Archive | November 2020

Part II Etiology and Pathogenesis of COPD – Chronic Obstructive Pulmonary Disease

copd-facts  copd-facts2



By far the most common etiological cause of COPD remains smoking. Even after the client quits smoking, the disease process continues to worsen. Air pollution and occupation also play an important role in COPD. Smog and second-hand smoke contribute to worsening of the disease.

Occupational exposure to irritating fumes and dusts may aggravate COPD. Silicosis and other pneumonoconioses may bring about lung fibrosis and focal emphysema. Exposure to certain vegetable dusts, such as cotton fiber, molds and fungi in grain dust, may increase airway resistance and sometimes produce permanent respiratory impairment. Exposures to irritating gases, such as chlorine and oxides of nitrogen and sulfur, produce pulmonary edema, bronchiolitis and at times permanent parenchymal damage.

Repeated bronchopulmonary infections can also intensify the existing pathological changes, playing a role in destruction of lung parenchyma and the progression of COPD.

Heredity or biological factors can determine the reactions of pulmonary tissue to noxious agents. For example, a genetic familial form of emphysema involves a deficiency of the major normal serum alpha-1 globulin (alpha-1 antitrypsin). A single autosomal recessive gene transmits this deficiency. The homozygotes may develop severe panlobular emphysema (PLE) early in adult life. The heterozygotes appear to be predisposed to the development of centrilobular emphysema related to cigarette smoking. The other better-known cause of chronic lung disease is mucoviscidosis or cystic fibrosis, which produces thickened secretions via the endocrine system and throughout the body.

Aging by itself is not a primary cause of COPD, but some degree of panlobular emphysema is commonly discovered on histopathologic examination. Age related dorsal kyphosis with the barrel-shaped thorax has often been called senile emphysema, even though there is little destruction of interalveolar septa. The morphologic changes consist of dilated air spaces and pores of Kohn.


The pathogenesis of COPD is not fully understood despite attempts to correlate the morphologic appearance of lungs at necropsy to the clinical measurements of functioning during life. Chronic bronchitis and centrilobular emphysema do seem to develop after prolonged exposure to cigarette smoke and/or other air pollutants. Whatever the causes, bronchiolar obstruction by itself does not result in focal atelectasis, provided there is collateral ventilation from adjacent pulmonary parenchyma via the pores of Kohn.

It has been proposed that airway obstruction at times may result in a check-valve mechanism leading to overdistension and rupture of alveolar septa, especially if the latter are inflamed and exposed to high positive pressure (i.e. barotrauma). This concept of pathogenesis of emphysema is entirely speculative. Airflow obstruction alone does not necessarily result in tissue destruction. Moreover, both centrilobular and panlobular emphysema may exist in lungs of asymptomatic individuals. It has been reported that up to 30% of lung tissue can be destroyed by emphysema without resulting in demonstrable airflow obstruction. Normally, radial traction forces of the attached alveolar septa support the bronchiolar walls. With loss of alveolar surface in emphysema, there is a decrease in surface tension, resulting in expiratory airway collapse. Additional investigative work continues in an effort to link disease states to pathogenesis.

Control of Ventilation

A brief description of respiratory control mechanisms will help the nurse better understand how the progression of COPD results in pathophysiologic changes. The respiratory centers impart rhythmicity to breathing. The sensory-motor mechanisms provide fine regulation of respiratory muscle tension and the chemical or humoral regulation that maintains normal arterial blood gases. This will help the nurse to understand why hypercapnia (increased PaCO2) results in the COPDers’ extreme reliance on the hypoxic drive.

The reticular formation of the medulla oblongata constitutes the medullar control center responsible for respiratory rhythmicity. The mechanism whereby rhythmicity is established is not clear, but it may be the end result of the interaction of two oscillating circuits, one for inspiration and one for expiration, which inhibit each other. Although medullar centers are inherently rhythmic, medullar breathing without pontine influence is not well coordinated; therefore, pontine as well as medullar centers participate in producing normal respiratory rhythm.

In the pons, a neural mechanism has been identified as the pneumotaxic center. Stimulation of this center leads to an increase in respiratory frequency with an inspiratory shift, whereas ablation of the center leads to a slowing of respiration. The pneumotaxic center has no intrinsic rhythmicity but appears to serve by modulation of the tonic activity of the apneustic center. The latter is located in the middle and caudal pons. Stimulation of the apneustic center results in respiratory arrest in the maximal inspiratory position, or apneusis.

Respiratory muscles, like other skeletal muscles, possess muscle spindles, which, by sensing length, form a part of a reflex loop that assures that the muscle contraction is appropriate to the anticipated respiratory load and required effort. This servo-­mechanism facilitates fine regulation of respiratory movements and may stabilize the normal respiration in spite of changes in mechanical loading. Breathing is automatic when the respiratory load is constant or when changes in load are subconsciously anticipated. Thus, because it is anticipated, we are not consciously aware of the increase in expiratory resistance during phonation. Under such circumstances the increase in effort is not sensed because it is appropriate to the expected load.

