Patho Exam 4 Flashcards

1
Q

How can we tell if our patient has adequate oxygenation if cyanosis can be present with
adequate oxygenation and inadequate oxygenation can be present without cyanosis?

A

The PaO2 should be measured to determine oxygenation

Severe anemia (inadequate hemoglobin concentration) and carbon monoxide poisoning (hemoglobin is bound to carbon monoxide instead of oxygen) cause inadequate oxygenation without cyanosis.
Polycythemia vera (too many red blood cells) may cause cyanosis even when oxygenation is adequate.
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2
Q

Differentiate between dead space and shunting.

A

Dead Space: When there is a ventilation-perfusion mismatch, an area of the lung has either too little perfusion in relation to ventilation or too little ventilation in relation to perfusion. A pulmonary embolus blocks the flow of blood to an area of the lung causing too little perfusion in relation to ventilation.

Shunting: Pulmonary edema (fluid in the alveoli) and pneumonia (mucous in the alveoli) cause too little ventilation in relation to perfusion. Oxygen is unable to move quickly from the alveoli into the blood because of the water or mucous in the alveoli.

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3
Q

While suctioning a patient, when should a clean technique be used and when should a sterile technique be used?

A

Clean procedure: When suctioning the mouth and throat

Sterile procedure: When suctioning below the glottis (between the epiglottis and the trachea)

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4
Q

What determines where an aspirated object is most likely to lodge in the lungs?

A

Aspiration is the passage of fluid or solid particles into the lungs.

Because of the anatomy of the lungs, aspirated objects are more likely to enter the right bronchus than the left.
This is because the right is slightly larger than the left and is at less of an angle with the trachea than the left bronchus

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5
Q

What is the most common source of a pulmonary embolus?

A

The most common source of the embolus is deep vein thrombosis in the legs and pelvis

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6
Q

What are signs of pulmonary embolus with infarction?

A

Embolus with infarction (death of lung tissue:
*The signs and symptoms include sudden onset of pleural chest pain, tachypnea, tachycardia, and dyspnea. The patient has a “feeling of doom” or unexplained anxiety. Syncope (fainting) may occur.

  • If infarction occurs, additional symptoms may be a pleural friction rub (sounds like sand paper rubbing together when auscultating), hemoptysis (coughing up blood), fever, and leukocytosis.
  • Diagnosis is confirmed by elevated levels of D-dimer in the blood and a CT scan.

Embolus without infarction (no permanent lung damage):
* If the embolus does not cause infarction, the clot is dissolved by the body and normal pulmonary function returns

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7
Q

What is the most common cause of pulmonary edema?

A

Left heart failure

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8
Q

What are clinical manifestations of pulmonary edema?

A
  • Dyspnea and crackles heard on inspiration when auscultating the lungs
  • Hypoxemia - because the oxygen has to diffuse through the fluid to reach the capillaries, decreased oxygen levels occur in the blood.
  • Sputum appears pink and frothy due to the capillary damage
  • Whitened areas bilaterally due to the fluid replacing the air in the alveolar sacs in an x-ray
  • The mediastinum is widened and the heart appears large due to excess fluid from left heart failure
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9
Q

What is atelectasis?

A

Atelectasis is collapse of alveoli in the lungs. There are three types of atelectasis. 1. compression atelectasis caused by external pressure such as fluid or air in the pleural space; 2. absorption atelectasis, caused by an obstruction in the airway causing the air to be absorbed from the alveoli but no fresh air coming in. 3. surfactant atelectasis, caused by lack of surfactant in the alveoli which causes increased surface tension

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10
Q

What are clinical manifestations of pneumothorax and pleural effusion?

A

Pneumothorax is air in the pleural space.

