Pathoma-Lecture-Notes

2. What's a complication of chronic rheumatic fever?
- Infective endocarditis

Aortic stenosis
1. What are some causes of aortic stenosis?
- Normal wear and tear of valve
- Bicuspid aortic valve (speeds up wear and tear)
- Chronic rheumatic fever

2. What is its presentation?
- Presents in late adulthood (>60 years)
- Crescendo-decrescendo murmur with systolic ejection click (click is when the valve opens?)

3. How do you distinguish stenosis from chronic rheumatic fever vs normal wear and tear?
- In chronic rheumatic fever, there is fusion of commissures of aortic valves. Also, we see mitral

stenosis.

4. What are complications of aortic stenosis?
- Concentric left ventricular hypertrophy - may progress to cardiac failure
- Angina with syncope with exercise (decreased perfusion of heart and brain)
- Microangiopathic hemolytic anemia (see schistocytes)

5. How do you treat aortic stenosis?
- Valve replacement

Aortic regurgitation
1. What are causes of aortic regurgitation?
- Isolated aortic root dilation (most common cause)
- Aortic dissection, Syphillis (causes aortic root dilation)
- Valve damage, ex - infective endocarditis

2. What are clinical features of aortic regurgitation?
- Increased pulse pressure (water-hammer pulse) - diastolic pressure is low due to regurgitation,

systolic pressure increases due to increased stroke volume (pulse pressure is difference between
systolic and diastolic pressures)
- LV dilation and eccentric hypertrophy due to volume overload

3. What is treatment of aortic regurgitation?
- Valve replacement once LV dysfunction develops

Cardiac Page 4.2

Mitral valve prolapse
1. What is mitral valve prolapse? What are some etiologies?
- Mitral valve prolapse is ballooning of mitral valve into left atrium during systole
- It occurs due to myxoid degenration of valve making it floppy
- Etiologies:
○ Marfan syndrome
○ Ehlers-Danlos syndrome

2. What is presentation of mitral valve prolapse?
- Mostly asymptomatic
- Mid-systolic click followed by regurgitation murmur
- Murmur is softer with squatting (increased systemic resistance decreases left ventricular

emptying)

3. What are complications?
- Rare but infective endocarditis, arrhythmia and severe mitral regurg

4. What is treatment of mitral valve prolapse?
- Valve replacement

Mitral regurgitation
1. What are some causes of mitral regurgitation?
- Complication of mitral prolapse
- LV dilation
- Infective endocarditis
- Acute rheumatic fever - vegetation on valve edge prevent smooth closing
- Papillary muscle rupture after MI

2. What is presentation of mitral regurgitation?
- Holosystolic "blowing" murmur; lower when squatting (increased systemic resistance decreases

LV emptying) and expiration (increases blood return to LV)
- Volume overload and left sided failure

Mitral stenosis
1. What are some causes of mitral stenosis?
- Chronic rheumatic valve disease most common cause

2. What are presentations of mitral stenosis?
- Opening snap followed by diastolic rumble
- Volume overload with dilation of left atrium:

○ Pulmonary congestion with edema and alveolar hemorrhage
○ Pulmonary HTN and eventual right sided heart failure
○ A-fib with mural thrombus

Cardiac Page 4.3

8.5 Endocarditis

1. What is endocarditis?
- Inflammation of endocardium (mostly valves) usually due to bacterial infection.

Pathogen

1 S. viridans Most common cause of Subacute endocarditis (small
endocarditis; dental vegetations)
procedure

2 S. aureus Most common cause of Acute endocarditis (large
endocarditis in IV drug vegetations)
users

3 S. epidermidis Key organism to cause

endocarditis of prosthetic

valves

4 Strep bovis Cause endocarditis in pt
with colorectal carcinoma
(HY)

5 HAECK organism Hemophilus, Cause endocarditis with negative
Actinobacillus, blood culture (because
Cardiobacterium, pathogens difficult to grow)
Eikenella, Kingella

6 Nonbacterial Occurs if pt is

thrombotic hypercoagulable or has

endocarditis adenocarcinoma

7 Libman-Sacks Sterile vegetations on Associated with lupus

endocarditis both side of mitral valve

8 Coxiella burnetti Most common cause of
culture -ve endocarditis

1. Describe endocarditis due to S. viridans.
- Most common cause of endocarditis.
- Low virulence pthogen; therefore mainly infects previously damaged valves
- Results in small vegetations that don't destroy valves (therefore called subacute endocarditis)

3. Describe pathogenesis of endocarditis due to S. viridans.
- Damaged endocardial surface develops thrombotic vegetations
- During transient bacteremia (ex - dental procedure), bacteria can be trapped in these vegetations

4. Describe endocarditis due to S. aureus.
- Most common cause of endocarditis in IV drug abusers
- High virulence organism; can infect normal valves (mainly tricuspid)
- Vegetations are large and destroy valve (called acute endocarditis)

Cardiac Page 5.1

Fig - staph aureus endocarditis
5. Describe clinical presentation of endocarditis. (FOR JANE)
- Fever
- Murmur
- Janeway lesion - mainly on palm and sole (painless)
- Osler nodules (hurts - ouch!) - mainly on finger and toes (painful)
- Roth nodules
- Hemolytic anemia (usually microcytic)
- Nailbed splinter hemorrhage
- Emboli

Fig - roth nodules (retinal hemorrhage); osler and roth nodules are immunologic.
Endocarditis may lead to glomerulonephritis and positive Rheumatic factor.
6. How does endocarditis lead to low blood iron.
- Acute phase reactant proteins are made (hepsidin being one major one). Hepsidin traps iron in
storage site. This leads to high ferritin. Also, bone marrow takes iron from blood because hepsidin
is trapping iron in storage site. That’s how serum iron decreases.
7. Describe nonbacterial thrombotic endocarditis.
- It is sterile vegetation seen on valves during hypercoagulable state or underlying adenocarcinoma.