It has been suggested that signals from respiratory muscle and joint mechano-receptors are integrated to produce a sensation that may reach consciousness when there is this “length tension appropriateness.”

Humoral regulation of the medullar centers is mediated by chemosensitive areas in the medulla and through peripheral chemoreceptors. Peripheral chemoreceptors are primarily responsible for the hypoxic drive. These receptors are highly vascular structures located at the carotid bifurcation and arch of the aorta. A diminution of oxygen supply results in anaerobic metabolism in cells of these carotid and aortic bodies. The resulting locally produced metabolites stimulate receptor nerve endings and, through signals conveyed to medullar control centers, lead to increased ventilation. The extremely high blood flow of the chemoreceptors and their almost immeasurable arterial-venous difference make them sensitive to reduced arterial oxygen tension (PaO2) but not to a reduction in oxygen content alone. However, a decrease in blood flow to these chemoreceptor organs, by permitting accumulation of metabolites, results in their stimulation and an increase in ventilation. Very high PaCO2 minimizes receptor stimulation regardless of blood flow.

A decrease in arterial pH also stimulates these peripheral chemoreceptors. The stimulation resulting from an increase in arterial carbon dioxide tension (PaCO2) is probably secondary to the increase in pH. The effect of pH has been attributed to dilatation of arteriovenous anastomoses in the periphery of the chemoreceptor bodies, with resulting reduction in blood flow to the chemosensitive cells. However, the effect of carbon dioxide and pH on respiration is mediated only to a limited extent by peripheral chemoreceptors. Denervation of these receptor organs abolishes the hypoxic drive to respiration but has little effect on the influence on ventilation of carbon dioxide or pH.

Changes in PaCO2 have a profound effect on central chemoreceptors located in the medulla. These are primarily responsible for mediating the hypercapnic respiratory drive. The precise location and characteristics of these central chemoreceptor sites nor their neural connections with the medullar respiratory control centers have been established. The chemosensitive areas appear to be directly responsive to hydrogen ions rather than to carbon dioxide.

Central chemoreceptors are sensitive to changes in pH, and through this mechanism they appear to be specifically responsive to PaCO2. Hydrogen ions themselves do not readily traverse the blood-brain barrier. Under normal circumstances, CO2 plays the primary role in chemical control of ventilation while PaO2 and extracellular pH have lesser roles. Normal subjects increase their ventilation more than two-fold while breathing 5% CO2 gas mixture.

Chronic elevation of PaCO2 (hypercapnia) is found in patients having COPD. The respiratory response to CO2 is markedly diminished in these clients and they become markedly sensitive to their diminished PaO2 (hypoxemia). An exuberant use of oxygen for hours may have dire consequences by removing the dominant respiratory stimulus in these clients.  If a patient has Emphysema whose brain is use to high carbon diozide levels in their blood secondary to bad breathing and getting low 02 blood levels in their body so their brain gets use to being messaged to tell the patient to breath on low levels of carbon dioxide blood levels when reaching the brain.  If this emphysema pt is given high doses of O2 for hours it turns the brain off making it think it doesn’t need to send messages to the person to breath.  A normal person with no emphysema COPD is use to breathing due to hypoxia but a emphysema is use to breathing when they have hypocapnia.  That is why when a emphysema pt who is no respiratory arrest is given 2L or less daily.  When is distress high 02 levels temporarily unlikely to hurt the pt, since the high 02 is given for a short period.


“Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Symptoms include breathing difficulty, cough, mucus (sputum) production and wheezing.”


Part I What actually is Chronic Obstructive Pulmonary Disease (COPD)?

COPD2  COPD3 Usually due to smoking

This is Healthy Lung Month covering COPD.  What is Chronic Obstructive Pulmonary Disease?

Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma. A brief review of normal functional anatomy will provide a background for the discussion of pathology.

The airway down to the bronchioles normally is lined with ciliated pseudo-stratified columnar cells and goblet cells. Mucus derives from mucus glands that are freely distributed in the walls of the trachea and bronchi. The cilia sweep mucus and minor debris toward the upper airway. Low humidity, anesthesia gases, cigarette smoking and other chemical irritants paralyze the action of these cilia. The mucociliary action starts again after a matter of time. This is why people awaken to “smokers cough.”

“Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma.”