Clinical manifestations of pneumothorax include, sudden pleural pain, tachypnea, and dyspnea.
In tension pneumothorax, the lung collapses and there is decreased or absent breath sounds on the affected side.
As more air collects in the pleural space, hypotension and tracheal deviation away from the affected side occurs.
A right pneumothorax causes left tracheal deviation, and vice versa.
Pleural effusion is the presence of fluid in the pleural space.

Common signs and symptoms include dyspnea, compression atelectasis, and pleural pain.
As with a large pneumothorax, a pleural effusion that is large enough will cause absent or decreased breath sounds on the affected side and tracheal deviation away from the affected side.

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11
Q

Why is tension pneumothorax life-threatening?

A

Pneumothorax is a condition that occurs as air accumulates in the pleural space and can lead to collapse of the lung. A tension pneumothorax occurs when air enters the pleural space upon inspiration but does not escape during expiration. This becomes problematic because as more air enters the pleural space, the pressure rises and compresses the lungs, heart, and the great vessels of the heart. This is a medical emergency as it affects oxygenation and tissue perfusion, as the heart is unable to pump effectively and send blood throughout the body.

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12
Q

What three conditions make breathing difficult in asthma?

A
  1. Exposure to the triggering agent leads to inflammation of the bronchi (animals, cold air, exercise, pollen, etc.)
  2. constriction of the bronchial smooth muscle
  3. mucous production in the bronchi

Untreated inflammation can lead to long-term airway damage that is irreversible called airway remodeling

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13
Q

Which of the obstructive lung diseases causes prolonged expiration?

A

asthmatic attack, chronic bronchitis, emphysema

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14
Q

What are the clinical manifestations of emphysema?

A

Expiration becomes difficult and the air is trapped in the lungs due to large air spaces in the lungs. This air trapping causes hyperexpansion of the chest (barrel chest). Prolonged expiration is always present. Dyspnea and wheezing are common and so is weight loss. Cyanosis is uncommon because polycythemia doesn’t occur until later in the disease.

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15
Q

What is the treatment for tuberculosis?

A

Treatment involves antibiotic therapy to control active disease or prevent reactivation of latent TB.

4 different drugs may be given for a minimum of 6 months.

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16
Q

What blood gas findings indicate acute respiratory failure?

A

Hypoxemia -
PaO2 less than or equal to 50mmHg (Normal PaO2 is 80-100 mmHg)

Hypercapnia-
PaCO2 greater than or equal to 50mmHg (Normal PaCO2 is 35-45mmHg)
pH less than or equal to 7.25 (normal 7.35-7.45)

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17
Q

What are clinical manifestations of acute respiratory distress syndrome (ARDS)?

A

Early Signs

  1. Marked Dyspnea
  2. Rapid, Shallow Breathing (Hyperventilation)
  3. Inspiratory Crackles (due to pulmonary edema

Late Signs
1. Respiratory Alkalosis (blowing off of CO2 (acid) with hyperventilation)
2. Hypoxemia (decreasing blood O2 levels due to pulmonary edema)
3. Lactic Acid Build-Up –> 4. Metabolic Acidosis (due to anaerobic metabolism without adequate oxygen)
Respiratory Acidosis (increased work of breathing causes CO2 retention (acid))
5. Organ Dysfunction, Hypotension, Decreased CO —> Eventual Death

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18
Q

What is the goal of treatment for pulmonary hypertension?

A

The goal is to prevent cor pulmonale or right-side heart failure

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19
Q

Which lung cancer can cause symptoms of endocrine diseases?

A

Small Cell Carcinoma causes symptoms of endocrine disease. It arises from neuroendocrine cells in the lungs that cause ectopic hormone production. Most commonly, antidiuretic hormone (ADH) is produced and symptoms of Syndrome of Inappropriate ADH (SIADH) occur. Other tumors may produce adrenocorticotropic hormone (ACTH), resulting in symptoms of Cushing Disease.

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20
Q

Which lung cancer has the weakest association with smoking and which has the strongest?

