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					A 66-Year-Old Man with Lung
Cancer
               Eugene G. Martin, Ph.D.
               Professor of Pathology & Laboratory Medicine

     Based upon: LABORATORY MEDICINE CASEBOOK.
     An introduction to clinical reasoning

     Jana Raskova, MD
       Professor of Pathology & Laboratory Medicine
     Stephen Shea, MD
       Professor of Pathology & Laboratory Medicine
     Frederick Skvara, MD
       Associate Professor of Pathology & Laboratory Medicine
     Nagy Mikhail, MD
       Assistant Professor of Pathology & Laboratory Medicine
     UMDNJ-Robert Wood Johnson Medical School
     Piscataway, NJ
History
   66 year old male brought to the emergency room after he was
    found to be unresponsive at home.
   Blood sugar was 28 mg/dL (Normal: 65-110).
   Regained consciousness after administration of dextrose.
   Diagnosed 3 months earlier as having diabetes mellitus and
    started on insulin.
   At the time of that diagnosis chest x-ray revealed a mass in left
    lung – Bronchogenic carcinoma
   Treated with three cycles of chemotherapy, the last 6 days
    ago.
What questions does this
history elicit?
   Why the sudden         Could the presence of
    onset of DM?            a lung cancer result in
   How come his            DM?
    glucose suddenly       What does
    dropped to 28           chemotherapy have to
    mg/dl?                  do with this story?
   How big a problem      Are there other
                            possibilities?
    is glucose of 28
    mg/dL                  What do you worry
                            about here?
    Physical findings:
    Physical Exam
        Confused and lethargic man.
        BP: 150/90 HR: 92bpm
        Temperature – 98.8 oC
        Respiratory rate – 26 per minute
        Decreased breath sounds on the left side
        Marked weakness of both legs
        “Puffy” appearance of the face
What questions do the
physical findings elicit?
1.   Does he have a
     history of                  Should they have done
     hypertension or is the       a supine and standing
     combination of               BP? Why?
     hypertension and an
     elevated HR
     suggestive of
     something reflexive?
     Such as?
2.   What is the meaning
     of “puffy”?
3.   Why is he so weak?
Questions from the physical
                          Does this patient have
   What is the            orthostatic
    significance of        hypotension? (Defn: A
                           fall in BP > 30/20 on
    determining a          standing). Answer:
                           YES
    supine and a          One of the
    standing BP?           consequences of
                           blood loss is an
   Is the HR 96           inability to maintain
                           blood pressure upon
    bpm significant?       standing. One of the
                           physiologic responses
                           is an increase in HR.
Cushing Syndrome
                                              SYMPTOMS:
   Excess secretion of hormone                   Acne or superficial skin infections
    cortisol = “Cushing syndrome”                 Backache
                                                  Buffalo hump (a collection of fat between the
    Also caused by:                               shoulders)
         Tumor of the pituitary gland            Central obesity with protruding abdomen and thin
          or adrenal gland                         extremities
                                                  Hair growth on the face
         Tumor elsewhere in the body             Headache
         Long-term use of anti-                  Impotence (men)
          inflammatory medicines                  Menstrual cycle stops (women)
          called corticosteroids                     Mental changes
                                                     Moon face (round, red, and full)
   TYPICAL LAB TESTS:                               Purple marks called striations on the skin of the
                                                      abdomen, thighs, and breasts
       WBC elevated                                 Thin skin with easy bruising
       Glucose elevated                             Weakness
       Potassium low                                Weight gain (unintentional)
                                                     Bone pain or tenderness
   FOLLOW-UP:                                       Fatigue
       Is it the pituitary or something             High blood pressure
                                                      Muscle atrophy
        else? – Check the feedback             
                                                     Red spots on the skin
        loop                                         Skin blushing or flushing
 HEMATOLOGY: At Admission
          Patient            Normal
WBC       8.14 X 103/uL      (3.6-11.2)

  Neut    88.6%              (44-88)

  Lymph   8.2%               (12-43)

  Mono    1.7%               (2-11)

  Eos     1.5%               (0-5)

RBC       3.18 X 106/uL      (4.0-5.8)

Hgb       9.9 g/dL           (12.6-17.0)
HCT       30.4 %             (42-52)
MCV       95.4 fL            (80-102 f1)
MCH       31.2 pg            (27-35)
Plts      205 thousands/uL   (130-400)
Peripheral Blood Smear
       Normal                          Patient