Bronchi run in septal connective tissue, but bronchioles are suspended in lung parenchyma by alveolar elastic tissue. The elastic tissue extends throughout alveolar walls, air passages, and vessels, connecting them in a delicate web. Bronchiolar epithelium is ciliated, single-layered and columnar or cuboidal. Beyond the bronchioles the epithelium is flat and lined with a film of phospholipid (surfactant), which lowers surface tension and thereby helps to keep these air spaces from collapsing. Remember that the phospholipid develops during later gestation in utero. This is the reason why premature infant’s lungs cannot stay inflated without the addition of surfactant therapy. Macrophages are found in alveolar lining. Smooth muscles surround the walls of all bronchi, bronchioles, and alveolar ducts and when stimulated they shorten and narrow the passages. Cartilage lends rigidity and lies in regular horse-shaped rings in the tracheal wall. Cartilage is absent in bronchi less than 1 mm in diameter.

The terminal bronchiole is lined with columnar epithelium and is the last purely conducting airway. An acinus includes a terminal bronchiole and its distal structures. Five to ten acini together constitute a secondary lobule, which is generally 1 to 2 cm in diameter and is partly surrounded by grossly visible fibrous septa. Passages distal to the terminal bronchiole include an average of three but as many as nine generations of respiratory bronchioles lined with both columnar and alveolar epithelium. Each of the last respiratory bronchioles gives rise to about six alveolar ducts, each of these to one or two alveolar sacs, and finally each of the sacs to perhaps seventy-five alveoli. Alveolar pores (pores of Kohn) may connect alveoli in adjacent lobules.

Two different circulations supply the lungs. The pulmonary arteries and veins are involved in gas exchange. The pulmonary arteries branch with the bronchi, dividing into capillaries at the level of the respiratory bronchiole, and supplying these as well as the alveolar ducts and alveoli. In the periphery of the lung, the pulmonary veins lie in the interlobular septa rather than accompanying the arteries and airways. The bronchial arteries are small and arise mostly from the aorta. They accompany the bronchi to supply their walls. In some cases of COPD, like bronchiectasis, extensive anastomoses develop between the pulmonary and bronchial circulations. This can allow major shunting and recirculation of blood, therefore contributing to cardiac overload and failure. Lymphatics run chiefly in bronchial walls and as a fine network in the pleural membrane. The lumina of the capillaries in the alveolar walls are separated from the alveolar lining surfaces by the alveolar-capillary membrane, consisting of thin endothelial and epithelial cells and a minute but expansile interstitial space. This interface between air and blood, only 2 microns in thickness, is the only place where gases may be exchanged effectively.

Disease Specific Review


Chronic Bronchitis

Chronic bronchitis is a clinical disorder characterized by excessive mucus secretion in the bronchi. It was traditionally defined by chronic or recurrent productive cough lasting for a minimum of three months per year and for at least two consecutive years, in which all other causes for the cough have been eliminated. Today’s definition remains more simplistic to include a productive cough progressing over a period of time and lasting longer and longer. Sometimes, chronic bronchitis is broken down into three types: simple, mucopurulent or obstructive. The pathologic changes consist of inflammation, primarily mononuclear, infiltrate in the bronchial wall, hypertrophy and hyperplasia of the mucus-secreting bronchial glands and mucosal goblet cells, metaplasia of bronchial and bronchiolar epithelium, and loss of cilia. Eventually, there may be distortion and scarring of the bronchial wall.


Asthma is a disease characterized by increased responsiveness of the trachea and bronchi to various stimuli (intrinsic or extrinsic), causing difficulty in breathing due to narrowing airways. The narrowing is dynamic and changes in degree. It occurs either spontaneously or because of therapy. The basic defect appears to be an altered state of the host, which periodically produces a hyperirritable contraction of smooth muscle and hypersecretion of bronchial mucus. This mucus is abnormally sticky and therefore obstructive. In some instances, the illness seems related to an altered immunologic state.

Histological changes of asthma include an increase in the size and number of the mucosal goblet cells and submucosal mucus glands. There is marked thickening of the bronchial basement membrane and hypertrophy of bronchial and bronchiolar smooth muscle tissue. A submucosal infiltration of mononuclear inflammatory cells, eosinophils and plugs of mucus blocks small airways. Patients who have had asthma for many years may develop cor pulmonale and emphysema.


Pulmonary emphysema is described in clinical, radiological and physiologic terms, but the condition is best defined morphologically. It is an enlargement of the air spaces distal to the terminal non-respiratory bronchiole, with destruction of alveolar walls.

Although the normal lung has about 35,000 terminal bronchioles and their total internal cross-sectional area is at least 40 times as great as that of the lobar bronchi, the bronchioles are more delicate and vulnerable. Bronchioles may be obstructed partially or completely, temporarily or permanently, by thickening of their walls, by collapse due to loss of elasticity of the surrounding parenchyma, or by influx of exudate. In advanced emphysema, the lungs are large, pale, and relatively bloodless. They do not readily collapse. They many contain many superficial blebs or bullae, which occasionally are huge. The right ventricle of the heart is often enlarged (cor pulmonale), reflecting pulmonary arterial hypertension. Right ventricular enlargement is found in about 40% of autopsies of patients with severe emphysema. The distal air spaces are distended and disrupted, thus excessively confluent and reduced in number. There may be marked decrease in the number and size of the smaller vascular channels. The decrease in alveolar-capillary membrane surface area may be critical. Death may result from infection that obliterates the small bronchi and bronchioles. There is often organized pneumonia or scarring of the lung parenchyma due to previous infections.