A

Weakest association- Adenocarcinoma

Strongest association- Small cell carcinoma

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21
Q

Differentiate immunity and inflammation

A

inflammation: first response to injury, nonspecific (the same way regardless of the stimulus that activated the response), cells (leukocytes, plasma proteins, and chemical mediators), no memory, cannot be induced artificially
immunity: specific against a microorganism, has memory, subsequent responses are rapid, permanent or long-term protection, induced through vaccination, cells (T lymphocytes and B lymphocytes), two purposes (destroy infectious microorganisms that are resistant to inflammation and provide long term protection against future exposure to the same organism)

22
Q

Differentiate active and passive acquired immunity

A

Active Immunity- Is produced after natural exposure to an antigen or after immunization. The Immune system produces T or B Lymphocytes which can provide long-term protection against that antigen.

Passive- Does not involve the immune system. Can occur naturally from a mother to her baby through the placenta and breast milk. Certain circumstances like rabies or hepatitis A virus in people who are unvaccinated T or B lymphocytes from a donor are administered (Immune Globin) which protects individuals because their T or B lymphocytes are eventually destroyed

23
Q

Differentiate humoral and cell-mediated immunity

A

Humoral Immunity - Involves B lymphocytes which produce proteins and antibodies. The antibodies are primarily responsible for protection against bacteria and viruses.

Cell - mediated immunity; Involves different types of T cells, these cells are important for protection against viruses, tumors, pathogens that are resistant to killing neutrophils and macrophages.

24
Q

What are the functions of the different immunoglobulins?

A

IgM- first antibody produced during initial/ primary response
IgG- fast-acting second exposure-response
IgA- protects mucous membranes in GI, pulmonary, and genitourinary tracts by preventing attachments and invasion of pathogens through mucous membranes
IgE- prevents infection from large parasites by initiating an inflammatory response that attracts eosinophils. Also, the primary cause of allergies when produced against environmental agents
IgD- antigen receptor on the surface of early B lymphocytes

25
Q

What are the functions of the different T lymphocytes?

A

T-cytotoxic cells: these cells directly attack and kills antigens (cells infected with viruses or cancerous cells)

T-helper cells: stimulate other leukocyte activity and control humoral and cell-mediated immune responses. Cytokine-producing T cells secrete cytokines that activate other cells (macrophages) in an inflammatory response

T-memory cells: remember an antigen, induce a quicker secondary response than the first response

26
Q

What are the functions of the different blood cells in the inflammatory response?

A

mast cells: most important, located close to blood vessels near the body’s outer surface.

Basophils: function the same way as mast cells. the release of histamine and chemotactic factors. the histamine causes dilation of blood vessels and increased capillary permeability. the chemotactic factors attacked neutrophils and eosinophils to the injured area.

Neutrophils: arrive 6-12 hrs after the injury. they remove debris and dead cells in non-infected injuries and destroy bacteria in infected injuries.

macrophages: replace neutrophils after 24hrs they start the healing process by cleaning the site through phagocytosis and promoting blood vessel formation and releasing growth factors.

Eosinophils: body primary defense against parasites and help regulate vascular effects of inflammation.

Platelets: work to form clots

27
Q

How does the complement system protect against bacterial infections?

A

The compliment system produces direct and indirect components of the inflammatory and adaptive immune response.
Opsonins- coat bacteria and increase susceptibility to phagocytosis by neutrophils and macrophages
Chemotactic factors- attract phagocytes to injury
Anaphylatoxins- cause release of histamine from mast cells which vasodilates and increasing capillary permeability

28
Q

What are the manifestations of acute inflammation?

A

Local: swelling, pain, heat, redness, altered function

Systemic: Fever, leukocytosis, increase in plasma proteins

29
Q

Give examples of chronic inflammation without a previous acute inflammatory response.

A

Examples of chronic inflammation without previous acute inflammatory response care tuberculosis and syphilis. In tuberculosis, the microorganisms are resistant to breakdown by phagocytes. In syphilis, the microorganisms are able to survive within the macrophage.

