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Differential Diagnosis > Screening for Cardiopulmonary Disorder Lecture > Flashcards

Screening for Cardiopulmonary Disorder Lecture Flashcards

1
Q

Symptoms of Cardiac disease include…

A

Chest pain or discomfort

Palpitation

Dyspnea

Cardiosyncope

Fatigue

Cough

Cyanosis

Claudication

Vital signs

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2
Q

What are the three categories of cardiac diseases?

A

Heart muscle

Heart valves

Cardiac nervous system

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3
Q

What are certain conditions which affect the heart muscle?

A

Obstruction or restriction

Inflammation

Dilation of distension

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4
Q

What is the epidemiology of atherosclerosis?

A

Contributes to 1/2 of all deaths in the western world

Can lead to ischemic heart disease (IHD), cerebral infarct, kidney failure, aneurysms, and peripheral vascular disease resulting in gangrene

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5
Q

What are some risk factors for atherosclerosis and ischemic heart disease?

A

Cigarette smoking
- smoking 1 or more packs/day increases mortality by 200%

High fat (especially cholesterol) diet

  • hypercholesterolemia (familial or dietary) is a major risk factor for atherosclerosis
  • cholesterol is found in high levels in animal fat, butter, and egg yolks

Hypertension
- Males aged 45-62 whose pressure is 169/95 or higher have 500% greater risk of ATH than those whose pressure is 140/90

Uncontrolled diabetes mellitus
- DM induces hypercholestrolemia

Age
- ATH is more common in middle age or older people

Sex
- Men are more commonly affected

Genetics
- Many factors leading to HTN/hypercholesterolemia

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6
Q

What is the pathogenesis of atherosclerosis? (Fatty streak)

A

Many think the first indication of vessel disease, which may progress to ATH, is the deposition of lipids in the tunica intima of arteries.

Streaks are particularly noticeable around the openings of vessels

They are thought to be due to the stresses on the endothelium caused by the loss of laminar flow near openings of vessels

All children have fatty streaks by the time they are 10 years old

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7
Q

What are the steps of atherosclerosis pathogenesis?

A
  1. Chronic endothelial “injury”
    - Hyperlipidemia
    - HTN
    - Smoking
    - Homocysteine
    - Hemodynamic factors
    - Toxins
    - Viruses
    - Immune reactions
  2. Endothelial dysfunction
    - Increased permeability, leukocyte adhesion, monocyte adhesion and emigration
  3. Smooth muscle emigration from media to intima. Macrophage activation
  5. Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
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8
Q

What are atheromas capable of doing?

A

Occlude the lumen of the vessel

Cause thrombus formation

Erode into the media leading to development of an aneurysm

Produce emboli

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9
Q

What is the epidemiology of HTN?

A

In its early stages, HTN is asymptomatic, but it can lead to:

Cardiac hypertrophy
Heart failure
Aortic dissection
Renal failure

Most of the time the cause is unknown

Often due to kidney disease

25% of general adult population is HTNsive

Most common in African Americans

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10
Q

What is the formula for blood pressure?

A

BP = Cardiac output x Peripheral resistance

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11
Q

How is blood pressure regulated?

A

Slide 18

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12
Q

What is the vascular pathology in HTN?

A

Athromas can occlude the renal arteries. Juxtaglomerular complex detects low BP and secretes renin. BP is raised by the angiotensin-aldosterone pathway

LEADING TO OR CAUSED BY:

Increased BP causes hemodynamic disturbances of the blood flow and the formation of athromas

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13
Q

What is an aneurysm?

A

Localized bulging of a blood vessel or of the heart

Due to weakening of the wall of the vessel

Major cause is atherosclerosis

HTN can cause aneurysm formation in a weakened artery

Can burst leading to sudden severe blood loss, or can cause damage by pressing on surrounding tissues

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14
Q

What is a dissection?

A

Occurs when blood enters the wall of a vessel, separating its layers. It usually (but not always) is a complication of aneurysm

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15
Q

Where is the most common site of aneurysm?

A

Lower abdominal aorta

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16
Q

What are varicose veins?