Cardiac Page 5.2

- It is sterile vegetation seen on valves during hypercoagulable state or underlying adenocarcinoma.
- These vegetations occur on bicuspid valves along lines of closure and lead to mitral regurg
8. Describe Libman-Sacks endocarditis.
- Sterile vegetations on both side of mitral valve - leads to mitral regurg
- Associated with lupus (HY)
9. Describe diagnosis of endocarditis.
- Surface Echo - 60% sensitive
- Transesophageal echo - 90% sensitive
- Endocarditis leads more often regurg of valves rather than stenosis
- If valve vegetation is >1cm, consider surgery of valves

Cardiac Page 5.3

8.6 Cardiomyopathy

1. Describe dialated cardiomyopathy.
- Most common type of cardiomyopathy
- Leads to systolic dysfunction (heart can't contract very well)
- Complications:

○ mitral and tricuspid regurg
○ Arrhythmia (heart's conduction system is stretched up)
2. What are some causes of dialated cardiomyopathy?
- Idiopathic in most cases
- Mutation - they are autosomal dominant
- Myocarditis - coxcakie virus most common pathogen
- EtOH abuse (HY)
- Drugs - doxorubicin, cocaine
- Pregnancy (HY) - occurs in 3rd trimester or soon after birth

Fig - myocarditis; notice the presence of lymphocytes. Most common cause is coxcakie virus;
acutely, it can cause death; in chronic cases, it can cause dialated cardiomyopathy
3. What is treatment for dialated cardiomyopathy?
- Nothing; pt need transplant
Hypertrophic cardiomyopathy
4. Describe hypertrophic cardiomyopathy.
- Massive hypertrophy of left ventricle
- Most common cause (HY): due to autosomal dominant mutations in sarcomere proteins
5. What are its clinical presentation?
- Diastolic dysfunction (heart doesn't fill well)
- Sudden death in young athletes due to ventricular arrhythmias.
- Syncope with exercise
- Biopsy (HY):

○ Myofiber hypertrophy with disarray

Cardiac Page 6.1

Fig - myofiber hypertrophy and disarray (fibers oriented in different directions)common in
hypertrophic cardiomyopathy
Restrictive cardiomyopathy
6. What is restrictive cardiomyopathy and it's causes?
- Diastolic dysfunction
- Causes
○ Amyloidosis
○ Sarcoidosis
○ Hemochromatosis
○ Endocardial fibroelastosis (in kids) - there's fibrosis and elastosis in endocardium
○ Loeffler syndrome - eosinophilic inflammation of endocardium and myocardium
7. What is EKG finding of restrictive cardiomyopathy?
- Low voltage EKG
- Diminished QRS amplitudes

Cardiac Page 6.2

8.7 Cardiac Tumors

Myxoma Rhabdomyoma Metastasis
Most common cardiac tumor
Most common cardiac tumor in Most common cardiac
adults tumor in children

Benign mesenchymal tumor with Benign hamartoma of
abundant ground substance in cardiac muscle
histology
Usually seen in ventricle Most commonly affects pericardium
Pedunculated mass in left atrium and seen as pericardial effusion

Associated with tuberous Breast, lung carcinoma, melanoma and

sclerosis lymphoma common source of

metastasis

Myxoma
1. What is most common primary cardiac tumor in adults?
- Myxoma

2. What type of tumor is myxoma?
- Benign mesenchymal tumor with abundant ground substance in histology

2. What is its presentation?
- Pedunculated mass in left atrium that can obstruct mitral valve (syncope)

Fig: biopsy (abundant ground substance) and autopsy of myxoma

Rhabomyoma
1. What is most common primary cardiac tumor in children?
- Rhabdomyoma

Cardiac Page 7.1

2. What kind of tumor is rhabdomyoma?
- Benign hamartoma of cardiac muscle
- Usually seen in ventricle
2. What is it associated with?
- Tuberous sclerosis (a genetic disorder that causes non-malignant tumors in many different organs,

primarily in the brain, eyes, heart, kidney, skin and lungs. Common presentation: seizures,
developmental delay, intellectual disability and autism)

Fig: rhabdomyoma
Metastasis

1. What is most common type of cardiac tumor?
- Metastasis (more common than primary tumors)
2. What are common sites of metastasis?
- Breast, lung carcinoma, melanoma and lymphoma
3. What is its most common presentation?
- Most commonly affects pericardium and seen as pericardial effusion

Cardiac Page 7.2

Chapter 9: Respiratory Tract
Pathology

9.1 Nasopharynx, 9.2 Larynx

Nasopharynx
1. Differentiate angiofibroma and nasopharyngeal carcinoma.

Angiofibroma Nasopharyngeal carcinoma

Defn Benign tumor of nasal mucosa Malignant tumor of nasopharyngeal epithelium
made up of large blood vessels
and fibrous tissue

Demograp Classically seen in adolescent - Classically seen in Chinese young adults and
hics males - very rare in females african kids

Presentati Presents with profuse epistaxis - Associated with EBV
on (nose bleed) - HY - Often involves cervical lymph nodes

Biopsy Biopsy - pleomorphic keratin positive epithelial
cells (poorly differentiated SCC) in background
of lymphocytes (HY)

2. Differentiate Rhinitis and Nasal polyp.

Rhinitis Nasal polyp

Cause Rhinovirus no 1 cause - Secondary to repeated rhinitis (HY)
- CF (if you see child with nasal polyp, suspect CF) -
HY
- Asprin intolerant asthma (HY)

Presentatio Runny nose, sneezing, Protrusion of edematous, inflamed nasal mucosa
n congestion

3. What is allergic rhinitis? What's it's associated with?
- A type of rhinitis caused due to type 1 hypersensitivity reaction (ex - pollen)
- Association:

