Kirshenbaums Review 1

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Kirshenbaums Review 1 ...

Kirshenbaum’s Review 1

    Spring Semester 2003 thThursday, February 6, 2003

    Written by: Frances E. Kim

A guy is lying dead and there are tons of bicycles around him. Is there an ice cream truck next to the bicycles? Are they

    playing cards? Yes! Was he cheating? Yes! Were they 51 bicycles? Yes. 53. Yes. He was cheating so someone killed him.

Game Plan:

    Lung, Bone and Soft Tissue


Normal Lung:

    R lung has 3 lobes; L has 2 lobes and lingual that takes place

    Upper lobes are more anterior; Lower more posterior:

    R is more vertical than L main bronchus so that’s why infections.

Histology- go from trachea into main bronchi then secondary, teritiary

    Bronchi into bronchioles- term bronchioles- resp bronchioles-

Definition of an acinus: A resp bronchiole and air spaces distal to that.

    Lobule: A lobule is several terminal bronchioles with their acini.

Emphysema: pancinar, distal acinar,

Dual blood supply: pulmonary artery and bronchiole arteries (coming off aorta).

Entire resp tree is lined with pseudostartified columnar and cuboidal as you get deeper. Vocal cords are lined by squamous


HISTO at level of alveolus:

    Endothelial cells lying on BM and actual interstitium of lung; other side you have type I and Type II; interstitium is actual

    alveolar septa.

Processes: interstitial, septal, or interalveolar spaces.

FUNCTION of the lung:

    2 essential functions:

    (1) ventilation

    (2) resp gas exchange.


    Big broad categories:

    (1) congenital

    (2) atelectasis

    (3) diseases of vascular origin

    (4) obstructive vs. restrictive lung disease

    (a) subcats of obstructive

    (b) subcats of restrictive

    (pulmonary infections fall under restrictive—it’s confusing in Robbins because it has its own category--

    - )

    (5) complications of therapy (read on own)

    (6) Neoplasms

    (7) Pleura




Bronchopulmonary sequestration:lung tissue that has no connection to the lungeither extra or intralobar


    We’ll be faced with this secondary to other things:

What is it?

    It’s simply collapse of the lung. We see it in 2 situations:

    (1) Neonate—primary or secondary: primary: alveoli never expand; secondary: don’t expand enough (seen in IRDS-

    we’ll talk about in vascular diseases)

    (2) Acquired:

    ? we’ll see this a lot

    3 situations there (think about it and you don’t have to memorize)

    (1) Obstruction: if you obstruct the airways and then distal to the obstruction the lung will collapse (a block

    or tumor will cause atelectasis)

    -- total vs. partial obstruction? Does it matter?

    You need total obstruction to get atelectasis.

    -- partial obstruction: you’ll get emphysema (a compensatory type)

    -- if you get obstructed: you get collapse of the lung and the mediastinum will go toward the collapsed lung

    (2) Compressive: something on the outside is squeezing down on the lung. The pressure causes the

    mediastinum to move the other way.

    Examples: pneumothorax; fluid in pleural space;

    (3) Contraction: Pleural scarring

VASCULAR DISEASES( tested from vascular/cardio)

    (1) Seen secondary to something going on in the heart:

    LEFT-SIDED HEART FAILURE leads to pulmonary congestion and edema

Review pathophysiology: back up of pressure, increased pressure, etc.

(2) Adult Resp Distress Syndrome (Know these synonyms!)

    Shot lung, diffuse alveolar damage

histologically similar to neonate:

    we see hyaline membranes outlining the septa:

    in RDS, you have non-cardiogenic pulmonary edema: you have diffuse damage to the alveoli and you have damage to type

    I pneumocytes, this forms the hyaline membranes.

Causes of ARDS:

    Shock, sepsis, chemicals, burns


    Once an adult has ARDS, the overall prognosis is BAD!

    The way you treat this is by treating the underlying condition and supportive therapy.

What big broad category are we talkinga bout?

(3) Pulmonary embolism, Hemorrhage, Infarction

    discussed in hemodynamics.

Pulmonary thrombosis: how often do we see this? Hardly EVER!

    PE usually comes from lower extremities due to inactivity.

    PE usually doesn’t cause an infarct in a healthy individual because of dual vascular supply.

(4) Pulmonary Hypertension:

    High blood pressure of pulmonary artery, arteriole system.

    Not seen very often.