   Normochromic, normocytic anemia.
   Red cell population is decreased in number
   Cell size and shape normal
   Platelets and neutrophils are unremarkable
   None of this information adds anything to the automated
    hematology count shown earlier
      Question from the Hematology
      Results
         Does this patient have               Normochromic, normocytic
          anemia? If so, what kind?             anemia
         What info do you still need?              Reticulocyte ↑
                                                        Hemolytic disease
RBC           3.18 X 106/uL   (4.0-5.8)                 Acute blood loss
                                                    Reticulocyte normal
                              (12.6-17.0)               Malignancy
Hgb           9.9 g/dL
                                                        Myeloma
                                                        Chronic Disease
HCT           30.4 %          (42-52)
                                               If this patient had a chronic blood
                                                loss for more than 6 months you
MCV           95.4 fL         (80-102 f1)
                                                would expect a hypochromic,
                                                microcytic anemia
MCH           31.2 pg         (27-35)
Anemia Assessment
   Normocytic, normochromic anemia
        Reticulocyte ↑
             Hemolytic disease
             Acute blood loss
        Reticulocyte normal
             Malignancy
             Myeloma
             Chronic Disease
   Macrocytosis is seen in:
        Megaloblastic anemias 
             vitamin B12 and folate deficiency
             Some forms of chronic liver disease
   Microcytosis and hypochromia
        Iron deficiency anemia
        Spherocytosis
        Some forms of anemia of chronic disease
       CHEMISTRY
Test          Patient      Normal       Test         Patient     Normal
Glucose       28 mg/dL!!   (65-110)     LDH          537 U/L     (100-220)
Creatinine    1.2 mg/dL    (0.7-1.4)     LDH1        23%         (17-27)
BUN           25 mg/dL     (7-24)        LDH2        37%         (28-38)
Uric Acid     8.1 mg/dL    (3.0-8.5)     LDH3        18%         (18-28)
Cholesterol   150 mg/dL    (150-240)     LDH4        11%         (5-15)
Calcium       8.5 mg/dL    (8.0-10.0)    LDH5        11%         (6-13)
Protein       5.5 g/dL     (6-8)
Albumin       2.7 g/dL     (3.2-4.6)    Alk. Phos.   194 U/L     (0-120)
                                        AST          30 U/L      (0-55)
                                        GGTP         247 U/L     (0-55)
                                        Bilirubin    0.6 mg/dL   (0.1-1.0)
Why:
   What is the
    significance of the
    elevated LDH?
   Why is LDH3 relatively
    low and LDH2
    relatively high?
   What is the
    significance of
    elevations of both
    LDH, GGTP and Alk.
    Phos.?
Lactate Dehydrogenase
   Found most everywhere                Normal
   Five fractions (isoenzymes):                 LDH Type 1 < LDH Type 2
       LDH-1 is found primarily in              LDH Type 5 < LDH Type 4
        heart muscle and RBCs               Abnormal
       LDH-2 - heart, red blood                 LDH Type 1 > LDH Type 2
        cells, kidney (lesser amounts                Myocardial Infarction
        than LDH-1)                                  Hemolytic Anemia
       LDH-3 - highest in the lung.                 Pernicious Anemia
       LDH-4 - highest in the kidney,               Renal infarction
        placenta, and pancreas.                  LDH Type 5 > LDH Type 4
       LDH-5 - highest in the liver                 Liver disease
        and skeletal muscle.
   Relative amounts of a
    particular isoenzyme of LDH in
    the blood can provide
    diagnostic clues.
Liver enzymes and cancer

   ↑ LDH – seen in 50% of patients with cancer
   ↑ GGTP is also commonly seen in patients
    with cancers WITH or WITHOUT liver mets.
   ↑ Alk. Phos. Also commonly seen in patients
    with cancers WITH or WITHOUT liver mets.
   If biliary obstruction by tumor  ↑ serum
    bilirubin and a MUCH greater ↑ in alk. Phos.
                                    Additional Studies:
Arterial Blood Gases Electrolytes



                                    Test             Patient      Normal
                                    pH               7.54         (7.35-7.45)
                                    pCO2             49 mmHg      (32-46)
                                    pO2              52 mmHg      (74-108)
                                    HCO3             43 mEq/L     (21-29)
                                    Base excess      + 18 mEq/L   (-2 -> +2)
                                    O2 saturation    89%          (92-96)