Classification of emphysema relies on descriptive morphology, requiring the study of inflated lungs. The two principal types are centrilobular and panlobular emphysema. The two types may coexist in the same lung or lobe.

Centrilobular emphysema (CLE) or centriacinar emphysema affects respiratory bronchioles selectively. Fenestrations develop in the walls, enlarge, become confluent, and tend to form a single space as the walls disintegrate. There is often bronchiolitis with narrowing of lumina. The more distal parenchyma (alveolar ducts and sacs and alveoli) is initially preserved, then similarly destroyed as fenestrations develop and progress.

The disease commonly affects the upper portions of the lung more severely, but it tends to be unevenly distributed. The walls of the emphysematous spaces may be deeply pigmented. This discoloration may represent failure of clearance mechanisms to remove dust particles, or perhaps the pigment plays an active role in lung destruction. CLE is much more prevalent in males than in females. It is usually associated with chronic bronchitis and is seldom found in nonsmokers.

Panlobular emphysema (PLE) or panacinar emphysema is a nearly uniform enlargement and destruction of the alveoli in the pulmonary acinus. As the disease progresses, there is gradual loss of all components of the acinus until only a few strands of tissue, which are usually blood vessels, remain. PLE is usually diffuse, but is more severe in the lower lung areas. It is often found to some degree in older people, who do not have chronic bronchitis or clinical impairment of lung function. The term senile emphysema was formerly applied to this condition. PLE occurs as commonly in women and men, but is less frequent than CLE. It is a characteristic finding in those with homozygous deficiency of serum alpha-1 antitrypsin. It has also been found that certain populations of IV Ritalin abusers show PLE.

Bullae are common in both CLE and PLE, but may exist in the absence of either. Air-filled spaces in the visceral pleura are commonly termed blebs, and those in the parenchyma greater than 1 cm in diameter are called bullae. A valve mechanism in the bronchial communication of a bulla permits air trapping and enlargement of the air space. This scenario may compress the surrounding normal lung. Blebs may rupture into the pleural cavity causing a pneumothorax, and through a valve mechanism in the bronchopleural fistula a tension pneumothorax may develop.

Paracicatricial emphysema occurring adjacent to pulmonary scars represents another type of localized emphysema. When the air spaces distal to terminal bronchioles are increased beyond the normal size but do not show destructive changes of the alveolar walls, the condition is called pulmonary overinflation. This condition may be obstructive, because of air trapping beyond an incomplete bronchial obstruction due to a foreign body or a neoplasm. Many lung lobules may be simultaneously affected as a result of many check-valve obstructions, as in bronchial asthma. Pulmonary overinflation may also be nonobstructive, less properly called “compensatory emphysema”, when associated with atelectasis or resection of other areas of the lung.


Bronchiectasis means irreversible dilation and distortion of the bronchi and bronchioles. Saccular bronchiectasis is the classic advanced form characterized by irregular dilatations and narrowing. The term cystic is used when the dilatations are especially large and numerous. Cystic bronchiectasis can be further classified as fusiform or varicose.

Tubular bronchiectasis is simply the absence of normal bronchial tapering and is usually a manifestation of severe chronic bronchitis rather than of true bronchial wall destruction.

Repeated or prolonged episodes of pneumonitis, inhaled foreign objects or neoplasms have been known to cause bronchiectasis. When the bronchiectatic process involves most or all of the bronchial tree, whether in one or both lungs, it is believed to be genetic or developmental in origin.

Mucoviscidosis, Kartagener’s syndrome (bronchiectasis with dextrocardia and paranasal sinusitis), and agammaglobulinemia are all examples of inherited or developmental diseases associated with bronchiectasis. The term pseudobronchiectasis is applied to cylindrical bronchial widening, which may complicate a pneumonitis but which disappears after a few months. Bronchiectasis is true saccular bronchiectasis but without cough or expectoration. It is located especially in the upper lobes where good dependent drainage is available. A proximal form of bronchiectasis (with normal distal airways) complicates aspergillus mucus plugging.

Advanced bronchiectasis is often accompanied by anastomoses between the bronchial and pulmonary vessels. These cause right-to-left shunts, with resulting hypoxemia, pulmonary hypertension and cor pulmonale.

Keeping a healthy lung prevents emphysema.  So for starters don’t smoke and exercise; which includes don’t be exposed to smoke frequently!