    Can be primary (essential) or secondary: Most of it is secondary to something else: that something else is some intrinsic lung disease. Or some l-sided heart backup of pressure. Congenital or acquired.

IF you’re doing an autopsy and you’re looking at the pulmonary artery, atherosclerosis is a sign that there’s pulmonary


Microscopically you’d see medial hypertrophy.



    Increased resistance to air flow as a result of that, you’re going to have the greatest degree of obstruction upon EXPIRATION. Therefore, that’s why in all PFTs, the major abnormalities are in forced expiratory volumes. All the FEVs

    are decreased in Obstructive lung diseases.

4 Subcategories:

    (1) Emphysema

    Chronic bronchitis.




    Reduced expansion of the lungs with a decrease in TLC.- difficulty inspiriting.

    2 situations give rise to a restrictive process:

    (1) chest wall disrorders

    (2) interstitial/infiltrating diseases: like pneumonia


    What’s COPD? Is that the same as obstructive lung diseases? Chronic Obstructive Pulmonary Disease. It’s pretty much the same thing. It comes in 4 flavors.

It’s a pathophysiologic syndrome.

    (1) Emphysema

    ? A morphologic definition: abrnomal permanent big airspaces with no fibrosis.

    ? Different types: 3 major types and some subtypes.

    (a) Centri-Acinar Emphysema:

    Emphysema of the central acinus: it’s the resp bronchiole that are mainly involves and distal alveolar spaces are


    Generally occurs in upper lobes.

    Strongest association is with smoking.

    Represents 95% of all the emphysema we’ll see in the next 50 years.

    (b) Pan-Acinar Emphysema:

    The whole acinus is involves.

    From resp bronchiole to all alveolar speaces.

    Esp lower lobes.

    Seen in alpha1antitrypsin deficiency (rare)

    (c) Distal Acinar (AKA para-septal):

    Dilated airspaces are bigger and bigger. The ones sitting right under pleural space can pop and lead to spontaneous

    pneumothorax seen more often in women.

    Compensatory: Seen with partial obstruction.

    Senile: part of aging process.

    Pathogenesis Theory:

    Protease and anti-protease balance.

    Elastase that produces the proteases

    Inflammatory cells prefer proteases and then you have

    A1AT deficiency: you don’t have the anti-

    A1AT deficiency:

    Autosomal dominant disease

    Occurs very early on (< 30 years old)

    Pan-acinar emphysema



    Air spaces are dilated because there’s been some destruction of septa and coalescence of spaces.

    Alveolar septa might club at the end


    CC: dyspnea, wheezing, prolonged expiration, barrel chest (the lungs have ballooned)

    Generally described as pink puffers: hyperventilate enough to maintain regular blood gases.

(2) Chronic Bronchitis

    It’s a clinical definition: a persistent cough with sputum production for 3 months in 2 consecutive years.

Histo changes:

    Increased mucous production.

    Mucous plugs may sit in bronchiole spaces and cause obstruction.


    (1) smoking

    (2) certain inhaled irritants

    (3) certain infections

    CB vs. Emphysema Age of onset: chronic is a little younger (40 years)

    Dyspnea: seen early in CB

    Cough: CB has a productive cough (there’s nothing in emphysematous alv spaces)

CB: blue bloater (can’t keep up with maintaining blood gases)

(3) Bronchial Asthma

    increased irriation of tracheobronchila tree with paroxysmal (comes and goes) narrowing of the airways which reverses

    spontaneously or with treatment.

SO, paroxysmal and reversible separate

Subcategories and causes of asthma:

    (a) Atopic Asthma: triggered by an antigen; increase in IgE and it’s a type I hypersensitivity reaction. The PGs, LKTs,

    cause it.

    (b) Non-Atopic Asthma: is usually precipitated by viral infection (rhinovirus)

    (c) Drug-induced Asthma: common drug is aspirin! (aspirin-sensitive asthma is associated with nasal polyps

    (d) Occupational/Industrial asthma: also a type I hypersensitivity reaction.

    (e) Allergic bronchopulmonary aspergillosis: Aspergillus is a fungus- you’re having an allergic reaction to the



    What kind of inflamm cells will be prominent in asthma? EOSINOPHILS!!!

    You may products of eosinophils: Charcot-Leyden crystals!

(4) Bronchiectasis

    Dilatation of the bronchi! (ectasis is dilation)

    Is due to a chronic, necrotizing infection that involve the bronchi! Patient coughs up funky, foul-smelling garbage.