                                    Test            Patient       Normal
                                    Na+             142 mEq/L     (134-143)
                                    K+              2.6 mEq/L     (3.5-4.9)
                                    Cl-             86 mEq/L      (95-108)
                                    CO2             53 mEq/L      (21-32)
          The primary acid-base
          disturbance is:
Test               Patient             Normal
pH                 7.54                (7.35-7.45)                      50%
pCO2               49 mmHg             (32-46)
pO2                52 mmHg             (74-108)
                                                                                     33%
HCO3               43 mEq/L            (21-29)


     1.   Respiratory acidosis                                                                     17%

     2.   Metabolic Alkalosis
                                                          0%
     3.   Metabolic Acidosis


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Learning Response:
   ANSWER: The primary disturbance is
    a partly compensated metabolic
    alkalosis:
       ↑ pH - alkalosis
       ↑ HCO3
       ↑ PCO2
       Total CO2
Diagnosis of Acid-Base Disorders
              Arteri   Arteria   [Total   [HCO   Test   Patient    Normal
              al pH    l PCO2    CO2]     3]

                                                 pH     7.54       (7.35-7.45)
Metabolic     ↓        ↓         ↓        ↓
acidosis
                                                 pCO2   49 mmHg    (32-46)
/w part                                          pO2    52 mmHg    (74-108)
resp c
                                                 HCO3   43 mEq/L   (21-29)
Metabolic     ↑        ↑         ↑        ↑
alkalosis
                                                 CO2    53 mEq/L     (21-32)
/w part
resp c
Respirator    ↓        ↑         ↑        ↑
y acidosis


Respirator    ↑        ↓         ↓        ↓
y alkalosis
Vomiting
   Acid-losing alkalosis (Metabolic alkalosis)
       The gastric mucosa produces HCl by carbonic anhydrase
        mediated conversion of H2CO3  HCO3- and H+
       Gastric HCl is lost in vomiting
           H+ is continually being lost. H2CO3 is continually being
            consumed
           CO2 component ↑ because the HCO3- that is released when
            HCl is produced remains in the blood stream and gets
            broken down
           Because H2CO3 is decreased the lungs tend to retain CO2
            to compensate – generally not sufficient to prevent an
            increase in the usual 20:1 ratio of HCO3- to H2CO3
Presentation of Lung Cancer
   Usually recognized
    late in its natural
    history – tumor can
    often grow a long time
    before symptoms
   Of 100 newly identified
    lung cancers, 80 will
    be inoperable at
    presentation
   5 year mortality – 85-
    90%
Presenting Symptoms
Metastatic spread of lung
cancer
   1/3 present with              Adrenal glands; and
    symptoms resulting            Intra-abdominal lymph
    from distant                   nodes;
    metastases                     Brain and spinal cord;
   Most common sites:             Lymph nodes; and
                                   Skin.
     Bones;

     Liver  Liver Function
       Tests rarely are
       abnormal until
       metastases are large
What is a Paraneoplastic
Syndrome?
   DEFINITION: Clinical syndrome involving non-metastatic,
    systemic effects that accompany malignant disease.
       Collections of symptoms that result from substances produced by
        the tumor.
            Substances include: Hormones or other biologically active products
             produced by the tumor.
       Actions:
            Activate hormone secretion
            Blockade the effect of hormones.
            Autoimmunity
            Immune-complex production, and
            Immune suppression..
   Symptoms may be endocrine, neuromuscular, cardiovascular,
    cutaneous, hematologic, GI, renal or misc.
Clinical Course
   Patient‟s glycemia stabilized
   Electrolyte abnormalities were
    corrected by appropriate replacement
    therapy
   MRI of brain was normal.
       Why did they do this?
   Additional studies ordered
       What would make sense?
        Adrenal Gland
   Medulla of adrenal gland                      What can happen?
    secretes:                                         Adrenals
        Epinephrine                                   themselves
                                                       malfunction  a
            ↑ HR, ↑ BP, ↑ Cardiac Output              change in hormone
            ↑ Blood glucose levels                    secretion (Adrenal
   Cortex of adrenal gland                            Hyperplasia)
    secretes:                                         Feedback loop has
        Cortisol (Glucocorticoids)                    been altered (e.g.
                                                       ↑↑ ACTH  ↑
        Aldosterone                                  Cortisol production)
            Electrolyte control (↑ Na+,↓ K+          A tumor mimics
             & Cl-)  ↑ BP control
                                                       either one of the
        Androgens                                     releasing factors 
            Testosterone (Virilization)               altered production
Hypothalamic Pituitary Axis
What studies would you
order? Why?
Test                                   Patient Result                Reference Range
Serum ACTH (7 AM)                      314 ρg/mL                     (0-100 pg/mL)
Serum Cortisol (7 AM)                  51.0 µg/dL                    (5.0-25.0 ug/dL)
Serum Cortisol (4 PM)                  45.2 µg/dL                    (2.5-12.5 ug/dL)
Serum Aldosterone                      13.7 ng/dL                    0.0-12.0 ng/dL

