Patho Exam #2 Flashcards

(99 cards)

1
Q

Lymph nodes

A

 Part of the immune and hematologic systems
o Facilitates maturation of lymphocytes
o Transports lymphatic fluid back to the circulation
o Cleanses the lymphatic fluid of MOs and foreign particles

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

Evaluation of the Hematologic System

A
•	Tests of bone marrow function
	Bone marrow aspiration
	Bone marrow biopsy
	Measurement of bone marrow iron stores
	Differential cell count
•	Blood tests
	Large variety of tests – CBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aging and the Hematologic System

A

• Erythrocyte lifespan is normal, but are replaced more slowly
 Possible causes
o Iron depletion
o Decreased total serum iron, iron-binding capacity, and intestinal iron absorption
 Lymphocyte function decreases with age
 Humoral immune system is less responsive

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

Quantitative disorders

A

 Increases/decreases in cell numbers
o Leukopenia
 Not normal and not beneficial
 Low WBC predisposes a patient to infection
o Leukocytosis
 Normal protective physiologic response to physiologic stressors
 Bone marrow disorders or premature destruction of cells
 Response to infectious MO invasion

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

Qualitative disorders

A

 Disruption of cellular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Neutropenia

A

• Reduction in circulating neutrophils
• Causes
 Prolonged severe infection
 Decreased production caused by chemotherapy
 Reduced survival
 Abnormal neutrophil distribution and sequestration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Leukemias

A

• Malignant disorder of the blood and blood-forming organs (Hematopoietic stem cells)
• Excessive accumulation of leukemic cells
 In bone marrow mutation
 Excessive accumulation of lymphocytic – B, T, or NK cells
 Excessive accumulation of myelogenous – monocytes or granular leukocytes

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

Acute leukemia

A

 Presence of undifferentiated or mature cells, usually blast (leukoblast) cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Chronic leukemia

A

 Predominant cell is mature but does not function normally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Leukemia Symptoms

A

• Related to suppressed bone marrow function
 Infection – severe and/or recurrent
 Night sweats, fever, lymphadenopathy
 Anemia, pallor, fatigue, weight loss
 Nose bleeds, bleeding gums, petechiae (small red or purple spot caused by bleeding into the skin), ecchymosis (bruise)
• Related to infiltration to other organs with immature cells
 Enlarged spleen, liver, lymph nodes, bone and joint pain
 CNS symptoms (ALL & AML): headache, nausea, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Leukemia Diagnosis

A

• Abnormalities in Complete blood cell count (CBC)
• X rays
• Bone marrow aspiration reveals leukemic blast cells and tumor markers
 Syringe is used to suck marrow from the iliac crest or the sternum
 Procedure used to examine bone marrow cells
• Lumbar puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chemotherapy

A

 Needs to be systemic
 Goal is to rid body of leukemic cells without completely destroying bone marrow
 Bone marrow transplant provides cure for some types of leukemia

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

Acute Lymphocytic Leukemia (ALL) & Acute Malloid Leukemia (AML)

A

 Induction Therapy
o Intense combo of chemotherapy and radiation
o Given at time of diagnosis
o Goal to achieve remission
 Consolidation Therapy
o Given once remission achieved
o Variation of chemotherapy given during induction
o Curative intent; may be one treatment or repeated cycles for 1 – 2 years
o CNS treatment in children
 Maintenance Therapy
o Purpose to maintain remission
o Decreased dose of chemotherapy
o Usually given in cycles over several years (2-5)

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

Chronic Malloid Leukemia (CML)

A

 Chemo agents – administered orally
 In blast crisis
o Drugs similar to those used in AML
 Leukapheresis (WBCs are separated from a sample of blood), plateletpheresis (platelets are separated from a sample of blood)
 Bone marrow transplant before blast crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic Lymphocytic Leukemia (CLL)

A

 Goal – palliation (make a disease or its symptoms less severe or unpleasant without removing the cause)
 Oral chemo agents to control WBC count