○ Asthma
○ Eczema
- Presentation:
○ Eosinophilic infiltrate

4. What is aspirin intolerant asthma?
- Presents as triad of asthma, aspirin induced bronchospasm and nasal polyps.

Pulmonary Page 1.1

- Presents as triad of asthma, aspirin induced bronchospasm and nasal polyps.
- Seen in 10% of asthma patients

Larynx
1. Differentiate laryngeal papilloma and laryngeal carcinoma

Laryngeal papilloma Laryngeal carcinoma

Defn Benign papillary tumor of vocal cord SCC of epithelial lining of vocal cord

Cause HPV 6 and 11; EtOH and smoking (papilloma rarely
progress to carcinoma)

Presentatio - Hoarseness of voice - Hoarseness of voice

n - Usually single in adults and multiple - Cough and stridor

in children (HY)

2. Differentiate acute epiglottitis and laryngotracheobronchitis (croup).

Acute epiglottitis laryngotracheobronchitis (croup)

Cause H. Influenzae type b most common cause (in Parainfluenza virus most common
immunized or non-immunized kids. cause

Present Too much drooling, dysphagia, sore throat, Barking cough and inspiratory
ation fever, muffled voice, inspiratory stridor stridor

xray Thumb sign on xray Steeple sign on Xray

Risk of actue airway obstruction (medical
emergency)

3. What is vocal cord nodule (singer's nodule)? What's its cause?
- Nodule on true vocal cord

Pulmonary Page 1.2

- Nodule on true vocal cord
- Caused due to excessive use of vocal cord; usually bilateral (wear and tear issue
- Composed on degenerative myxoid connective tissue
- Treat with rest

Fig: vocal cord nodule (usually bilateral and seen on true vocal cord)

Pulmonary Page 1.3

9.3 Pulmonary Infections

1. What is pneumonia? What causes it?

- It's infection of lung parenchyma.

- Causes:
○ Lack of cough reflex
○ Damage to mucociliary escalator
○ Mucus plugging

2. What are presentation of pneumonia?
- Fevers and chills (organism usually leak out to blood)
- Cough with yellow-green (pus) or rusty (blood) sputum
- Tachypnea with pleuritic chest pain (inflammation produces bradykinin and PGE2 which causes pain)
- Decreased breath sounds and dullness to percussion (loss of air volume due to exudates will result in dullness

to percussion)
- Elevated WBC count (due to infection)

3. How do you diagnose pneumonia?
- X-ray
- Blood culture/ sputum stain and culture

4. What are patterns of pneumonia seen on Xray?

Lobar pneumonia Bronchopneumonia Interstitial pneumonia (aka atypical pneumonia)

- Affects whole lobe - Affects area around - Inflammation of interstitium without consolidation of air
bronchioles (mostly sacks (see increased lung markings in X-ray)
multifocal)

- Cause is mostly - Cause is mostly - Called atypical because need special media to grow the
bacterial bacterial bacteria. Viruses also cause it

- Most common Bacterial causes:
cause: - Mycoplasm pneumoniae
- Chlamydophilla
• Strep. - Legionella (pathoma puts legionella in broncho)
Pneumoniae
(95%)

• Klebsiella
pneumoniae

• H influenziae

Treat: ceftriaxone Treatment:

Fig - lobar pneumonia (right), bronchopneumonia (middle), interstitial pneumonia (left). Note lack of alveolar
exudate in interstitial pneumonia

Pulmonary Page 2.1

exudate in interstitial pneumonia

Lobar pneumonia Bacteria Association

Strep pneumo • Most common cause of community acquired pneumonia

Klebsiella pneumoniae • enteric flora that's aspirated.
• Common seen in alcoholics, nursing home pt.
• Bacteria has thick mucoid capsule, so see currant jelly sputum.
• Often complicated by lung abscess

Broncho pneumonia Association
bacteria
Staph aureus • Most common cause of secondary pneumonia (pneumonia superimposed on viral
upper respiratory tract infection)
Haemophilus
influenzae • Often complicated by abscess or emphyema (free pus in pleural space)
Pseduomonas • Common cause of secondary pneumonia
aeruginosa • Associated with COPD
Moxarella catarrhalis • Associated with cystic fibrosis patients

Legionella • Associated with COPD
pneumophila • Community acquired
• Transmitted from water source
• Associated with COPD and immunocompromised states
• Intracellular organism visualized by silver stain
• Pt. Presents with pneumonia, diarrhea, and hyponatremia

Atypical pne Association
organism

Mycoplasma • Most common cause of atypical pneumonia
pneumoniae • Affects young adult in close quarters (military recruits, dorm students)
• Complications: autoimmune hemolytic anemia (IgM against I antigen on RBC),

erythema multiforme

Chlamydia • 2nd most common cause of atypical pneumonia in young adults
pneumoniae

Respiratory • Most common cause of pneumonia in infants

syncytial virus (RSV)

Cytomegalovirus • Associated with posttransplant immunosuppressive therapy
(CMV)

Influenza virus • Commonly seen in elderly, immunocompromised, or people with preexisting lung
disease

• Increases risk for S aureus or H influenza secondary pneumonia

Coxiella burnetti • Pneumonia with high fever (Q fever; generally, pneumonia has low fever)
• Associated with farmers and veterinarians
• Coxiella is different from rickettsia in 3 ways: causes pneumonia, does not require

arthropod for transmission (transmitted as spores), does not produce rash

5. What are four classic phases of lobar pneumonia?
- Congestion - due to edema
- Red hepatization - due to neutrophil and RBC exudate. Hepatization because previously spongy lung is now

tough due to fluid

Pulmonary Page 2.2

tough due to fluid
- Grey hepatization - breaking down of RBC makes lung gray.
- Resolution - lung tissue is regenerated by type II pneumocytes

6. What is aspiration pneumonia? What are it's causes? What's it's presentation?
• Seen in patients at risk for aspiration (ex - comatose, alcoholics)
• Causes: anaerobic bacteria of oropharynx:

