflexes; Cardiac dysrhythmias; Anorexia, nausea, emesis, Fatigue, Polyuria, Constipation, Headache, confusion, lethargy, personality change, Renal calculi, Pathological fractures. (Common paraneoplastic syndrome**** IMPORTANT)