30
Q

Differentiate the functions of the neutrophils and macrophages during wound healing.

A

Neutrophils remove debris and dead cells in non-infected injuries and destroy bacteria in infected injuries. They are the first to arrive after the initial injury.

Macrophages come after the neutrophils. Macrophages begin the healing process by cleaning the injury through phagocytosis, angiogenesis (promoting blood vessel formation), and releasing growth factors.

31
Q

What factors contribute to dysfunctional wound healing?

A

Factors that can cause dysfunctional wound healing are ischemia, excessive bleeding, excessive fibrin deposits, diabetes mellitus, wound infection, inadequate nutrients, medications, and tobacco smoke

32
Q

What are the two most common causes of wound dehiscence

A

The two most common causes are wound infection and excessive strain on the suture line (obesity).

33
Q

What symptoms are caused by histamine release in Type I hypersensitivity reaction?

A

Histamine is released during a Type I hypersensitivity reaction causing bronchoconstriction, edema, vasodilation, and increased gastric acid secretion. The gastrointestinal tract, skin, and respiratory tract are the areas affected. Gastrointestinal tract symptoms include vomiting, diarrhea, or abdominal pain. Skin symptoms are urticaria (hives) and edema. Respiratory tract symptoms include rhinitis and wheezing caused by bronchoconstriction. Type I hypersensitivity can also lead to anaphylaxis shown by bronchospasm, hypotension, and dysrhythmias

34
Q

Give examples of Type II, III, and IV hypersensitivity reactions.

A

Type ll- Graves disease, antibody stimulates the thyroid to produce thyroid hormone results in hyperthyroidism, blood transfusion reactions

Type lll- sunlight and medication. Sun exposure can cause lupus skin lesions or trigger an internal response. Anti-seizure meds, blood pressure meds, and antibiotics can cause lupus and usually stops when meds are discontinued

Type lV- contact dermatitis, transplant reaction, positive tuberculosis test

35
Q

What is the “window period” in HIV infection?

A

The window period is when an individual who is serologically negative but can still transmit HIV to a partner. The tests for HIV are negative because the immune system has not produced enough antibody to be detected by the tests, but the person is still able to transmit the disease.

36
Q

During which stage(s) can a patient infected with HIV pass on the virus?

A

early-stage (ARS): with or without symptoms the risk of transmitting HIV is high because the levels of HIV in the blood are very high.

Clinical Latency (asymptomatic/chronic HIV infection): the virus is developing without symptoms. They can still transmit HIV to others even when on drug therapy, but antiretroviral therapy reduces the risk of transmission.

37
Q

During the stage of resistance/adaptation, what happens when cortisol and epinephrine/norepinephrine are released?

A

Cortisol: Affects carbohydrate and protein metabolism. Stimulates gluconeogenesis in the liver –> Increases blood glucose. Triggers the breakdown of protein stores in some tissues (connective tissues, bones, muscles, skin). –> Increases circulating levels of amino acids.

Cortisol aims to provide the body with more energy for “flight or flight” (glucose in blood) and the means to repair damaged tissues (amino acids for protein synthesis).

Epinephrine/Norepinephrine: Also stimulates an increase in blood glucose. Sympathetic response –> Increased heart rate, increased blood pressure, and increased respirations.

38
Q

What is the link between stress, immune system, and disease?

A

inflammation

39
Q

Differentiate benign and malignant tumors

A

Benign tumors are not cancerous. Malignant tumors are cancerous. Both can be life-threatening, depending on what they are compressing.

40
Q

Which cancer terms indicate malignant tumors?

A

The root word indicates the cell or tissue of origin. The suffixes carcinoma and sarcoma always indicate malignant tumors. The suffix -oma indicated benign tumors, with the exceptions of melanoma, glioma and lymphoma, which are malignant.