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

Malignant Lymphomas

A

• Uncontrolled proliferation of lymphocytes arising from lymphoid tissues
• Invade bone marrow and other organs
Hodgkin’s Lymphoma
Non-Hodgkin’s Lymphoma

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

Hodgkin’s Lymphoma (Disease)

A

 Associated with Epstein-Barr Disease (EBV)
 Form of lymphoma demonstrating the Reed-Sternberg cell, seen after doing a biopsy on a patient’s lymph node]
 Bimodal incidence peak
o Teens to mid-twenties or after 50
 Thought to be associated with inflammatory reaction to infectious agent, virus – EBV
 Painless progression of single node or group of nodes; spreads in continuous pattern
 Usually good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Non-Hodgkin’s Lymphoma:

A

 Linked with chromosomal translocation
 Worst type
 Heterogeneic group of neoplastic disorders of lymphoid tissue; absence of Reed-Sternberg cell
 More prevalent than Hodgkin’s Lymphoma
o More common in older adults
o Common among persons who are immunosuppressed
 Viruses also implicated as possible cause
 Multi-centric in origin, non-continuous spread to lymph nodes and early to liver, spleen, and bone marrow
 Poorer prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Malignant Lymphomas Symptoms

A

 Painless, enlarged lymph nodes
 Low grade fever, night sweats, weight loss, fatigue
 Enlarged liver, spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Malignant Lymphomas Diagnosis

A

 Biopsy lymph node
 CT scan
 Bone marrow aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Malignant Lymphoma: Treatment

A

• Hodgkin’s Lymphoma
 If localized, radiation therapy alone (Stage I & II)
 Stage IIIA: radiation therapy and combination chemotherapy
 Stage IIIB & IV: combination chemotherapy
• Usually combination of radiation therapy and chemotherapy as multicentric (multiple centers of origin) in nature

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

Multiple Myeloma

A

• Malignant disease of plasma cells – abnormal B cells
• Malignant plasma cells produce
 Immune deficiency
 Increased amount of nonfunctional immunoglobulin
o Called the M protein – increases blood viscocity
 Substance that stimulates and enhances angiogenesis
• Malignant plasma cells can infiltrate other tissues

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

Multiple Myeloma Symptoms

A

 Bone pain
 Osteoclastic activity increased
o Osteolytic lesions and evidence of osteoporosis on X-ray
o Pathologic fractures
 Hypercalcemia, anemia, leukopenia, thrombocytopenia
 Renal failure (damage due to Bence Jones protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Multiple Myeloma Diagnosis