A

Superficial leg veins which do not cause serious problems and even though they are usually thrombosed, they do not often throw an emboli

Deep leg veins, on the other hand, when thrombosed (thrombophlebitis) do form emboli

Factors contributing to thrombophlebitis include:

  • Cardiac failure
  • Prolonged bed rest
  • Immobilization
  • Obesity
  • Pregnancy
  • Neoplasia
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17
Q

When does congestive heart failure (CHF) occur?

A

When the heart is unable to pump out as much blood as enters (or tries to enter) it

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18
Q

What are the most common causes of CHF?

A

HTN–peripheral resistance too great to pump against

Mitral or aortic valve disease–when the heart pumps , blood flows both forward into the aorta and backward into the heart chambers

Ischemic heart disease–lack of blood supply to the heart muscle reduces its capacity to pump

Infarction–a healed infarct leaves scar tissue that reduces the ability of the heart to pump

Primary diseases of the myocardium

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19
Q

What is the pathogenesis of CHF?

A

As the heart fails, several adaptive responses occur:

Increase in sympathetic stimulation–increasing heart rate and force of contraction

Hypertrophy of the individual heart muscle cells occur most commonly in situations of increased pressure (HTN)

DILATION of the heart chambers occurs most commonly when there is an increase in volume (as in valvular disease)

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20
Q

What is the pathogenesis cascade of CHF?

A

Hypertrophy often leads to dilation–enlarged cells need more oxygen. If the coronary blood supply cannot enlarge fast enough, the hypertrophied heart becomes ischemic, preventing it from performing adequately and leading to increased heart failure. The increased pressures generated stretch the muscle cells causing dilation

Compensated CHF–the hypertrophied and dilated heart can meet the needs of the body

Decompensated CHF–the heart cannot meet the needs of the body

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21
Q

What is the pathogenesis of CHF associated with the lungs?

A

Failure of the left side of the heart causes pulmonary HTN and congestion of the pulmonary venous system. The increased pressure leads to pulmonary edema in which edema fluid fills the interstitial tissue and ultimately the alveoli. Pulmonary HTN can also cause right side heart failure as the right ventricle tries to push more blood into the pulmonary circulation

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22
Q

What is the pathogenesis of CHF pertaining to the kidneys?

A

Kidney reacts to decreased perfusion as it would to HTN. To increase the BP, it releases renin activating the renin-angiotensin system. Sodium and water are resorbed and more fluid is added to the already overburdened heart

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23
Q

What is the pathogenesis of CHF pertaining to the liver?

A

The venous HTN causes congestion in liver. Lack of oxygen due to pulmonary edema affects the cells in the central part of each liver lobule and may lead to their death. A liver with this pattern of cell death is called a “nutmeg liver”

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24
Q

What are the clinical features of CHF?

A

Dyspnea–SOB due to pulmonary edema. In severe cases the patient may feel as though he/she is drowning. The dyspnea may be more severe during physical activity or when lying down. A patient with pulmonary edema may need to sleep with his head elevated

Atrial fibrillation–leading to an “irregularly irregular” heartbeat. The pulse is extremely erratic

Soft tissue edema due to venous congestion. Fluid retention and edema are very common in CHF. Unlike inflammatory edema, CHF edema has a low protein content. The edema may affect dependent areas such as the feet and legs, cause ascites, or be generalized

Cyanosis due to poor oxygenation and delivery of the blood

The average length of time from diagnosis of CHF to death in 5 years

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25
Q

What is ischemic heart disease?

A

Occurs when the cardiac muscle does not get enough blood to meet its demands. Note that ischemia refers to lack of nutrients brought by the blood in addition to oxygen

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26
Q

What is the etiology of ischemic heart disease?

A

Over 90% of IHD cases are due to atherosclerosis of the coronary arteries. For this reason it is often called “coronary heart disease”

  • HTN
  • Smoking
  • Uncontrolled diabetes
  • Hypercholesterolemia
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27
Q

What is the epidemiology of IHD?

A

Most common in older people

Men are more commonly affected–except in the very elderly

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28
Q

What is the pathogenesis of IHD?