○ Bacteroides
○ Fusobacterium
○ Peptococcus
○ Kliebsiella (is it anaerobic?)
• Classic presentation:
○ Right lower lobe abscess

Tuberculosis
1. Describe presentation of primary TB.
• Caused by inhalation of bacteria.
• Presentation:
○ Focal caseating necrosis classically in lower lobe and hilar lymph nodes
○ The foci undergo fibrosis and calcification resulting in Ghon complex
○ Mostly asymptomatic
○ Leads to positive PPD

Fig: Ghon complex (calcified and fibrosed lung): classic location is subpleural region near hylar nodes

1. Describe presentation of secondary TB (aka reactivated TB).
• Commonly seen due to immunosuppression, AIDS, or old age
• Presentation:

○ Usually affects upper lobes
○ Forms many focal caseating necrosis, or miliary TB or TB bronchopneumonia
○ Symptoms:

▪ Fevers and night sweats
▪ Cough with hemoptysis
▪ Weight loss

9. What are classic locations for spread of miliary TB?
• Kidney - most common organ to be involved - gives sterile pyura
• Meninges (classic location is base of brain)
• Cervical lymph nodes
• Lumbar vertebrae (pott disease)

Pulmonary Page 2.3

9.4 Chronic Obstructive Pulmonary Disease

1. What is COPD? What are some findings?
• COPD is obstruction to getting air out of lungs.
• Findings:

○ Low FEV1:FVC ratio - Decreased FVC, even more low FEV1
○ Normal FEV1:FVC is 80%. Normal TLC = 7 L.
○ Increased TLC due to air trapping
2. What are some causes of COPD?
- Chronic bronchitis (blue bloaters)
- Emphysema (pink puffers)
- Asthma
- Bronchieatasis

Chronic bronchitis
3. What is chronic bronchitis? What is the mechanism?
- chronic productive cough lasting at least 3 months over a minimum of 2 years
- hypertrophy of bronchial mucinous glands--patients cough up cups of mucous
4. Describe pathophysiology of chronic bronchitis and histology of airway?
- Below lamina propria are serous glands (secrete water to humidify air) and mucous glands
(secrete mucus to trap pollutants).

Pulmonary Page .1

(secrete mucus to trap pollutants).
- With chronic smoking, mucus glands undergo hypertrophy and hyperplasia. This causes tons of

mucus production, and the mucus can plug airways causing hypoxemia.
- Other:

○ Epithelium is pseudostratified columnar
○ Lamina propria has venules that warm the cold air coming from outside

Fig: Cross section of chronic bronchitis. Top right portion has respiratory epithelium, bottom left
has cartilage. It's clearly visible that mucus glands make >50% thickness of airway.
5. With what is chronic bronchitis highly associated?
- Smoking
6. What are the clinical features of chronic bronchitis?
- productive cough due to excessive mucous production,
- cyanosis ('blue bloaters') - mucus plugs trap CO2;
- increased risk of infection (anytime you plug a tube, it increases risk of infection behind the block)
- Reid index Increases to >50 from <40%;
- Cor pulmonale (pulm HTN) - due to globally low PAO2 in lungs (low PAO2 induces
vasoconstriction)
7. What is Reid index?
- It's the ratio of thickness of airway mucous gland to total thickness of airways. Normally, it's <40%.

Emphysema
8. What is emphysema?
• Destruction of alveolar air sac and multiple sacs combine to become one.
• Due to loss of elasticity of air sacs, lung becomes like a shopping bag, not effectively expelling air
out.
• Also, elasticity of air sacs attached to bronchioles keep the bronchiole open during expiration.
When the sacs are gone, then bronchioles collapse during expiration.

Pulmonary Page .2

Fig: Histology of emphysema showing multiple air sacs combining to make one.

9. What is pathophysiology of emphysema?
• Imbalance between protease and antiprotease. Inflammation induces high protease activity. So,

smoking leads to inflammation which leads to emphysema.

10. Differentiate two classic causes of emphysema (destruction of alveolar air sacs).

Smoking (no. 1 cause of emphysema) A1AT deficiency (alpha 1 antitrypsin) -

Pollutants cause inflammation that induce A1AT is an important antiprotease that
protease mediated damage to alveoli inhibits protease damage to alveoli

Centriacinar emphysema seen mainly in upper Panacinar emphysema seen mainly in lower
lobes (upper lobes have more air) lobes

Can cause liver cirrhosis too

Complications: hypoxemia and cor pulmonale Complications: hypoxemia and cor pulmonale
(pulm HTN) (pulm HTN)

11. What is acinus?
• Functional unit of lung (a terminal broncheole and alveoli associated with it)

12. Why does A1AT deficiency cause cirrhosis?
- A1AT deficiency is due to misfolding of mutated protein, mutant A1AT accumulates in ER of
hepatocytes which results in liver damage.
- A1AT is doesn't go to blood and lung because it's not exported by liver.

13. What does liver biopsy in A1AT deficiency show? (HY)
- Pink-purple, PAS-positive (a stain) globules in hepatocytes. Note - mucin and tropheryma whipplei
are also PAS +ve

Pulmonary Page .3

14. Describe the genetics of A1AT transmission.
- PiM - normal allele
- PiZ - mutant allele

PIMM • Norman healthy person

PiMZ - Haterogytoes; usually asymptomatic (low circulating A1AT)
- Significant emphysema risk with smoking

PiZZ - Homozygous mutant
- Significant risk for panacinar emphysema and cirrhosis

15. What are clinical presentation of emphysema?
- Dyspnea and cough
- Minimum sputum - contrast to chronic bronchitis
- Prolonged expiration with pursed lips (pink puffer) - pursed lips create back pressure to prevent
airway collapse (pt are not cyanotic because they are oxygenated; in chronic bronchits,
broncheoles are plugged up)
- Barrel chest - increased anterior-posterior diameter of lung
- Weight loss - use muscles to breathe
- Late complication:
○ Cor pulmonale
○ Hypoxemia in late stage due to loss of capillaries

Asthma
16. What is asthma?