A

 Serum protein electrophoresis
o Elevated monoclonal protein spike
 Bone marrow aspiration
o Sheets of plasma cells present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Multiple Myeloma Treatment
 Chemotherapy: control illness o Various cheme agents + corticosteroids (Decadron)  Thalidomide (Thalomid) to prevent angiogenesis (used to be used to treat, but caused deformed limbs if mother took in early pregnancy)  Biologic agents – alpha-interferon to maintain remission  Radiation for bone lesions  Bisphosphonates to diminish osteoclastic activity  Promote renal function  Symptom management o Pain, hypercalcemia, increased blood viscosity o Prevent, treat infections
26
Anemia
``` • Reduction in total number of erythrocytes in circulating blood or in the quality or quantity of hemoglobin  Impaired erythrocyte production  Acute or chronic blood loss  Increased erythrocyte destruction  Combination of the above ```
27
Anemia Morphology
```  Morphology o Based on MCV, MCH, and MCHC values o Size  Identified by terms that end in “-cytic”  Macrocytic, microcytic, normocytic o Hemoglobin content  Identified by terms that end in “-chromic”  Normochromic and hypochromic ```
28
Anemia Physiology Manifestation
o Reduced oxygen-carrying capacity o Heme iron: organ meats good source o Non-heme irons: Vitamin C helps observe
29
Classic Anemia Symptoms
Fatigue, dypsnea, weakness, and pallor
30
Microcytic-Hypochromic Anemia
• Iron deficiency anemia  Most common type of amemia worldwide  Nutritional iron deficiency  Metabolic or functional deficiency  Characterized by RBCs that are abnormally small and contain reduced amounts of hemoglobin  Related to: o Disorders of iron metabolism o Alcoholism o Progression of iron deficiency causes:  Brittle, thin, coarsely ridged, and spoon-shaped nails  A red, sore, and painful tongue
31
Macrocytic-Normochromic Anemia
• Folate deficiency anemia  Absorption of folate occurs in the upper small intestine  Not dependent on any other factor  Neurologic manifestations generally not seen  Treatment requires daily oral administration of folate
32
Normocytic-Normochromic Anemia
``` • Hemolytic anemia  Accelerated destruction of RBCs  Autoimmune hemolytic anemias  Immunohemolytic anemia: blood transfusion reaction  Drug-induced hemolytic anemia ```
33
Pernicious Anemia
• Lack in intrinsic factor, no B12 absorption • Signs and symptoms  Nerve demyelination  Atrophic glossitis (redness and swelling of tongue, beefy red) • People at risk usually obese due to surgeries
34
Mononucleosis
Infection of B lymphocytes • Epstein Barr virus • Most infectious two weeks before symptoms start to show • Ruptured spleen can be caused by this which can cause death • Diagnosed by monospot test
35
Burkitt-lymphoma
* B-cell, Epstein Barr * Most common types of non-Lodgkins lymphoma in children * Found in jaw and facial muscles
36
Gas transport
 Ventilation of the lungs  Diffusion of oxygen from the alveoli into the capillary blood  Perfusion of systemic capillaries with oxygenated blood  Diffusion of oxygen into systemic capillaries into the cells  Diffusion of CO2 occurs in reverse order
37
Factors Affecting Alveolar-Capillary Gas Exchange
* Surface area available for diffusion * Thickness of the alveolar-capillary membrane * Partial pressure of alveolar gases * Solubility and molecular weight of the gas
38
Lung compliance
* C=△V/△P | * △V Lung volume can be accomplished with given △P respiratory pressure
39
Airway resistance
* Volume of air that moves into and out of the air exchange portion of the lungs * Directly related to the pressure difference between the lungs and the atmosphere * Inversely related to resistance the air encounters as it moves through the airways
40
Cheyne-Stokes Respirations
o Characterized by oscillation of ventilation between apnea and hyperpnea o Compensate for changing serum partial pressures
41
Kussmaul Respirations
o Deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA), but also renal failure o Form of hypertentilation (reduces CO2 in blood due to increased rate or depth of respiration)
42
Signs and Symptoms of Pulmonary Disease