A

Fixed obstruction: 75% occlusion = angina pectoralis
- Stable angina

Plaque instability plaque rupture, fissure, hemorrhage

  • Thrombus formation
  • Embolus formation
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29
Q

What is stable angina?

A

Usually 70% or greater occlusion

Occurs after exercise

Treatment–nitroglycerin

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30
Q

What is prinzmetal angina?

A

Occurs at rest

Probably due to coronary artery spasm

Treatment–nitroglycerin

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31
Q

What is unstable angina?

A

Attacks with increased frequency and severity

Usually due to thrombus formation on a plaque

Often a precursor of infarction

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32
Q

What are treatments for IHD?

A

Balloon angioplasty–a catheter is inserted into the affected coronary artery and, when in place, a “balloon” at its tip is expanded. This compresses the arthroma and enlarges the lumen of the vessel

Coronary stent

  • Bare metal stent–a mesh tube that is inserted after balloon angioplasty holds the vessel open. Endothelium grows over the wire mesh preventing contact with blood
  • Drug eluting stents–are impregnated with anti-proliferation drugs that prevent restenosis. These are being closely watched as some research indicates that the drugs prevent the endothelium from covering the stent resulting in late thrombosis

Coronary bypass surgery–affected coronary arteries are replaced by veins or synthetic vessels

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33
Q

What is the epidemiology of myocardial infarction (IHD)?

A

Most common cause of death in industrialized nations

1.5 million/year in U.S: 1 in 3 die

5 times as common in middle aged men than women

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34
Q

What is the pathogenesis of MI?

A

Most acute cases are caused by coronary artery thrombosis which is commonly due to the rupture of an atherosclerotic plaque

Roughly 1/2 of all infarcts involve the anterior interventricular artery (left anterior descending coronary artery) which is the major supply to the left ventricle and the anterior portion of the interventricular septum

Stages of injury:

  • Coagulation necrosis
  • Inflammation
  • Formation of granulation tissue
  • Fibrosis and scar formation

Subendothelial and transmural infarcts

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35
Q

What is the pathogenesis of coagulation necrosis?

A

First stage of infarction is coagulation necrosis. Dead cardiac myocytes are highly eosinophilic (red is dead). The spaces between the cells are filled with edema fluid and nuetrophils

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36
Q

What is the pathogenesis of inflammation following MI?

A

A 3-4 ay old infarct shows coagulation necrosis and infiltration by numerous neutrophils

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37
Q

What is the pathogenesis of removal of debris following MI?

A

After a week, necrotic tissue removed and fibroblasts are invading infarct

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38
Q

What is the pathogenesis of granulation tissue following MI?

A

After 3 weeks, infarct area is filled with granulation tissue

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39
Q

What is the pathogenesis of fibrosis following MI?

A

Healed infarct showing blue stained fibrous scar tissue on a slide

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40
Q

What are some complications which result from MI?

A

EXTERNAL RUPTURE OF THE WALL OF THE HEART

  • Usually occurs during first week when the damaged myocardium is being replaced by granulation tissue
  • Occurs in 10% of patients who die in the hospital of MI
  • Death is due to cardiac tamponade (fluid around the heart)

RUPTURE OF THE IV SEPTUM

  • Usually occurs during the first week when the damaged myocardium is being replaced by granulation tissue
  • Occurs in 1% of patients with MI
  • Results in left-to-right shunt and CHF

PAPILLARY MUSCLE RUPTURE
- Results in severe valvular dysfunction

VENTRICULAR ANEURYSM

  • Develop at the site of a healed infarct
  • Frequently contain mural thrombi
  • Non-contractile
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41
Q

What are the clinical features of MI?

A

SEVERE, CRUSHING SUB-STERNAL PAIN that may radiate to the left shoulder and arm, neck and jaw, and/or epigastric region. Pain lasts for hours-days and is not helped by nitroglycerin

PULMONARY CONGESTION AND EDEMA which may lead to dyspnea

ECG ABNORMALITIES
and ARRHYTHMIAS

SUDDEN DEATH–25% of MI sufferers never make it to the hospital

42
Q

What does uncontrolled hypertension lead to?