“The stage of a cancer describes how much cancer is in the body. It helps determine how serious the cancer is and how best to treat it. The staging system used most often for pancreatic cancer is the AJCC (American Joint Committee on Cancer) TNM system, which is based on 3 key pieces of information: 1-extent of the tumor (T) 2- spread to nearby lymph nodes (N) 3- The spread (metastasized) to distant sites (M).”

American Cancer Society

Part IV Pancreatic Cancer – Staging and RX


Pancreatic Cancer, its incidence cuts across all racial and socio-economic barriers and is nearly always fatal. 90% die within the 1st yr of diagnosis.


Stage is a term used in cancer treatment to describe the extent of the cancer’s spread. The stages of pancreatic cancer are from 0 to IV.

The best treatment for pancreatic cancer depends on how far it has spread, or its stage. The stages of pancreatic cancer are easy to understand. What is difficult is attempting to stage pancreatic cancer without resorting to major surgery. In practice, doctors choose pancreatic cancer treatments based upon imaging studies, surgical findings, and an individual’s general state of well being.

Stages of Pancreatic Cancer

Stage is a term used in cancer treatment to describe the extent of the cancer’s spread. The stages of pancreatic cancer are used to guide treatment and to classify patients for clinical trials. The stages of pancreatic cancer are:

  • Stage 0: No spread. Pancreatic cancer is limited to top layers of cells in the ducts of the pancreas. The pancreatic cancer is not visible on imaging tests or even to the naked eye.
  • Stage I: Local growth. Pancreatic cancer is limited to the pancreas, but has grown to less than 2 centimeters across (stage IA) or greater than 2 but no more than 4 centimeters (stage IB).
  • Stage II: Local spread. Pancreatic cancer is over 4 centimeters and is either limited to the pancreas or there is local spread where the cancer has grown outside of the pancreas, or has spread to nearby lymph nodes. It has not spread to distant sites.
  • Stage III: Wider spread. The tumor may have expanded into nearby major blood vessels or nerves, but has not metastasized to distant sites.
  • Stage IV: Confirmed spread. Pancreatic cancer has spread to distant organs.

Determining pancreatic cancer’s stage is often tricky. Imaging tests like CT scans and ultrasound provide some information, but knowing exactly how far pancreatic cancer has spread usually requires surgery.

Since surgery has risks, doctors first determine whether pancreatic cancer appears to be removable by surgery (resectable). Pancreatic cancer is then described as follows:

  • Resectable: On imaging tests, pancreatic cancer hasn’t spread (or at least not far), and a surgeon feels it might all be removable. About 10% of pancreatic cancers are considered resectable when first diagnosed.
  • Locally advanced (unresectable): Pancreatic cancer has grown into major blood vessels on imaging tests, so the tumor can’t safely be removed by surgery.
  • Metastatic: Pancreatic cancer has clearly spread to other organs, so surgery cannot remove the cancer.

If pancreatic cancer is resectable, surgery followed by chemotherapy or radiation or both may extend survival.

Treating Resectable Pancreatic Cancer

People whose pancreatic cancer is considered resectable may undergo one of three surgeries:

Whipple procedure (pancreaticoduodenectomy): A surgeon removes the head of the pancreas and sometimes the body of the pancreas, parts of the stomach and small intestine, some lymph nodes, the gallbladder, and the common bile duct. The remaining organs are reconnected in a new way to allow digestion. The Whipple procedure is a difficult and complicated surgery. Surgeons and hospitals that do the most operations have the best results.

About half the time, once a surgeon sees inside the abdomen, pancreatic cancer that was thought to be resectable turns out to have spread, and thus be unresectable. The Whipple procedure is not completed in these cases.

Distal pancreatectomy: The tail and/or portion of the body of the pancreas are removed, but not the head. This surgery is uncommon for pancreatic cancer, because most tumors arising outside the head of the pancreas within the body or tail are unresectable.

Total pancreatectomy: The entire pancreas and the spleen is surgically removed. Although once considered useful, this operation is uncommon today.

Chemotherapy or radiation therapy or both can also be used in conjunction with surgery for resectable and unresectable pancreatic cancer in order to:

  • Shrink pancreatic cancer before surgery, improving the chances of resection (neoadjuvant therapy)
  • Prevent or delay pancreatic cancer from returning after surgery (adjuvant therapy)

Chemotherapy includes cancer drugs that travel through the whole body. Chemotherapy (“chemo”) kills pancreatic cancer cells in the main tumor as well as those that have spread widely. These chemotherapy drugs can be used for pancreatic cancer:

  • 5-fluorouracil (5-FU) or capecitabine
  • Gemcitabine

Both 5-FU and gemcitabine are given into the veins during regular visits to an oncologist (cancer doctor). An oral drug, capecitabine, may be substituted for 5-FU, especially with radiation.