• Dyspnea: not breathing properly  Subjective sensation of uncomfortable breathing • Orthopnea: difficulty breathing when laying down • Paroxysmal nocturnal dyspnea (PND): sleeping and then wake up sharply, can be associated with cardiac
43
Mechanisms Involved in Dyspnea
• Stimulation of lung receptors • Increased sensitivity to changes in ventilation perceived through CNS mechanisms • Reduced ventilatory capacity or breathing reserve • Stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm and of receptors in the skeletal joints • Associated conditions  Primary lung disease  Heart disease  Neuromuscular disorders
44
Signs and Symptoms of Pulmonary Disease
``` • Hypoventilation  Hypercapnia • Hyperventilation  Hypocapnia • Cough  Acute cough  Chronic cough • Hemoptysis: coughing up blood • Cyanosis • Pain: chest pain • Clubbing: finger nails, pulmonary obstructive disorders • Abnormal sputum: look for color (green, yellow, pink, brown), consistency, thickness, copious amounts of sputum, smell • Pulmonary edema: fluid in or around lungs, congestive heart failure (CHF) ```
45
Hypoxemia
• Shortness of breath, increased respiration, changing mental status (esp in elderly), pale or cyanosis • Results from:  Inadequate O2 in air  Disease of respiratory system  Dysfunction of the neurological system  Alterations in circulatory function • Mechanisms  Hypoventilation  Impaired diffusion of gases  Inadequate circulation of blood through the pulmonary capillaries  Mismatching of ventilation and perfusion
46
Mild Hypoxemia
```  Metabolic acidosis  Increase in heart rate  Peripheral vasoconstriction  Diaphoresis  Increase in blood pressure  Slight impairment of mental performance ```
47
Chronic Hypoxemia
```  May be insidious in onset and attributed to other causes o Compensation masks condition  Increased ventilation  Pulmonary vasoconstriction  Increased production of RBCs  Cyanosis ```
48
Hypercapnia
• Increased arterial PCO2 • Caused by hyperventilation or mismatching or ventilation and perfusion • Effects  Acid-base balance (decreased pH, respiratory acidosis)  Kidney function  NS function  Cardiovascular function
49
Pleural effusion
Abnormal collection of fluid in pleural cavity  Transudate or exudate, purulent (containing pus), chyle (fluid that consists of fat droplets and lymph), or sanguineous (bloody)
50
Spontaneous Pneumothorax
 Occurs when air-filled blister on the lung surface ruptures
51
Traumatic Pneumothorax
 Caused by penetrating or non-penetrating injuries |  Can be from car accident, incident is involved
52
Tension Pneumothorax
 Occurs when the intrapleural pressure exceeds atmospheric pressure  Build-up of air within pleural space, usually due to a laceration which allows air to escape in pleural space but doesn’t return
53
Characteristics and Symptoms of Pleural Pain
* Abrupt in onset * Unilateral, localized to lower and lateral part of the chest * May be referred to the shoulder * Usually made worse by chest movements * Tidal volumes are kept small * Breathing becomes more rapid * Reflex splinting of the chest may occur
54
Diagnosis of Pleural Effusion
 Chest radiographs, chest ultrasound |  Computed tomography (CT)
55
Treatment of Pleural Effusion
* Thoracentesis: inserting needle in lungs to draw out fluid * Injection of sclerosing agent (develops scar tissue) into the pleural cavity * Open surgical drainage (chest tube, usually used to inflate lungs that collapse)
56
Actelectasis
Incomplete expansion of a lung or portion of a lung
57
Causes of Actelectasis
 Airway obstruction  Lung compression such as occurs in pneumothorax or pleural effusion  Increased recoil of lung due to loss of pulmonary surfactant
58
Causes of Respiratory Failure
``` • Impaired ventilation  Upper airway obstruction  Weakness of paralysis of respiratory muscles  Chest wall injury • Impaired matching of ventilation and perfusion • Impaired diffusion  Pulmonary edema  Respiratory distress syndrome ```
59
Treatment of Respiratory Function
* Respiratory supportive care directed toward maintenance of adequate gas exchange * Establishment of an airway * Use of bronchodilating drugs * Antibiotics for respiratory infections * Ensure adequate oxygenation
60
Acute Respiratory Distress Syndrome (ARDS)