- Reversible airway bronchoconstriction, most commonly seen due to allergic stimuli (atopic
asthma)

- Associated with allergic rhinits, eczema (atopic dermatitis) and family history of atopy (tendency
of type I hypersensitivity reactions)

- Commonly seen in kids

17. What is pathogenesis of asthma? (HY)
- Allergens induce TH2 phenotype in genetically susceptible patient. TH2 secretes:

IL-4 Induces class switching to IgE

IL-5 Attracts eosinophils

IL-10 Stimulates TH2 and inhibits TH1

- IgE coats mast cells and next time same allergen is encountered, massive mast cell degranulation
occurs.

- Histamines (arteriolar vasodilation and increase vascular permeability) and leukotriene
(vasoconstriction, increased vascular permeability (by constricting pericytes), and
bronchoconstriction) are released by mast cells.

Pulmonary Page .4

bronchoconstriction) are released by mast cells.
18. What is late phase reaction in asthma? (HY)

- Eosinophils release MAJOR BASIC PROTEIN that damages cells and induces bronchoconstriction
19. What are clinical features of asthma?

- Productive cough, dyspnea, wheezing in response to allergen exposure (episodic).
20. What are biopsy findings in asthma?

- Curschmann spirals (spiral shaped mucus plug)
- Charcot-leyden crystals (HY) (eosinophil derived MAJOR BASIC PROTEIN that indicate eosinophilic

inflammation)

Fig: Carcot leyden crystal on left and curschmann spiral on right
21. What are nonallergic causes of asthma?

- Exercise
- Viral infection
- Asprin (HY)
- Occupational exposure
22. What is presentation of asprin intolerant asthma?
- Nasal polyps (nasal polyp in kids highly associated with CF)
- Bronchospasm with aspirin
Bronchiectasis
1. What is bronchieatasis?
- Necrotizing damage to airway walls lead to permanent dilation of bronchioles
- Imagine if you blow air into a big tube, the air will just move randomly inside the tube and might

not come out

Pulmonary Page .5

Fig: large dilated structures are airway, not coeleaced alveoli
2. What is pathophys of bronchiectasis?
- Loss of muco-ciliary clearance system is the main problem. Mucus accumulation followed by

bacterial overgrowth leads to pus filled infection and permanent dilation of airways.
3. What are come cauases of bronchiectasis?

Causes:
○ CF (classic pt)
○ Allergic bronchopulmonary aspergillosis - classically seen in asthamits and CF pt.
○ Kartagener syndrome (mutation of dyenin arm cilia)
○ Tumor or foreign body that blocks airway (infection behind block can cause necrosis).

3. What is presentation and complication of bronchiectasis?
- Cough, dyspnea and foul smelling sputum
- Complication:

○ secondary systemic amyloidosis (HY) - systemic increase in SAA (an acute phase reactant)
produced chronically due to chronic inflammation. SAA is converted to AA that's deposited.

○ Hypoxemia and cor pulmonale
4. What is presentation of Kartagener syndrome?
- Sinusitis (cilia in nasal sinus not working well)
- Infertility
- Inversion of body organs (ex - heart on right)
- Bronchiectasis

Pulmonary Page .6

9.5 Restrictive Diseases

1. What are 4 examples of restrictive lung disease?
- Idiopathic (10), 20 pulmonary fibrosis
- Pneumoconioses
- Sarcoidosis
- Hypersensitivity pneumonitis (pigeon breeder's lung)

2. What are etiologies of 10 and 20 pulmonary fibrosis?
Primary Increased TGF beta --> induce fibrosis
Secondary Amiodorone, bliomycin, radiation
You need lung transplant for pulmonary fibrosis

3. What is pneumoconiosis? What's its pathophysiology?
- Interstitial lung disease caused due to chronic occupational exposure with fibrogenic material.
- Pathophys - macrophages ingest fibrogenic material and induce fibrosis

4. What are some examples of pneumoconiosis?

Example Risk group Complication Presentation

Silicosis Sand blasters - High risk of TB (inhibits - Silicotic nodule (lots of collagen with
phagolysosome formation) minimum inflammation)
- High risk for lung
carcinoma

Berylliosi Beryllium High risk for lung cancer Non caseating granuloma in hylar nodes
s miners and other organs

Aerospace
workers

Asbestos Construction High risk of lung carcinoma - Asbestos body (ferruginous body) in
is workers (more) and mesothelioma biopsy - ferritin and hemosiderin coat
asbestos
Plumbers - Pleural plaques
Shipyard
workers

Pulmonary Page .1

Fig: A: Asbestos body (ferritin and hemosiderin coated asbestos particle); B: pleural plaque on
diaphragmatic pleura; C: Silicotic nodule, notice lots of collagen with minimum inflammation

5. What is presentation of sarcoidosis?
- Sarcoidosis is non-caesating granuloma in multiple organs (most commonly localized in lungs and

hyalar lymph nodes)
- Presentation: non specific - fatigue, wt loss, joint pain and arthritis
- Others: uveitis, erythema nodosum, cardiac sarcoidosis, neurosarcoidosis (affects CN often)etc
- Hypercalcemia (HY) -

○ 1 alpha hydroxylase activity of epithelial histiocytes convert vit D to active form
- Asteroid bodies are seen in biopsy (not-specific; can be seen in giant cells of any granulomas)

Fig: asteroid bodies seen in giant cells of granulomas (present in sarcoidosis)

6. What is hypersensitivity pneumonitis (aka extrinsic allergic alveolitis)?
- It is granuloma and interstitial inflammation caused due to inhaled organic or non-organic matter

(aka pigeon breeder's lung).
- Pathophys:

○ Ab-Ag complex forms in lung that activates neutrophils and eventually lymphocytes.
Lymphocytes mediate most damages

- Cause:
○ many organic and non-organic matters

- Presentation:
○ fever/cough hours after exposure
○ Chronic exposure leads to interstitial lung diseaese

7. How is iron stored in body?
- Free Fe produces ROS by Fenten reaction so cells store free Fe in ferretin protein or hemosiderin

Ferretin Hemosiderin

Intracellular protein that acts as buffer against Fe overload or Intracellular complex made of

shortage (protein can be secreted too) Ferretin and other stuff

Fe in Ferretin can be given out when needed Fe here is poor source to supply
to body

Pulmonary Page .2

to body
Plasma Ferretin correlates well with total Fe in body; so serum
ferretin a common test to access anemia.