In radiation therapy, a machine beams high-energy X-rays to the pancreas to kill pancreatic cancer cells. Radiation therapy is done during a series of daily treatments, usually over a period of weeks.

Both radiation therapy and chemotherapy damage some normal cells, along with cancer cells. Side effects can include nausea, vomiting, appetite loss, weight loss, and fatigue as well as toxicity to the blood cells. Symptoms usually cease within a few weeks after radiation therapy is complete.

The best treatment for pancreatic cancer depends on how far it has spread, or its stage. The stages of pancreatic cancer are easy to understand. What is difficult is attempting to stage pancreatic cancer without resorting to major surgery. In practice, doctors choose pancreatic cancer treatments based upon imaging studies, surgical findings, and an individual’s general state of well being.

Treating Metastatic Pancreatic Cancer

In metastatic pancreatic cancer, surgery is used only for symptom control, such as for pain, jaundice, or gastric outlet obstruction. Radiation may be used for symptom relief, as well.

Chemotherapy can also help improve pancreatic cancer symptoms and survival. Gemcitabine has been the most wildly used chemotherapy drug for treating metastatic pancreas cancer. Other drug combinations include gemcitabine with erlotinib, gemcitabine with capecitabine, gemcitabine with cisplatin, and gemcitabine with nab-paclitaxel. If you’re in fairly good health you may receive FOLFIRINOX (5-FU/leucovorin/oxaliplatin/irinotecan). Other combinations include gemcitabine alone or with another agent like (nab)-paclitaxel or capecitabine. Next line drug combinations to treat pancreatic cancer include oxaliplatin/fluoropyrimidine, or irinotecan liposome (Onivyde) in combination with fluorouracil plus leucovorin.

Palliative Treatment for Pancreatic Cancer

As pancreatic cancer progresses, the No. 1 priority of treatment will shift from extending life to alleviating symptoms, especially pain. Numerous treatments can help protect against the discomfort from advanced pancreatic cancer:

  • Procedures like bile duct stents can relieve jaundice, thus reducing itching and loss of appetite associated with bile obstruction.
  • Opioid analgesics and a nerve block called a celiac plexus block can help relieve pain.
  • Antidepressants and counseling can help treat depression common in advanced pancreatic cancer.

Clinical Trials for Pancreatic Cancer

New pancreatic cancer treatments are constantly being tested in clinical trials. You can find out about clinical trials for the latest treatments for pancreatic cancer on the websites of the American Cancer Society and the National Cancer Institute






“Oncologists will conduct tests to classify the type and stage of your disease.  Staging is a process that determines the spread of the cancer cells within and around the pancreas.  Diagnosis and staging of pancreatic cancer usually happen at the same time.”


Part III Continuation on Pancreatic Cancer Diagnostic Testing!

6.) Angiography

This is an x-ray test that looks at blood vessels. A small amount of contrast dye is injected into an artery to outline the blood vessels, and then x-rays are taken.

An angiogram can show if blood flow in a particular area is blocked by a tumor. It can also show abnormal blood vessels (feeding the cancer) in the area. This test can be useful in finding out if a pancreatic cancer has grown through the walls of certain blood vessels.  Usually the catheter is put into an artery in your inner thigh and threaded up to the pancreas.

Blood Tests

Several types of blood tests can be used to help diagnose pancreatic cancer or to help determine treatment options if it is found.

Liver function tests: Jaundice (yellowing of the skin and eyes) is often one of the first signs of pancreatic cancer. Doctors often get blood tests to assess liver function in people with jaundice to help determine its cause. Certain blood tests can look at levels of different kinds of bilirubin (a chemical made by the liver) and can help tell whether a patient’s jaundice is caused by disease in the liver itself or by a blockage of bile flow (from a gallstone, a tumor, or other disease).

Tumor markers: Tumor markers are substances that can sometimes be found in the blood when a person has cancer. Tumor markers that may be helpful in pancreatic cancer are:

  • CA 19-9
  • Carcinoembryonic antigen (CEA), which is not used as often as CA 19-9

Neither of these tumor marker tests is accurate enough to tell for sure if someone has pancreatic cancer. Levels of these tumor markers are not high in all people with pancreatic cancer, and some people who don’t have pancreatic cancer might have high levels of these markers for other reasons. Still, these tests can sometimes be helpful, along with other tests, in figuring out if someone has cancer.

In people already known to have pancreatic cancer and who have high CA19-9 or CEA levels, these levels can be measured over time to help tell how well treatment is working. If all of the cancer has been removed, these tests can also be done to look for signs the cancer may be coming back.

Other blood tests: Other tests, like a CBC or chemistry panel, can help evaluate a person’s general health (such as kidney and bone marrow function). These tests can help determine if they’ll be able to withstand the stress of a major operation.