Damaged alveoli, oxygenation severely impaired • Injury to pulmonary capillary endothelium • Inflammation and platelet activation • Surfactant inactivation • Atelectasis
61
Causes of ARDS
* Aspiration in gastric contents * Major trauma (with or without fat emboli) * Sepsis secondary to pulmonary or non-pulmonary infections * Acute pancreatitis * Hematologic disorders * Metabolic events * Reactions to drugs and toxins
62
ARDS Manifestations
```  Hyperventilation  Respiratory alkalosis  Dyspnea and hypoxemia  Metabolic acidosis  Hypoventilation  Respiratory acidosis  Further hypoxemia  Hypotension, decreased cardiac output, death ```
63
ARDS Evaluation and Treatment
* 100% oxygen * Keep O2 levels above 90% * Physical examination, blood gases, and radiologic examination * Supportive therapy with oxygenation and ventilation and prevention of infection * Surfactant to improve compliance
64
Chronic obstructive airway disease (COPD)
• Expiration is affected • Progression can be slowed with treatment • Inflammation and fibrosis of bronchial wall • Hypertrophy of submucosal glands • Hypersecretion of mucus (asthmatic patients, chronic bronchitis patients) • Loss of elastic lung fibers  Impairs the expiratory flow rate, increases air trapping, and predisposes to airway collapse • Alveolar tissue  Decreases the surface area for gas exchange
65
Causes of COPD
* Chronic bronchitis * Emphysema * Bronchiectasis * Cystic fibrosis
66
Types of COPD
• Emphysema  Enlargement of air spaces (beyond terminal bronchioles, loss of recoil, harder and not as quick) and destruction of lung tissue • Chronic obstructive bronchitis  Obstruction of small airways
67
Pulmonary Emphysema
* Smoking history * Age of onset: 40-50 years * Often dramatic barrel chest (1:1 ratio) * Weight loss * Decreased breath sounds * Normal blood gases until late in disease process * Slowly debilitating disease
68
Chronic Bronchitis
* Smoking history * Age of onset 30-40 years * Barrel chest may be present * Shortness of breath predominant early symptom * Rhonchi often present * Sputum frequent early manifestation * Often dramatic cyanosis * Hypercapnia and hypoxemia may be present * Frequent cor pulmonale and polycythemia * Numerous life threatening episodes due to acute exacerbations
69
Pulmonary Embolism
• Development  Blood-borne substance lodges in a branch of the pulmonary artery and obstructs the flow  Thrombus: arising from DVT  Fat: mobilized from the bone marrow after a fracture or from a tramatized fat depot  Amniotic fluid: enters the maternal circulation after rupture of the membranes at the time of delivery
70
Asthma
```  Environmental o Construction (concrete dust) o Smoking o Pet hair  Preventable o Control whatever triggers asthma attack  Exercise induced  Allergen induced  Stress Induced ```
71
Asthma Symptoms
Wheezing, coughing throughout the night, difficulty breathing, and excess sputum
72
Pneumonia
```  6th leading cause of death  Nosocomial Infection  Spread of respiratory droplets  Hospital/environmental acquired  Can be caused by bacteria (strep)  Haemophilis influenza most common cause ```
73
Tuberculosis
```  Caused by mycobacteria (rod-shaped)  Acid-fast bacillus  Airborne  Patients in negative air-pressure rooms  Droplet precautions  Causeous necrosis (cheesy-looking granules)  TB skin tests o Pos. needs further testing o Chest x-ray o 3 sputum cultures ```
74
Hyperthyroidism
 Thyrotoxicosis: caused by too much thyroid hormone in body, most common type of hyperthyroidism o Exopathalmos: bulging of eyes o Too much T3 and T4 in body o Cured with iodine  Graves disease o Pretibial myxedema o Most common type of hyperthyroidism  Hyperthyroidism resulting from nodular thyroid disease o Goiter: result of iodine deficiency  Thyrotoxic crisis: immediate care needed, most extreme form of hyperthyroidism
75
Hypothyroidism
``` • Primary hypothyroidism  Subacute thyroiditis  Autoimmune thyroiditis (Hashimoto disease)  Painless thyroiditis  Postpartum thyroiditis  Myxedema coma: life threatening • Congenital hypothyroidism • Thyroid carcinoma • Overweight, fatigue, thyroid gland can atrophy, constipation, sensitivity to cold, dry skin and nails, constant pain • Creatinism  44 in or less  Scamp or no hair  Umbilical hernia  Underdeveloped breasts ```