Boards question:

bronchiectasis is usually seen with a congenital type of disease and that’s Cystic Fibrosis. Must know this. CF is you have

    a problem with secretions (e.g., sweat) with the lungs you have problems with secretions in other places like bile ducts in

    the liver (cirrhosis); pancreas: malabsorption syndrome.

Different kinds of infections you can get with bronchiectasis:

    Pseudomonas is most common. KNOW THIS!

That’s it for obstructive!!!



Infections of the lung:

    (1) Upper RTIs: trachea, bronchus: Called Acute Tracheobronchitis.

    (2) Lower RTIs: What is that? That’s the alveoli, alv septa.: Pneumonia

    Different ways to classify pneumonia:

    (a) Anatomic location

    (b) etiology

    (c) adj descriptors in front of the word: suppurative, fibrinous [not too useful]

Anatomic classification helps you in the etiology:

    Intraalveolar: bacterial pneumonias (inside the alveoli)

     2 types process types:

     (1) Lobar pneumonia

     (2) Bronchopneumonia

     Histologically you’d see the same thing.


    Pathcy, Consolidation of the lung that generally occurs at extremes of age (infancy and old age).

    usually bacterial

    HIstologically: in the alveoli you see a suppurative exudates (neutrophils, fibrin, necrosis); may see some of the bacterial


Stages are similar histologically in bronchopneumonia but because it’s SO patchy you don’t something that looks like liver

Lobar pneumonia

    Same histo process that knocks out a good part of the lung.

    Age: not at extremes

    Most frequent org (95%): Strep pneumonia (aka pneumococcal pneumonia)

Stages of lobar pneumonia: gross description.

    (1) Congestion: vessels are engorged with blood

    (2) Red Hepatization: it looks like red liver: PMNs, neutorphils, fibrin, bacteria

    (3) Grey Hepatization: exudates is digested

    (4) Resolution: it’s resolved.

Interstitial Pneumonia:

    Inflamm cells are in the interstitium.

    The interstitium of the lung is alveolar septa.

    Alveolar septae are thickened because you’ve got inflammatory cells (not bacterial) that are more chronic inflammatory


    VIRUSES cause this (not bacteria), mycoplasma (primary atypical pneumonia, walking pneumonia), Chlamydia


The cough with Interstitial P vs. Intralveolar/Bacterial Pneumonia:

    Non-productive = productive cough

Interstitial Pneumonia:

Symptoms are out of proportion to the physical findings: i.e., they’re very sick (can’t breathe) but when you listen to the

    lungs you don’t hear rowls, etc.

CXR: radiologists can distinguish between these two types!


    A complication of pneumonia



    Pulmonary infection

3 stages:

    Primary: classic thing you see is the GHON COMPLEX.

     The Ghon complex is a subpleural lesion along with caseating lymph nodes.

     Remember cheese-like? Caseous necrosis and is a type of granulomatous inflammation.

     Patient with this is usually asymptomatic.

Secondary: a reactivation of the infection particularly at apex of the lung.

     This patient is sick already.

Late/Progressive: More cavitation, more orgs, more caseating necrosis

     Danger is spread of the infection via lymphatic and hematogenous

     Then you end up with Miliary (Disseminated) Tuberculosis.

     White dots in lung (Like birdseed) and you can see the infection


    Restrictive lung diseases:

Causes known:

    (1) infections

    (2) Drugs and toxins

    (3) Pneumoconioses: lung reactions to inhaled substances

    Causes Unknown:

Pneumoconioses: lung reactions to inhaled substances like mineral dust

    ? most frequent: anthracosis (coal-workers pneumoconiosis)

    ? simple, asymptomatic and you see black lung and you see carbon-laden macrophages

    ? occasionally you can get complicated anthracosis where you get fibrosis too

    (a) you can sometimes RA and pneumoconiosis: Caplan’s Syndrome (boards-type question)

    (b) Silicosis: the most prevalent chronic occupational disease of the wold

    ? you breathe in the silicate fibers that evoke a fibrous reaction

    ? breathe it in, digested by macrophages, and the release of LKTs, and fibrogenic reactions

    ? Nodular concentric fibrosis eventually wipes out the lung

(c) Asbestosis:

    ? what happens is you breathe in the asbestos and it elicits a fibrosing reaction: pleural, calcification, and/or

    interstitial fibrosis.

    ? Thickened alveolar septae with destruction you get coalescence of spacesit looks like a HONEYCOMB!