A

Left ventricular hypertrophy

43
Q

What is valvular heart disease?

A

Usually affects the mitral valve and leads to stenosis of the left atrioventricular orifice and/or regurgitation

44
Q

What are some common causes of valvular heart disease?

A

Rheumatic heart disease

Sensile calcification

Non-infective inflammation

Inflammation

Congenital defects

45
Q

What are “Vegetations” associated with valvular heart disease?

A

Inflammatory swellings that contain inflammatory cells, necrotic tissues, and may include microorganisms

46
Q

What is rheumatic heart disease?

A

An inflammatory response that develops in a small number of patients after strep throat.

Some strains of strep seem more likely to lead to rheumatic fever than others.

Rheumatic fever develops 3-4 weeks after pharyngitis and may be acute or chronic.

It is thought that anti-strep antibodies react to connective tissue elements normally found in the heart and other tissues

47
Q

What is infective endocarditis most commonly caused by?

A

Bacterial infection

48
Q

What is coarcation of the aorta?

A

Drastic narrowing of the vessel

49
Q

What does an atrial septal defect look like?

A

See ppt (61)

50
Q

What does an atrioventricular septal defect look like?

A

See ppt (62)

51
Q

What does transposition of the great vessels look like?

A

See ppt (63)

52
Q

What is persistent truncus arteriosus?

A

See ppt (64)

53
Q

What are the characteristics of tetralogy of fallot?

A

Stenosis of the pulmonary trunk

Ventricular septal defect

Overriding aorta

Enlarged right ventricle

54
Q

What does tetralogy of fallot look like?

A

see ppt (65)

55
Q

What are the different diseases of the respiratory system?

A

Collapsed lung

Asthma

COPD

  • Emphysema
  • Chronic bronchitis

Restrictive lung diseases

  • ARDS (acute respiratory distress syndrome)
  • Chronic restrictive lung diseases

Vascular lung diseases

  • Thromboembolism
  • Hemorrhage
  • Infarction pulmonary HTN

Pulmonary infections

Lung cancer

56
Q

What are the characteristics of Asthma?

A

Edema

Bronchoconstriction

Excessive mucous prodction

Thick mucous

Chemotaxis of eosinophils

57
Q

What is asthma categorized as?

A

Type I Hypersensitivity reaction

58
Q

What is the epidemiology of emphysema?

A

3 million Americans have symptomatic emphysema

COPD is 4th leading cause of mortality in America (100k deaths/yr)

Beginning in 2000, women exceeded men in COPD deaths

59
Q

What is the etiology of emphysema?

A

Smoking #1 cause

Air pollution is a rising cause

Hereditary emphysema caused by deficiency of alpha-1-antitrypsin, but is only a fraction of the total number of cases

60
Q

What are other risk factors for emphysema?

A

Exposure to second-hand smoke

Age

Occupational exposure to chemical fumes

Air pollution

HIV infection

61
Q

What is the pathogenesis CASCADE for emphysema?

A

Stimulus increases number of macrophages which secrete chemoattractants for neutrophils. Neutrophils accumulate in the alveolar lumen and interstitium

  1. Neutrophils release elastase into the alveolar lumen
  2. Serum alpha-1 antitrypsin neutralizes elastase and prevents its destructive effect on the alveolar wall
  3. Persistent stimulus continues to increase the number of neutrophils and macrophages in the alveolar lumen and interstitium
  4. Neutrophils release elastase into the alveolar lumen and interalveolar space
  5. Serum alpha-1-antitrypsin levels decrease and elastase starts the destruction of elastic fibers, leading to the development of emphysema. Damaged elastic fibers cannot recoil when stretched
62
Q

What are the characteristics of CENTRIACINAR emphysema?

A

Wall of respiratory bronchioles is destroyed by elastases and other proteases

63
Q

What are the characteristics of PANACINAR emphysema?

A

Wall of respiratory bronchioles, alveolar ducts, and alveoli are destroyed by elastases and other proteases

64
Q

Generally, what is the pathogenesis behind emphysema?

A

Alveolar septa are destroyed resulting in the formation of large air spaces. In bullous emphysema, large hollow “bubbles” replace normal lung architecture

65
Q

What are the clinical features of emphysema?