Pulmonary Page .3

9.6 Pulmonary Hypertension

1. What is pulmonary hypertension?
- Mean arterial pressure in pulmonary circulation >25 mm Hg (normal is 10 mm Hg) is pulmonary

hypertension

2. What are causes of pulmonary HTN?
- Causes can be divided to primary and secondary.

Primary pulmonary HTN Secondary pulmonary HTN

- Etiology unknown (some familial forms - Hypoxemia (COPD, interstital lung disease)
related to BMPR2 mutation (HY) - see - Increased volume in pulm circuit (congenital heart
proliferation of vascular smooth muscle) disease)
- Recurrent pulmonary embolism (HY)

- Classically seen in young adult females

3. What are clinical characters of pulmonary hypertension?
- Characterized by atherosclerosis of pulmonary trunk (HTN leads to artherosclerosis) and smooth

muscle hypertrophy of pulmonary arteries, intimal fibrosis
- See plexiform lesions with severe long standing disease
- Right ventricular hypertrophy with cor pulmonale
- Exertional dyspnea and right sided heart failure - if you see a young woman with exertional

dyspnea, think pulmonary hypertension

Fig: plexiform changes - tuft of capillaries that arise as a complication of HTN

Pulmonary Page 5.1

9.7 Respiratory Distress Syndrome (RDS)

Acute respiratory distress syndrome
1. What is ARDS?
- Respiratory distress due to damage to alveolar-capillary interface (diffuse alveolar damage).
Protein rich fluid leaks into air sac. Protein rich fluid and epithelial cells are reorganized to make
hyaline membrane.
- Membrane blocks air exchange; membranes are sticky and promote alveoli collapse.

Fig: hyaline membrane seen on alveoli represents ARDS (right); diffuse whiteout seen in Xray in
ARDS (left)

2. What are causes of ARDS?
- Mechanism is activation of neutrophils that induces protease and free radical damage of type I

and II pneumocytes.
- It's occurs secondary to (100's of causes)

○ Sepsis
○ Infection
○ Shock
○ Trauma
○ Aspiration
○ Pancreatitis
○ DIC
○ Hypersensitivity reactions
○ Drugs

3. What's presentation of ARDS?
- Hypoxemia and cyanosis (due to thickened diffusion barrier and collapse of air sacs)
- White out on chest x-ray
- Hyaline membrane in alveoli on biopsy

4. How do you treat ARDS? What makes recovery complicated?
- Ventilation with positive end-expiratory pressure (PEEP) - every time patient breathes out, the

lung collapses a little more due to hyaline membrane. Positive pressure at end of respiration
prevents this.
- Treat underlying cause
- Recovery may be complicated due to interstitial fibrosis. Type II pneumocytes (stem cells) are
damaged and new cells can't be generated. (HY)

Pulmonary Page 6.1

Neonatal respiratory distress syndrome
1. What is neonatal respiratory distress syndrome?
- Respiratory distress in newborn due to inadequate surfactant production. Alveoli collapse and
hyaline membranes are seen.
2. How is enough surfactant production determined in fetus?
- Surfactant (phosphatidylcholine aka lecithin) is produced by type 2 pneumocytes from 28 weeks;
enough levels are not reached until 34 weeks (childbirth occurs in 40th week)
- Amniotic fluid ratio of lechitin to sphingomyelin >2 indicates enough surfactant production
3. What are some causes of neonatal respiratory distress syndrome?
- Premature birth
- Caesarian section delivery - child lacks stress induced steroids; steroids increase surfactant
production and release from pneumocytes
- Maternal diabetes - insulin decreases surfactant production (high blood sugar from mom causes
high insulin production in baby)
4. What is presentation of neonatal respiratory distress syndrome?
- Hypoxemia and cyanosis
- Ground glass appearance on X-ray
- Increased use of respiratory muscle; use of accessory muscle, grunting
5. What are it's complication?
- High risk of patent ductus arteriosus and necrotizing enterocolitis (decreased
- Supplemental oxygen used for treatment increases risk of free radical injury
○ retinal injury leads to blindness (O2 treatment for ARDS imp cause of blindness in neonates)
○ lung damage leads to bronchopulmonary dysplasia

Pulmonary Page 6.2

9.8 Lung Cancer

1. What are key risk factors for lung cancer?
- Cigarette smoking (85% of lung cancer)

○ Risk directly linked to duration and amount of smoking (pack years)
- Radon (2nd most common cause) - most common ionizing radiation exposure in USA

○ Colorless, odorless gas
○ Decay product of uranium
○ Found in soil, accumulates in closed space (basement)
- Asbestos

2. What is carcinogenicity of cigarette smoking?
- Contains > 60 carcinogens
- Polycyclic aromatic hydrocarbons and arsenic are particularly carcinogenic
- Cancer risk directly increases with duration and amount of smoking (pack years)

2. What is presentation of lung cancer?
- Average age at presentation is 60.
- Most common cause of cancer death in USA
- Nonspecific presentation -

○ Cough, wt loss, hemoptysis, post obstructive pneumonia

3. How do you diagnose lung cancer?
- Diagnosis requires biopsy
- Imaging reveals solitary nodule (coin-lesion) - growing lesion concerning
- Coin lesions also seen in (HY):