   ACTH too high  ↑ cortisol secretion
        Body fat redistribution  „Moon facies‟
        Excessive fat at top of back – „Buffalo hump‟
        Muscles loose their bulk  weakness
        ↑ BP , weakens bones (osteoporosis), diminished resistance to infection
        ↑ Kidney stones, ↑ diabetes, mental disturbances (depression & hallucination)
   Testing in AM & PM – Ordinarily, diurnal rthymn – high in AM, falls in PM. Not here! –
    Loss of control
   ↑ Aldosterone  Na+ retention, K+ secretion
 HEMATOLOGY
           Day 3 Day 6        Day 7     Day 8     Reference Range
WBC        6.02     0.83      0.65      .84       (3.6-11.2)

  Neut     97%      96%       25%       5%        (44-88)

  Lymph    3.00     2.00      71.00     88.00     (12-43)

  Mono     0        2         4         7         (2-11)

Hgb        9.3      7.6       7.5       8.4       (12.6-17.0)
HCT        28.2     22.00     22.1      24.3      (42-52)
MCV        95       90.2      93.2      93.9      (80-102 f1)

Plts       187      96        66        66        (130-400)



Death due to septic shock on day 9 (15 days after the last cycle of
chemotherapy
AUTOPSY FINDINGS
Bone Marrow findings
                  Normal bone marrow
                   biopsy
                      Cellularity is normal with
                       adequate numbers of fat
                       cells and a heterocellular
                       hematopoietic cell
                       population



                  Bone marrow at autopsy
                   (15 days post
                   chemotherapy) –
                      Marked hypocellularity
                      No evidence of tumor is
                       present
Liver
           Note edge of
            tumor nodule with
            infiltration by
            clumps of tumor
            cells between
            adjacent hepatic
            cords.
           Tumor cells
            spindle shaped
            consistent with
            small cell CA of
            the lung
Chest x-Ray

                 Left Lung Mass –
                  Primary lung CA
                 Possible adjacent
                  pneumonia
Histopathology – Lung Mass
                  H&E x12
                      Sheets of darkly staining
                       cells, areas of necrosis
                       and fibrosis.
                       No glandular or
                       squamous differentiation
                       is apparent

                  H&E x50 – Small Cell CA
                      Small cells with little
                       cytoplasm
                      Nuclei are oval and
                       spindle-shaped and
                       mitoses are frequent
                      Focus of necrosis present
CT Abdomen

                Bilateral adrenal
                 hyperplasia
                Right gland
                 appears larger than
                 left at this level
Case Summary

   Final Diagnosis:
       Small Cell CA of lung
       Post chemotherapeutic sepsis
       Ectopic ACTH production by Small Cell
        CA
            Hyperglycemia and Diabetes Mellitus
            Bilateral adrenal hyperplasia documented
               Hypercortisolism -
               Hyperaldosteronism  Electrolyte abnormalities
Small Cell CA
   Strongly associated with a history of
    cigarette smoking
   Only 1% occur in non-smokers.
   Originates in central or hilar area of the
    lung
   Metasizes early and widely
   Initial response to chemotherapy or
    radiation is good
QUESTIONS:
     Why the sudden onset of DM?
1.   Loss of Insulin Production by the Pancreas -                  20% 20% 20% 20% 20%
     Type I Diabetes
2.   He’s old. It’s just natural Type II Diabetes                                                                  60
3.   A substance that either interferes with
     insulin secretion or inhibits cellular
     responses to insulin has been released
4.   Vitamin B12 deficiency
5.   Post-chemotherapeutic myelosuppression?