    ? Interstitial fibrosis and dilated airspaces don’t make this diagnosis

    ? You have to see ferruginous (asbestos) bodies: this is the fiber that’s been coated with hemosiderin!

    ? Asbestos bodies are intra- and/or extracelluar

    ? IC bodies will be in what kind of cell? Macrophages! What kind of macrophages? Multi-nucleated giant cells?

    The foreign body type.

    ? Increased incidence of developing malignancies:

    o 5X risk of general population: Bronchogenic carcinoma

    o 1000X of general population: Mesothelioma

    Now we have to go through this potpourri of restrictive lung diseases of unknown etiology:

    (1) Sarcoidosis:

    Systemic disease that (definitely on boards/exams) involves a non-caseating, granulomatous inflammation

    Can involve lung, lymph nodes

    Females > Males.

    Blacks > whites.

Diff dx: TB, fungi, sarcoidosis.

(2) Diffuse Idiopathic interstitial fibrosis AKA Hammond-Rich Syndrome

    - what you’ll see is interstitial fibrosis (of alveolar septa thickened) - maybe see some inflammation

(3) Desquamated Interstital Pneumonitis (DIP):

    - be able to figure out what you’ll see based on this name - alveolar septae inflammation and you’ll see cells that look like they’re desquamating into the alveolar spaces

    (macrophages are sitting in the spaces)

(4) Hypersensitivity pneumonitis:

    - inflammation is going to be in the alveolar septa (interstitium)

    - this inflammation is pretty far deep

    - hypersensitivity reaction is further down in resp tract (that’s how it differs from asthma)

    - Farmer’s Lung Disease: hay is secondarily infected and that’s how the farmer gets infected

(5) Pulmonary eosinophilia:

    - you’ll see a bunch of eosinophils

    - w/ or w/o peripheral eosinophilia

    - 3 stutuations where we see this:

    (1) Loffler’s syndrome: a transient pulm lesion with eosinophilia + peripheral eosinophilia; benign; resolves

    on own.

    (2) Microfilaria

    (3) Chronically seen due to misc infection

(6) BOOP: Bronchiolitis Obliterans Organizing Pneumonia

    - what you’ll see: inflammation and fibrosis in the alveolar septa AND the alv spaces is being obliterated (scarring,

    fibrosis, inflammation)

(7) Diffuse Pulmonary Hemorrhage Syndrome:

    - interstitial disease that are associated with HEMOPTYSIS

    - know this for boards!

    - Also comes in with renal failure: Goodpasture’s Syndrome

    o Abs directed against BMs in glomeruli and in lungs

    o 1/only causes of hemoptysis and renal failure

    o (WEgener’s Granulomatosis may cause this too) - lung involvement w/o renal involvement: Idiopathic Pulmonary Hemosiderosis

(8) Autoimmune CT diseases:

    - lupus, scleroderma can lead

(9) Pulmonary Alveolar Proteinosis

    - main finding: proteinaceous material in the alveolar; alveolar septum’s probably involved.

    - Pink, bubbly material in alveoli may be confused with Pneumocystic Carinii Pneumonia (PCP)

    - How do you differentiate between PAP and PCP?

    o In GMS stain you have to find the PC orgs! That’s how you differentiate.


    Do you think you’ll see more benign or malignant?


3 terms: synonyms? Yes or no?

    Lung cancer? Lung carcinoma? Bronchogenic carcinoma?

    Broadest term- 1 type of lung cancer.

    Lung and bronchogenic carcinoma is the SAME thing!

    98% carcinomas in lung.

    Different types of carcinomas: Depends on epithelium it comes from: Squamous


    Small cell carcinoma (seen from neuroendocrine cells)


Risk Factors for Bronchogenic Carcinoma:

    (1) smoking

    (2) radiation

    (3) certain industrial hazards like asbestos

    (4) air pollution

    (5) molecular genetics (new one in Robbins this edition)

Most carcinomas arise from what structure in the lung? Bronchi? Alveoli? Proximal? Distal?

    Bronchi-- Proximal! So most carcinomas are centrally located!

Squamous Carcinoma: most common

    Associated with smoking.


    Location is more peripherally located (subpleural)

    Grows more slowly than squamous

    Associated with scarring for some reason

Small cell carcinoma (AKA Oat Cell Carcinoma):

    Strong correlation with smoking

    Cells are dark, round with little cytoplasm and have molding of the nuclei Aggressive, incurable

    Who cares? Why does it matter to differentiate between these 3? SCC is incurable and thus no surgery will be done.