76
Type 1 Diabetes Mellitus
* Demonstrates pancreatic atrophy and specific loss of beta cells * Macrophages, T- and B-lymphocytes, and natural killer cells are present
77
Type 1 Diabetesx Mellitus
* T cells attack and destroy islet cells in pancreas * Body can make insulin but body can’t use it * Obesity * Hypertension * Poor wound healings * Peripheral neuropathy * Amputations * Frequent infections * Liver and kidney disease * End-stage renal disease * retinopathy
78
Type 1 DM
• Genetic susceptibility  Glycogen • Environmental factors • Immunologically mediated destruction of beta cells by T cells • Manifestations  Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue  Have to have insulin
79
Type 2 DM
 Insulin resistance • Body makes insulin, but doesn’t produce enough for glucose in body • Usually seen in 35 years + • Normal should be 70-100 • Orange juice given to help instantly (monosaccharide) • Milk if no OJ present (dissacharide) • Glucose given under gum or by IV
80
Acute Complications of DM
* Hypoglycemia * Diabetic ketoacidosis * Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) * Somogyi effect * Dawn phenomenon
81
Diabetic ketoacidosis
 Sweet smelling pee  Fat begins to be broken down  Carbs aren’t broken down, glucose not used for energy  Ketones enter bloodstream
82
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
 Life threatening  Enough insulin produced to not get NKA  Not enough insulin produced to not prevent hyperglycemia  High blood sugarm but body still making enough insulin  Ketones aren’t spilled into blood
83
Somogyi effect
Blood glucose drops in sleep, Hormones increase blood sugar too much
84
Dawn phenomenon
Higher blood sugar than anticipated when waking up
85
Chronic Complications of DM
``` • Hyperglycemia and nonenzymatic glycosylation • Hyperglycemia and the polyol pathway  Protein kinase C • Microvascular disease  Retinopathy  Diabetic nephropathy • Macrovascular disease  Coronary artery disease  Stroke  Peripheral arterial disease • Diabetic neuropathies • Infection ```
86
Disseminated Intravascular Coagulation (DIC)
• Complex, acquired disorder in which clotting and hemorrhage simultaneously occur • Result of increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis • Endothelial damage is the primary initiator of DIC • By activating fibrinolytic system (plasmin), patient’s fibrin degradation product (FDP) and D-dimer levels will increase • Because of the patient’s clinical state, the disorder has a high mortality rate • Treatment is to remove the stimulus and maintain hemodynamic status • Clinical signs and symptoms demonstrate wide variability  Bleeding from venipuncture sites  Bleeding from arterial lines  Purpura, petechiae, and hemotomas  Symmetric cyanosis of the fingers and toes
87
Vitamin K deficiency | Alteration of Coagulation
Necessary for synthesis and regulation of prothrombin, the prothrombin factors (II, VII, XI, X) and proteins C and S (anticoagulants)
88
Liver disease
 Causes a broad range of hemostasis disorders | o Defects in coagulation, fibrinolysis, and platelet number and function
89
Thrombocytopenia
Platelet count <150,000/mm3
90
Hemorrhage from minor trauma
<50,000/mm3
91
Spontaneous bleeding
<15,000/mm3
92
Severe bleeding
<10,000/mm3
93
Sickle Cell Anemia
Mutation in beta chains of HbG | When HbG deoxygenated, beta chains link together forming long protein rods that make the cell sickle
94
Problems caused by Sickle Cell
Blocked capillaries, causing acute pain, infarctions cause chronic damage to liver, spleen, heart, kidneys, eyes and bones Pulmonary infarction > acute chest syndrome Cerebral infarction > stroke Sickled cells more likely to be destroyed
95
Ventilation
the movement of air between the atmosphere and the respiratory portion of the lungs
96
Inspiration
air is drawn into the lungs as the respiratory muscles expand the chest cavity
97
Expiration
air moves out of the lungs as the chest muscles expand the chest cavity becomes smaller
98
Perfusion
the flow of blood through the lungs
99
Diffusion
transfer of gases between air-filled spaces in the lungs and the blood