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Learning Response:
   ANSWER 3 -- A substance that either interferes with insulin
    secretion or inhibits cellular responses to insulin has been
    released
       Rapid onset of diabetes requires that insulin secretion be
        turned off, or that cells become unresponsive to insulin.
       Type I diabetes with destruction of the pancreas is
        uncommon in a 66 year old
       The onset of Type II diabetes is usually gradual
       Vitamin B12 has nothing to do with sudden diabetes
       Myelosuppression by chemotherapeutic agents would not
        effect glucose uptake or utilization by insulin.
     What was the most likely cause for his
       glucose suddenly dropped to 28 mg/dl?
                                                   20% 20% 20% 20% 20%
1.   Increased secretion of
                                                                                                60
     cortisol
2.   Insulin administration
3.   Increased secretion of
     aldosterone
4.   Vomiting
5.   Diarrhea




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Learning Response:
   ANSWER 2 – Insulin administration
       Secretion of ACTH  Stimulation of the adrenal
        cortex and the production of cortisol. Cortisol 
        ↑ glycogen stores to be release and increases
        blood glucose levels
       Increased secretion of aldosterone  ↑ Na+,↓
        K+, but has little effect on glucose levels
       Prolonged vomiting might cause cortisol to be
        released as a response to stress, which would ↑
        glycogen release  ↑ blood glucose, but it
        would not lower glucose levels because it would
        not increase insulin levels
     What is the greatest danger of a sugar of 28?

1.   Loss of consciousness                       25% 25% 25% 25%
2.   Spontaneous recovery
     will occur, it‟s not
     dangerous
3.   Mild delerium
4.   Death




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Learning Response:

•   Answer (4) - Death
       A blood sugar of 28 is a medical emergency. Symptoms of an
        insulin overdose reflect very low blood sugar levels and include
        headache, irregular heartbeat, increased heart rate or pulse,
        sweating, tremor, nausea, increased hunger, and anxiety. Insulin
        overdose -> resultant hypoglycemia and its effects on the central
        nervous system can be life threatening
       Hypokalemia, hypophosphatemia and hypomagnesemia can
        develop with excess insulin administration
     How could the presence of a lung cancer
       result in DM?
1.   The pancreas is one of the
     principle sites for metastases                     25% 25% 25% 25%
                                                                                                     60
2.   Ectopic production of ACTH by
     small cell carcinomas (SCC)
     leads to cortisol release from the
     adrenals and conversion of
     glycogen to glucose  diabetes
3.   The pituitary is often a target of
     metastases. In response the
     pituitary releases ACTH ->
     diabetes
4.   Small cell carcinomas release
                                                      ..




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     glucose directly from the tumor




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Learning Response:
   Answer (2) - Ectopic production of ACTH by small
    cell carcinomas (SCC) leads to cortisol release from
    the adrenals and conversion of glycogen to glucose
     diabetes
   The pancreas is rarely a site for SCC metastases
   The pituitary is also an extremely rarely target for
    metastases. The feedback loop is broken because
    exogenous ACTH is released by the tumor and
    overrides the reflex control.
   Small cell carcinomas do not release glucose
    directly from the tumor
     Most common type of lung cancer associated with
     ectopic hormone production is:

1.    Small cell carcinoma                25% 25% 25% 25%
2.    Adenocarcinoma
                                                                                      60
3.    Squamous cell
      carcinoma
4.    Large cell carcinoma


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Learning Response:

   ANSWER: (1) The most common type of lung
    cancer associated with ectopic hormone
    production is a small cell carcinoma – (10%)
       Small cell carcinomas originate from
        neuroendocrine cells of the bronchial
        epithelium
       Neuroendocrine cells are capable of
        producing ACTH
     The most common lung cancer in
     women and non-smokers?
1.   Small cell carcinoma(SCC)
                                      60
2.   Adenocarcinoma
3.   Squamous cell carcinoma
4.   Large cell carcinoma
Learning Response:
   Answer: (2) Adenocarcinoma
       Adenocarcinoma of the lung is the MOST
        COMMON primary lung cancer in women
        and non-smokers
       Pulmonary adenocarcinomas are
        occasionally associated with
        paraneoplastic syndromes, but rarely with
        ACTH secretion!
     Which is INCORRECT?...
1.   Small cell carcinoma of the
     lung most often starts in the
     central or hilar region
2.   Small cell carcinoma of the
     lung is usually NOT
     associated with a history of
     cigarette smoking
3.   Small cell carcinoma of the
     lung tends to metastasize                            0% 0% 0% 0%
     widely


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4.   Small cell carcinoma of the

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     lung best responds to
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Learning Response:

   Answer: (2) Small cell carcinoma of the lung is
    strongly associated with a history of cigarette
    smoking
     Only 1% of Small Cell Carcinomas occur in non-
        smokers.
     Small cell carcinoma‟s originate in the central or
        hilar region, metastasize early and widely, and
        initially respond well to chemotherapy and/or
        radiation therapy.