41
Q

What are the characteristics of a benign tumor?

A
  1. Well differentiated- resemble normal, mature cells.
  2. Proliferating cells are cohesive, encapsulated, and push surrounding cells aside as they grow.
  3. Do not metastasize- benign tumor cells do not spread to distant body sites.
  4. The rate of growth is usually slow- size may be stable for months to years
42
Q

What are the characteristics of a benign tumor?

A
  1. Well differentiated- resemble normal, mature cells.
  2. Proliferating cells are cohesive, encapsulated, and push surrounding cells aside as they grow.
  3. Do not metastasize- benign tumor cells do not spread to distant body sites.
  4. The rate of growth is usually slow- size may be stable for months to years
43
Q

How do malignant cells metastasize?

A
  1. Invasion or local spread (break away from the parent cells and invade local blood vessels and lymphatics)
  2. first to local lymph nodes through the lymphatics and then to distant organs through the bloodstream
  3. the cancer cells must avoid detection by the immune system and then successfully extravasate or leave the blood vessel and continue to proliferate at the new secondary site

*Cancer cells can also spread across body cavities, such as ovarian cancer spreading across the peritoneal cavity to the bladder or colon

44
Q

How do tumor markers follow the clinical course of prostate cancer?

A

Malignant tumors of the prostate secrete prostate-specific antigen (PSA) into the blood. A falling PSA level after treatment for prostate cancer indicates successful treatment. A subsequent rise in PSA level may indicate recurrence.

45
Q

What is the most common mutation to produce oncogenes?

A

The most common mutation to produce oncogenes is a small-scale change in DNA (point mutation), which means one or a few nucleotide base pairs are altered.

46
Q

How do mutations in apoptosis genes produce cancer?

A

Apoptosis genes control programmed cell death to eliminate aging cells or damaged cells from the body. Mutations cause failure of these cells to die which leads to an increase of these cells. B-cell lymphoma occurs when B-lymphocytes are not eliminated from the body and that produces cancer.

47
Q

What chemical modifications cause epigenetic silencing of genes?

A

DNA methylation (adding a methyl group) and histone modifications (adding a methyl or acetyl group) are both chemical modifications that cause epigenetic silencing of genes.

48
Q

What properties must cancer cells develop to survive and grow?

A

They must either gain the ability of secreting their own growth factors, or increase in growth factor receptors. They must become insensitive to anti-growth signals. They have to become resistant to apoptosis. They have to have their own blood supply for oxygen and nutrients. They are able to develop immortality by activating an enzyme called telomerase which places and maintains caps on each chromosome - so they don’t become smaller and signal the cell to die.

49
Q

What are causes of cancer?

A

VIRAL

  • Chronic Hepatitis B (HBV)
  • Chronic Hepatitis C (HCV)
  • Human papillomavirus (HPV)

BACTERIAL
-Helicobacter pylori (H. pylori)

ENVIRONMENTAL

  • Tobacco use
  • Alcohol
  • Diet/activity
  • Air pollution
  • Ultraviolet sunlight
  • Ionizing radiation
50
Q

Differentiate the two common staging systems for cancer.

A

The stage system goes like this:
Stage 1- indicates cancer is confined to the organ or tissue of origin.
Stage 2- the cancer is locally invasive
Stage 3- it has spread to regional structures, like the lymph nodes, for example.
Stage 4- cancer has spread to distant sites.

TNM system:

  • T - indicates the primary tumor. Using 0-3 equals the size of tumor and the extent of spread. For example in breast cancer, T0 means that the breast is tumor free, while T3 means the tumor has invaded the skin or chest wall.
  • N- indicates if there is lymph node involvement. 0-2 indicates node involvement. For example, N1 means there are mobile nodes involved, and N2 means there are fixed nodes involved which means greater involvement.
  • M- indicates the extent of metastasis. 0-2 indicates the degree of metastases.