A

First sign of emphysema is usually dyspnea

Cough and wheezing

Weight loss

“Barrel chest” due to accumulation of air in the lung

In late stages of disease, especially when accompanied by chronic bronchitis, patients become cyanotic and obese. They are commonly called “blue bloaters”

66
Q

What are the treatments of emphysema?

A

STOP SMOKING

Supplemental oxygen

Protein therapy for hereditary cases

Antibiotics and vaccination to treat/prevent associated infections

Surgery for some cases

Aerobic exercise to increase fitness

67
Q

What is the epidemiology of chronic bronchitis?

A

20-25% of all men ages 40-65 have chronic bronchitis

Common in cigarette smokers and often occurs with emphysema

68
Q

What is the clinical definition of chronic bronchitis?

A

Persistent cough with sputum production that occurs several times/week for a minimum of three months in two consecutive years

69
Q

What is the possible sequelae of chronic bronchitis?

A

Emphysema

Heart failure

Metaplasia, dysplasia, cancer

70
Q

What is the pathogenesis of chronic bronchitis?

A

Exposure to smoke and/or other pollutants results in inflammation first of the large airways

Irritants of smoke cause hypersecretion of mucous from epithelium and underlying mucosal glands

With continued irritation, respiratory epithelium undergoes metaplasia to stratified squamous epithelium resulting in the loss of the “ciliary elevator” that moves particulate matter out of the lungs

Submucosal mucous glands hypertrophy

71
Q

What is the clinical course of chronic bronchitis?

A

Presents with a chronic cough with sputum production

May progress to emphysema

Loss of “ciliary elevator” resulting in even more lung infections

72
Q

What is the definition of restrictive lung diseases?

A

Diseases which make it difficult for the lungs to inflate (reduced compliance)

Sometimes called interstitial lung diseases because the CT interstitium becomes prominent

73
Q

What are the characteristics of acute restrictive lung disease?

A

Sudden onset

Pulmonary edema

Inflammation

74
Q

What are the characteristics of chronic restrictive lung disease?

A

Chronic inflammation

Interstitial fibrosis

75
Q

What is the pathogenesis of acute respiratory distress syndrome (ARDS)?

A

Injury to respiratory membrane and type II alveolar cells resulting in increased vascular permeability and decreased surfactant production

Injury is thought to be due to an imbalance between pro-inflammatory and anti-inflammatory cytokines

Neutrophil infiltration of the alveoli, interstitium, and vessels leads to the release of proteases, LTs, reactive oxygen molecules, and P.A.F.

76
Q

What is the pathogenesis of acute respiratory distress syndrome (ARDS)?

A

EARLY DISEASE (0-7 days)

  • Grossly lungs are dark red, heavy, airless (look like liver)
  • Microscopically, lungs are congested, epithelium is necrotic, interstitial and alveolar edema, hemorrhage
  • Hyaline membranes (fibrinous edema fluid and cellular debris)

PROLIFERATIVE PHASE (1-3 weeks)

  • Proliferation of type II alveolar cells
  • Phagocytosis of hyaline membranes
77
Q

What is the clinical course of acute respiratory distress syndrome (ARDS)?

A

80% of patients develop ARDS within 72 hours of injury

Mortality has been reduced to ~40% from 100% by treatment methods

Patients who survive and do not develop chronic sequelae, return to normal function in 6-12 months

78
Q

What are the major types of chronic restrictive lung disease?

A

IMMUNOLOGIC:

  • SLE
  • RA
  • Systemic sclerosis

OCCUPATIONAL OR ENVIRONMENTAL PNEUMOCONIOSES:

  • Asbestosis
  • Silicosis
  • Coal worker’s pneumoconiosis (“black lung disease”)

DRUG OR TREATMENT RELATED:

  • Chemotherapeutic agents
  • Ionizing radiation
  • Oxygen
79
Q

What is some info related to Pneumoconiosis?