○ Granulomas - TB, fungus (ex - histoplasma in midwest)
○ Bronchial hamartoma - benign tumor of lung tissue + cartilage; often calcified in imaging
○ Harmartoma - disorganized mass that grows at same rate as surrounding tissue; made of same cells that

makes the tissue

4. Describe the TNM staging of lung cancer.
- T - tumor size

i. Pleural involvement classically seen in adenocarcinoma (adenocarcinoma is peripheral)
ii. Obstruction of SVC (superior vena cava syndrome) - distended head and neck veins with edema and blue

discoloration of arms and face
iii. Involvement of recurrent laryngeal nerve (hoarseness) or phrenic nerve (diaphragmatic paralysis)
iv. Horner's - compression of sympathetic chain (ptosis, anhydrosis - in skin, miosis) - especially if tumor is at

apex of lung (pancoast tumor)
- N-

○ Spread to hilar and mediastinal lymph nodes
- M-

○ Unique site of distant metastasis is adrenals (HY)
○ Others - brain, bone, liver

5. What's prognosis of lung cancer?
- Poor (no effective screening method) - 5 year survival rate is 15%

6. What are two categories of lung cancer?
Small cell carcinoma (15% of all lung carcinoma) Non-small cell carcinoma (85% of all lung carcinoma)

Pulmonary Page 7.1

- Usually no amenable to surgery (treat with - Adenocarcinoma (40%) - glands or mucus production
chemotherapy and radiation) - Squamous cell carcinoma (30%) - keratin pearls or intercellular
bridges
- Large cell carcinoma (10%) - none of above features seen
- Carcinoid tumor (5%)

- Treat upfront with surgery (doesn't respond well to
chemotherapy)

7. What are different types of lung cancer?

S.N Cancer type Remarks

1 Small Cell carcinoma - Treat with chemotherapy

2 Non-small cell carcinoma Subtype

Squamous cell carcinoma

Adenocarcinoma

Broncheoalveolar carcinoma (Adenocarcinoma in situ)

Large cell carcinoma

(Bronchial) carcinoid tumor

3 Mesothelioma - related to asbestos
4 Metastasis - Common origin of metastasis - breast, colon

8. Classify the different types of lung cancer.

Neuroendocrine Adenocarcinoma Related to smoking - small, Paraneoplastic Undifferentiat Excellent
syndrome ed and poor prognosis
(NE) tumor large, squamous, adeno prognosis

- Small cell - Adenocarcinom - Squamous cell carcinoma - Squamous cell - Small cell - Bronchoal
carcinoma a (most common in male veolar
(poorly carcinoma carcinoma carcinoma
differentiated smokers
NE cells) (PTHrp)

- (Bronchial) - Bronchioalveola - Small cell carcinoma (male - Small cell - Large cell

carcinoid tumor r carcinoma smokers) carcinoma carcinoma

(well (adenocarcinom (ADH, ACTH, Ab

differentiated a in situ) for Ca channel)

NE cells)

- Adenocarcinoma (most - Large cell

common in female smokers carcinoma (B-

and non-smokers) - HCG)

broncheoalveolar carcinoma

not associated with smoking

- Large cell carcinoma

9. Describe the following types of cancer.

Cancer Histology Association Location Remarks

Small cell - Poorly differentiated small cell - Male smokers Central - Associated with 5A and 1B
carcinoma and very aggressive (99% of small cell - Produces ACTH
carcinoma pt are - Produces ADH
- Arise from neuroendocrine smokers) - Produces Ab for Eaton-
cells (Kulchitsky cells) Lambert syndrome
- Chromogranin +ve (less +ve

Pulmonary Page 7.2

- Chromogranin +ve (less +ve Lambert syndrome
than carcinoid tumor) (presynaptic Ca channel Ab)
(paraneoplastic syndromes)

- Anti-neuronal antibody
syndrome (limbic encephalitis,
cerebellar degeneration,
opsoclonus, GI dysmotility,
poly radiculopathy)
- Amplification of myc
oncogene
- LOVES TO GO TO BRAIN - give
prophylactic cranial
irraditation
- MOST AGGRESSIVE TYPE OF
LUNG CANCER

Adenocar - Glands or mucin - Most common Peripheral
cinoma tumor in
nonsmokers and
female smokers

Fig: glandular structure in - Most common Central - May produce PTHrp
adenocarcinoma tumor in male (paraneoplastic syndrome)
smokers - Hilar mass from bronchus
Squamous - Keratin pearls or intercellular - Associated with double C
cell bridges (by definition)
carcinoma • HyperCalcemia- due to
PTHrp

• Cavitation

Fig: keratin pearl Fig-
intracellular
Large cell - Poorly differentiated and highly - Smoking bridge
carcinoma anaplastic cells (no keratin
Central or - Poor prognosis
pearls, intercellular bridges, peripheral - Poor response to
glands or mucin) chemotherapy; remove
surgically
- Paraneoplastic - may secrete
B-HCG

(Bronchial - Well differentiated - Not related to Central or - MOST COMMON PRIMARY
) neuroendocrine cells; smoking
Carcinoid chromogranin positive peripheral LUNG CANCER IN CHILDREN
tumor
(when central, - Low grade malignancy; rarely,

makes polyp can cause carcinoid

like mass in syndrome - caused due to

bronchus) release of vasoactive

substance (mainly serotonin) -

flushing, diarrhea, restrictive

cardiomyopathy due to

Pulmonary Page 7.3

Carcinoid (when central, Low grade malignancy; rarely,
tumor makes polyp can cause carcinoid
like mass in syndrome - caused due to
Fig: chromogranin positivity bronchus) release of vasoactive
substance (mainly serotonin) -
flushing, diarrhea, restrictive
cardiomyopathy due to
endocardial fibrosis

Bronchiol - Columnar cells that grow along - Not related to Peripheral - Excellent prognosis
- Pneumonia like consolidation
oalveolar preexisting bronchioles and smoking on imaging

carcinoma alveoli; arise from clara cells

(adenocar

cinoma in

situ)

Fig: normal alveoli top right; Canon-ball - More common than primary
columnar cells on rest nodules on tumors
imaging
Metastasi - Most common source are
s breast and colon carcinoma

Mesotheli - See psammoma bodies in - Highly associated - Malignant tumor of
oma biopsy (concentric with asbestos mesothelial cells
exposure (lung (mesothelium is a membrane
calcifications - other HY cancer more of simple squamous cells that
cancer - papillary thyroid, common in lines body cavities: pleura ,
meningioma, papillary serous asbestos peritoneum, mediastinum and
ovarian) exposure) pericardium)
- Tumor encases the lung

- Small cell carcinoma is poorly differentiated neuroendocrine tumor; carcinoid tumor is well differentiated
neuroendocrine tumor.