A person’s medical history, physical exam, and imaging test results may strongly suggest pancreatic cancer, but usually the only way to be sure is to remove a small sample of tumor and look at it under the microscope. This procedure is called a biopsy. Biopsies can be done in different ways.

Percutaneous (through the skin) biopsy: For this test, a doctor inserts a thin, hollow needle through the skin over the abdomen and into the pancreas to remove a small piece of a tumor. This is known as a fine needle aspiration (FNA). The doctor guides the needle into place using images from ultrasound or CT scans.

Endoscopic biopsy: Doctors can also biopsy a tumor during an endoscopy. The doctor passes an endoscope (a thin, flexible, tube with a small video camera on the end) down the throat and into the small intestine near the pancreas. At this point, the doctor can either use endoscopic ultrasound (EUS) to pass a needle into the tumor or endoscopic retrograde cholangiopancreatography (ERCP) to place a brush to remove cells from the bile or pancreatic ducts.

Surgical biopsy: Surgical biopsies are now done less often than in the past. They can be useful if the surgeon is concerned the cancer has spread beyond the pancreas and wants to look at (and possibly biopsy) other organs in the abdomen. The most common way to do a surgical biopsy is to use laparoscopy (sometimes called keyhole surgery). The surgeon can look at the pancreas and other organs for tumors and take biopsy samples of abnormal areas.

Some people might not need a biopsy

Rarely, the doctor might not do a biopsy on someone who has a tumor in the pancreas if imaging tests show the tumor is very likely to be cancer and if it looks like surgery can remove all of it. Instead, the doctor will proceed with surgery, at which time the tumor cells can be looked at in the lab to confirm the diagnosis. During surgery, if the doctor finds that the cancer has spread too far to be removed completely, only a sample of the cancer may be removed to confirm the diagnosis, and the rest of the planned operation will be stopped.

If treatment (such as chemotherapy or radiation) is planned before surgery, a biopsy is needed first to be sure of the diagnosis.



“While your initial assessment may include CT scanning and magnetic resonance imaging (MRI), we use more advanced tools to confirm your pancreatic cancer diagnosis and to determine its extent—a process called staging.”

Columbia Presbyterian Hospital NYC

Part II on Pancreatic Cancer – Diagnostic Testing from the start.


The top of pancreas attaches to the gall bile duct (allowing it into the head of the pancreas) and than there is the mesenteric artery.  Blood supply to the liver, pancreas and gallbladder is via the celiac artery (or celiac axis or celiac trunk). The celiac artery also supplies the duodenum, stomach and esophagus (the foregut and its derviatives). The pancreas is also supplied to some extent by the superior mesenteric artery that goes through the head of the pancreas.  This is how metastasis occurs (spreading) of pancreatic cancer can occur.  These arteries allow cancerous cells thorough the head into the bile duct into the blood stream and metastasis can now happen This can’t occur in the tail of the pancreas, its not attached to anything; which is the best place for it to occur & be diagnosed versus the head of the pancreas due to location.

Pancreatic cancer is hard to find early. The pancreas is deep inside the body, so early tumors can’t be seen or felt by health care providers during routine physical exams. People usually have no symptoms until the cancer has become very large or has already spread to other organs.

For certain types of cancer, screening tests or exams are used to look for cancer in people who have no symptoms (and who have not had that cancer before). But for pancreatic cancer, no major professional groups currently recommend routine screening in people who are at average risk. This is because no screening test has been shown to lower the risk of dying from this cancer, unfortunately.

Genetic History is one of the most common risk factors in getting most cancers, including Pancreatic.  Some people might be at increased risk of pancreatic cancer because of a family history of the disease (or a family history of certain other cancers). Sometimes this increased risk is due to a specific genetic syndrome.

Genetic testing looks for the gene changes that cause these inherited conditions and increase pancreatic cancer risk. The tests look for these inherited conditions, not pancreatic cancer itself. Your risk may be increased if you have one of these conditions, but it doesn’t mean that you have (or definitely will get) pancreatic cancer. 

Knowing if you are at increased risk can help you and your doctor decide if you should have tests to look for pancreatic cancer early, when it might be easier to treat. But determining whether you might be at increased risk is not simple. The American Cancer Society strongly recommends that anyone thinking about genetic testing talk with a genetic counselor, nurse, or doctor (qualified to interpret and explain the test results) before getting tested. It’s important to understand what the tests can − and can’t − tell you, and what any results might mean, before deciding to be tested.

For people in families at high risk of pancreatic cancer, newer tests for detecting pancreatic cancer early may help. The two most common tests used are an endoscopic ultrasound or MRI. These tests are not used to screen the general public, but might be used for someone with a strong family history of pancreatic cancer or with a known genetic syndrome that increases their risk. Doctors have been able to find early, treatable pancreatic cancers in some members of high-risk families with these tests.