A

Caused by inhalation and deposition of mineral dusts in the lungs

Generally taken 20-40 years for development of clinical effects

Early pneumoconiosis is usually asymptomatic, but advanced disease results in disability and early death

There is no effective treatment for these diseases

Between 1968 and 2000, there were 124,846 deaths listed as being due to pneumoconiosis

Comparing 1968-1981 with 1982-2000, there has been a decline in silicosis (-70%) and coal worker’s pneumoconiosis (-36%), but an alarming increase in asbestos (+400%)

80
Q

What is the most common lung disease in the world?

A

Silicosis

81
Q

What is some info related to Silicosis?

A

Caused by inhalation of airborne crystalline silica

Most common form of crystalline silica used is ground quartz

Silica is used in concrete and asphalt, ceramics and pottery, electronics, and as abrasives

If the silica is powdered and aerosolized, it can be inhaled where it lodges in the alveoli

Silicosis takes years to develop and symptoms are not present until late in the disease when decreased respiratory function may severely limit activity

Silica crystals initially deposit in the upper lobes of the lungs

May be phagocytized by macrophages, but commonly kill the cells

Before dying, the macrophages release cytokines and other mediators that stimulate fibrosis

82
Q

What is coal worker’s pneumoconiosis (“black lung disease”)?

A

Occurs as a result of the inhalation of coal dust and takes three forms:

  1. Asymptomatic anthracosis–accumulation of coal with no cellular reaction
  2. Simple coal worker’s pneumoconiosis (CWP)–macrophages congregate around the coal with no pulmonary dysfunction
  3. Complicated coal worker’s pneumoconiosis AKA “progressive massive fibrosis (PMF)”–severe fibrosis occurs and pulmonary function is compromised

From 1968-1998, CWP was the most commonly diagnosed pneumoconiosis, but it has recently declined due to safety equipment in mines

Antharcosis is seen in city-dwellers, smokers, and coal workers

Inhaled carbon is engulfed by macrophages and accumulates in the connective tissue of the lung

CWP is seen in both smokers and coal workers

May progress to centrilobar emphysema or to PMF (10% of cases)

In the absence of smoking, CWP does not progress to cancer

PMF takes many years to develop

PMF is characterized by multiple black scars 2-10 cm in diameter

83
Q

What is some information on asbestosis?

A

Asbestos is the commercial name given to any of 6 silica-based minerals that form long fibers

Because of its resistance to abrasion and heat, it is used to manufacture various insulation materials and auto brakes

There are types of asbestos, defined by the shape of the fibers:

  1. Chrystolite–form long, flexible, curly fibers (used in most of industry)
  2. Amphibole–more toxic

Takes 20-40 years to develop

Smokers exposed to asbestos have a 55% greater chance of developing asbestosis than non-smokers

84
Q

Why are the reasons why amphibole asbestos is so toxic?

A

Straight fibers align with the airways and can be carried all the way to the alveoli

They easily break into many small pieces

85
Q

Asbestosis can cause what?

A

Pleural effusion

Pleural fibrous plaques

Bronchogenic carcinoma

Mesotheliomas

86
Q

What makes asbestosis so dangerous?

A

Macrophages can not “digest” asbestos fibers–septa becomes thick with fibrosis

87
Q

What is some general information on influenza?

A

Belongs to the orthomyxoviridae family of viruses

Three types: A, B, & C which can all infect humans

Some type A also affects birds, pigs, horses, and seals

Typically in humans, it is type A which causes “the flu”

88
Q

What is community-acquired pneumonia?

A

Abrupt onset characterized by high fever, chills, chest pain, productive cough

89
Q

What is community-acquired pneumonia most common in?

A

CHF, COPD, and diabetic patients

Immunosuppressed (AIDS, transplant patients)

Decreased splenic function (sickle-cell or post splenectomy patients)

90
Q

What are some bacterial infections that often follow viral infections of the upper respiratory tract?

A

Strep (most common)

Haemophilus influenzae (most common pneumonia in COPD patients)

Moraxella catarrhalis (seen in COPD patients and the elderly)

Staph (most common secondary pneumonia after virus)

Legionella pneumophilia (“Legionnaire’s disease” associated with air condition)

Enterobacteriaceae (seen in the malnourished)

91
Q

What is the epidemiology of tuberculosis?