    Maybe fever

    Maybe chest pain

    Weight loss

ParaNeoplastic Syndromes

    Signs and symptoms may be unrelated to the lung itself

    These may be secondary to the tumor

(1) reason is due to the production of hormones

    e.g., Adeno? Produce ADH.

    Squamous: produce PTH.

(2) Myopathy or a peripheral neuropathy

    (3) Acanthosis nigricans (skin problem)

    (4) hypertrophic pulmonary osteoarthropathy (aka clubbing of the fingers)

    Pan-Coasts Tumor Tumors sits in apex of the lung and you’ll develop a Horner’s Syndrome:





Involvement of cervical sympathetic plexus

    1 variant of adenocarcinoma that occurs really peripherally (bronchi, bronchioles, alveolar) is called Bronchioalveolar Carcinoma

Tumor that’s kind of like a carcinoma (neuroendocrine tumor) that presents as a polyploid mass that protrudes: Carcinoid


If it mets, it can produce 5HT and you can develop Carcinoid Syndrome.

3 types of other malignancies in the lung:


    Leiomyosarcoma, liposarcoma, angiosarcoma



    & Metastases


    Big broad categories

    (1) Inflammation

    (2) Tumors

    (1) inflammation

    can be suppurative, chronic inflamm

    usually secondary to something going on in the lung

    Accumulation of diff substance in pleural spaces:

    Hydrothorax: fluid in the pleural space (AKA Pleural effusion)

     -- most common pathophysiologic: Heart failure

    Pneumothorax: knife in lung,

    Hemothorax: blood in the pleural space due to sharp knife

    (2) Tumors

    Mets is most frequent can come from anywhere

    Lung, Breast is most common

    Primary tumor of mesothelium= solitary fibrous tumor

    Primary malignancy is a mesothelioma (terrible term); poor prognosis

     -- strongly associated with pneumoconiosis of the lung due to asbestos


Big broad categories:

    (1) Congenital/Developmental

    (2) Infections

    (3) Neoplasms

    (4) Diseases associated with a bnormal matrix

    (5) Diseases associated with abnormal mineral

    (6) Diseases caused by osteoclastic dysfunction

    (7) Fractures

    (8) Avascular (Osteo-) necrosis


    bone = mineral (calcium hydroxyapatite) + Matrix (collagen) + Cells (osteocytes, osteoblasts, osteoclasts) + protein (is 90% type I collagen)

Subcat of bone:

    Lamellar vs. woven bone:

    Woven bone is new bone: collagen bundles are randomly dispersed.

    Woven bone is eventually replaced by Lamellar (mature bone)

Spongy or Cancellous bone VERSUS Cortical or Compact bone:

    Inside of long bones

Remodeling (osteo--)


2 types of bone formation:

    (1) Endochondral: mainly in long bone at epiphysis (cartilage first, etc.)

    (2) Intramembranous: no cartilage- occurs mainly in skull


    Absent/extra digit

    Cranioraschisis: failure of closure of spinal column in the skull

    Achondroplasia: failure of cartilage to develop, long bones are short relative to size of torso and skull

     (circus dwarfs)

Diseases associated with abnormal matrix:

    (1) problem with Type I collagen-- not seen often

    (2) seen often (50.4% of world): osteoporosis

    (1) Osteogenesis Imperfecta (AKA Brittle Bone Disease)

    this is the most common hereditary bone diseass and several different subtypes.

    Usually autosomal dominant.

    Problem with type I collagen

    Main problem is multiple, frequent fractures.

    Patients have blue sclera, deafness, loose joints, teeth discoloration.

    (2) Osteoporosis:

    A loss of bone mass (making sekelton vulnerable to fractures).

    There’s a decrease in osteoblastic activity relative to an increase in osteoclastic activity. It’s common as you get older,

    particularly seen in post-menopausal women.

    Increasing age, decrease in physical activity, problems with Vit D and thus calcium, and hormonal influence (estrogen

    decreases osteoclastic activity) are risk factors.

    Diagnosis is made by doing a bone scan and X-ray (see bone density).

    Calcium phosphorus, alkaline phosphatase is NORMAL in the blood.

Diseases Caused by Osteoclast Dysfunction

    Remember that

    (1) Decrease in osteoclastic activity

    (2) Increase in osteoclastic activity

    (1) ALBERS-SCHONBERK DISEASE AKA Marble Bone Disease AKA OSTEOPETROSIS: (AKA Osteosclerosis)

    Decrease in osteoclastic activity

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