Tests for Pancreatic Cancer and even other Cancers:

A.)  Doctor’s Visit

The M.D. is usually the first thing done and the M.D. will ask about your medical history to learn more about your symptoms. The doctor might also ask about possible risk factors, including smoking and your family history.  Your doctor will also do a physical examine you to look for signs of pancreatic cancer or other health problems.

Doctors are also studying other new tests to try to find pancreatic cancer early.  Interested families at high risk may wish to take part in studies of these new screening tests.

B.)  Imaging Testing=It can be used:

  • To look for suspicious areas that might be cancer
  • To learn how far cancer may have spread
  • To help determine if treatment is working
  • To look for signs of cancer coming back after treatment

1.) CT Scan-detailed cross-sectional images of the body/pancreas.  Their are special types of CT known as a multiphase CT scan or a pancreatic protocol CT scan. During this test, different sets of CT scans are taken over several minutes after you get an injection of an intravenous (IV) contrast.  CT-guided needle biopsy: CT scans can also be used to guide a biopsy needle into a suspected pancreatic tumor.

2.) MRI(magnetic resonance imagery)-uses radio waves and strong magnets instead of x-rays to make detailed images of parts of your body. Most doctors prefer to look at the pancreas with CT scans, but an MRI might also be done.  Special types of MRI scans that can also be used are:

-MR cholangiopancreatography (MRCP), which can be used to look at the pancreatic and bile ducts, is described below in the section on cholangiopancreatography.

-MR angiography (MRA), which looks at blood vessels, is mentioned below in the section on angiography.

3. ) Ultrasound (US) tests

These tests use sound waves to create images of organs such as the pancreas. The two most commonly used types for pancreatic cancer:

A-Abdominal ultrasound – If it’s not clear what might be causing a person’s abdominal symptoms, this might be the first test done because it is easy to do and it doesn’t expose a person to radiation. But if signs and symptoms are more likely to be caused by pancreatic cancer, a CT scan is often more useful.

B-Endoscopic ultrasound (EUS): This test is more accurate than abdominal US and can be very helpful in diagnosing pancreatic cancer. This test is done with a small US probe on the tip of an endoscope, which is a thin, flexible tube that doctors use to look inside the digestive tract and to get biopsy samples of a tumor (more invasive but more detailed in results of the pancreas).

4.) Cholangiopancreatography

Abdominal This is an imaging test that looks at the pancreatic ducts and bile ducts to see if they are blocked, narrowed, or dilated. These tests can help show if someone might have a pancreatic tumor that is blocking a duct. They can also be used to help plan surgery.  If signs and symptoms are more likely to be caused by pancreatic cancer, a CT scan is often more useful.

A – Endoscopic ultrasound (EUS): This test is more accurate than abdominal US and can be very helpful in diagnosing pancreatic cancer. This test is done with a small US probe on the tip of an endoscope, which is a thin, flexible tube that doctors use to look inside the digestive tract and to get biopsy samples of a tumor.

SPYGLASS. This novel technology provides a direct view of the bile duct system, enabling our doctors to visualize lesions and narrowed areas (strictures) in the ducts and to biopsy them to see if they are cancerous. This approach ensures highly accurate sampling of the area in question. It is an excellent tool to use with confocal endomicroscopy.

B – Magnetic resonance cholangiopancreatography (MRCP):This is a non-invasive way to look at the pancreatic and bile ducts using the same type of machine used for standard MRI scans. Unlike ERCP, it does not require an infusion of a contrast dye. Because this test is non-invasive, doctors often use MRCP if the purpose is just to look at the pancreatic and bile ducts. But this test can’t be used to get biopsy samples of tumors or to place stents in ducts; like ERCP. can do also.

5.) Percutaneous transhepatic cholangiography (PTC): In this procedure, the doctor puts a thin, hollow needle through the skin of the belly and into a bile duct within the liver. A contrast dye is then injected through the needle, and x-rays are taken as it passes through the bile and pancreatic ducts. As with ERCP, this approach can also be used to take fluid or tissue samples or to place a stent into a duct to help keep it open. Because it is more invasive (and might cause more pain), PTC is not usually used unless ERCP has already been tried or can’t be done for some reason.

5.) Positron emission tomography (PET) scan

For a PET scan, you are injected with a slightly radioactive form of sugar, which collects mainly in cancer cells. A special camera is then used to create a picture of areas of radioactivity in the body.

This test is sometimes used to look for spread from exocrine pancreatic cancers.

PET/CT scan: Special machines can do both a PET and CT scan at the same time.

Pancreatoscopy. Here what is used is a small camera to visualize the pancreatic duct.

This test can help determine the stage (extent) of the cancer.  It might be able to detect metastasis (spreading beyond the pancreas).  See the top anatomy picture provided to understand this better by knowing the location of the organ to other parts of the body, if needed.