A

Infects 1/3 of the world’s population and kills 3 million people/yr

After introduction of antibiotics, the incidence declined in industrialized countries

New, drug-resistant strains have emerged and TB is on the rise again

92
Q

What is the etiology of tuberculosis?

A

Caused by mycobacterium tuberculosis or M. bovis, aerobic bacili

M. Tuberculosis evades killing by macrophages and induces delayed hypersensitivity reactions

It can live in phagosomes

93
Q

What is the pathogenesis of tuberculosis?

A

Organism is inhaled and carried to the lungs where it is taken up by alveolar macrophages

Organism grows and reproduces in phagosomes of macrophages, ultimately killing the cell

Released bacteria then spreads to other cells

Primary infection is the GHON COMPLEX which consists of a subpleural lesion (usually along the oblique fissure) shown here at the upper pale arrow, and enlarged caseous lymph nodes draining the lesion shown at the lower dark arrows

Cellular immunity develops after a few weeks

T-cells kill M. tuberculosis in two ways:

  1. CD4 cells secrete interferon-gamma which activates macrophages to kill the bacteria through reactive nitrogen intermediates (NO, NO2, HNO3)
  2. CD8 cells secrete toxins that lyse infected macrophages and kill the bacteria resulting in caseous necrosis

Most cases are asymptomatic, but in children or immunosuppressed adults, TB can either become dormant forming a latent infection or progress to disseminated TB

Latent infections can be reactivated to produce a massive secondary infection of the lungs, which erodes the bronchioles causing cavitation

Either a primary or secondary TB can become disseminated by traveling through the lymphatics to infect other organs

Common sites of spread are to the bone marrow, liver, spleen, and retina. This is termed TB

94
Q

What is the epidemiology of lung cancer?

A

Most common cause of cancer deaths in both men and women

Peak incidence is from 55-65 years of age

At diagnosis, 75% already have metastases

  • 50% have distant metastases
  • 25% have metastases to regional lymph nodes
95
Q

What is the etiology of lung cancer?

A

TOBACCO SMOKING

  • The amount of daily smoking
  • The tendency to inhale
  • Duration of the smoking habit

Average smokers have a 10x greater risk; heavy smokers have a 20x greater risk than non-smokers

96
Q

What is the pathogenesis of lung cancer?

A

Nearly all lung cancers develop from respiratory epithelium

Most lesions originate at branch-points where inhaled particles impact on the epithelium

97
Q

What are the difference classifications of lung cancer?

A

Squamous cell carcinoma

Adenocarcinoma

Small cell carcinoma (Oat cell carcinoma)

Large cell carcinoma

98
Q

What are some characteristics of squamous cell carcinoma?

A

Closely correlated with smoking history

Arises in larger bronchi

Rapidly progresses through squamous metaplasia, dysplasia, to carcinoma

99
Q

What are some characteristics of Adenocarcinoma?

A

Most common type in non-smokers (but 75% are in smokers)

More peripherally located and slower growing than squamous cell carcinoma

100
Q

What are some characteristics of Small cell carcinoma (oat cell carcinoma)?

A

Closely related to smoking history (only 1% in non-smokers)

Highly malignant, most aggressive, metastasizes widely, incurable by surgery

Cells look like large lymphocytes (oat cells)

Probably derived from neuroendocrine cells of the epithelium

101
Q

What are some characteristics of Large cell carcinoma?

A

Probably represent squamous cell and adeno- carcinomas that are so undifferentiated they cannot be classified

102
Q

What is the clinical course of lung cancer?

A

PRESENTING COMPLAINTS:

  • Cough
  • Weight loss
  • Chest pain
  • Dyspnea

5 YEAR SURVIVAL RATE

  • Squamous cell carcinoma and adenocarcinoma 10%
  • Large cell (undifferentiated) carcinoma 3%
  • Small cell (oat cell) carcinoma 0% (1 year with treatment)

ONLY 20-30% are operable

30-40% survival for surgical removal of solitary tumors < 4 cm (uncommon since most tumors have already metastasized when diagnosed)

Differential Diagnosis (5 decks)

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