- Neuroendocrine cells have neurosecretory granules; chromogranin stains positive for neurosecretory granule.

Pulmonary Page 7.4

- Neuroendocrine cells have neurosecretory granules; chromogranin stains positive for neurosecretory granule.

Pulmonary Page 7.5

9.9 Pleura

1. Describe anatomy of pleura?
- It's lined by mesothelial cells
- It produces pleural fluid

2. What are differences between spontaneous and tension pneumothorax?

Spontaneous pneumothorax Tension pneumothorax

- Often due to rupture of - Often due to penetrating chest wall injury
emphysematous bleb

- Often seen in young adults

- Xray - trachea deviates to side of - X-ray - trachea pushed to opposite side of injury; medical

collapse emergency; put chest tube

Fig: spontaneous pneumothorax (no tracheal shift)

3. Describe mesothelioma (malignant neoplasm of mesothelial cells).
- Presentation:

○ Recurrent pleural effusion (mesothelial cells make pleural fluid)
○ Tumor encases the lung
- Risk factor:

Asbestos (lung cancer far more likely)

Pulmonary Page 8.1

○ Asbestos (lung cancer far more likely)
Fig: mesothelioma (tumor encasing the lung)

Pulmonary Page 8.2

Chapter 10: Gastrointestinal
Pathology

10.1 Oral Cavity

1. Describe the following oral cavity pathologies

Presentation Cause

Cleft palate - Cleft lip and palate usually occur Due to failure of facial prominence to fuse -
one superior, two from sides and two from
and lip together inferior - in early pregnancy

-

Apthous - Painful superficial ulceration of oral - Arise in relation to stress but resolves
ulcer mucosa - gray base (granuloma) with spontaneously
surrounding erythema

Behcet - Recurrent apthous ulcer, genital - Can be seen in viral infection
syndrome ulcer and uveitis - Unknown etiology

Oral herpes - Dew drops in petal appearing painful - HSV 1 - usually occur in childhood

ulcer - Virus remains dormant in trigeminal

ganglia; stress and sunlight can activate

virus and cause ulcers again

2. Describe the squamous cell carcinoma of oral cavity.

Description - Malignant neoplasm of squamous epithelia of oral cavity

Risk factor - EtOH and tobacco

Common site - Floor of mouth

Precursor - Leukoplakia
lesions • White plaque that can't be removed (unlike candida) - represents
dysplasia

- Erythroplakia (red plaque)
• Vascularized leukoplakia and highly suggestive of squamous cell
dysplasia

3. Differentiate leukoplakia from hairy leukoplakia
- Both can't be scraped off.
- Hairy leukoplakia is caused by EBV, usually seen in immunocompromized patients on side of

tongue and is NOT precancerous
- Leukoplakia is cancerous.

Fig: erythroplakia (right), leukoplakia (middle), hairy leukoplakia (left - not precancerous)

GI Page 1.1

10.2 Salivary Gland

1. Describe the following pathologies of the salivary gland.

Presentation Cause Labs Risk

Mumps - Bilateral inflammation Mumps virus - Increased amylase Sterility,
of salivary glands (can be from especially in
- Orchitis pancreas too) teenagers
- Pancreatitis
- Aseptic meningitis

Sialaden - Mostly unilateral - Mostly due to obstructive
tis inflammation of stone leading to staph
Aureus infection
salivary gland

2. Describe the following cancers of salivary gland (SG)

Cancer Epidemiology Location Composition Presentation

Pleomorphic Most common Mostly in Stromal (cartilage) and - Mobile painless circumscribed
parotids epithelial cells - mass in angle jaw
adenoma tumor of SG biphasic tumor - High recurrence; irregular
margins and extension across
capsule makes resection hard
- Rarely becomes carcinoma - if it
does, it will involve CN 7

Warthin 2nd most Mostly in Cystic tumor with
tumor common tumor parotids germinal center and
of SG lots of lymphocytes

Mucoepiderm Most common Mostly in Mucinous and - Involves CN 7
oid carcinoma malignant tumor parotids squamous cell

of SG

GI Page 2.1

10.3 Esophagus

1. Talk about features of following pathologies. Presentation

Pathology Description - Vomiting,
- polyhydroamnio
Tracheoesop Most common variant has proximal esophageal atresia with s,
hageal fistula distal esophagus arising from trachea - aspiration,
- abdominal
distension

Esophageal Protrusion of esophageal mucosa, most often in upper - Dysphagia for
web esophagus poorly chewed
food

Plummer ○ Severe iron deficiency anemia
venson ○ Esophageal web
syndrome ○ Beefy red tongue due to atrophic glossitis (inadequate cell

turnover)
○ Usually seen in post-menopausal woman

Zenker - (false diverticulum) - only mucosa protrudes in upper - Halitosis (rotting
food in
diverticulum esophagus at junction of esophagus and pharynx diverticulum)
- Dysphagia
- Obstruction

Mallory - Longitudinal laceration of mucosa at gastroesophageal - Painful

GI Page 3.1

Mallory - Longitudinal laceration of mucosa at gastroesophageal - Painful
Weiss junction hematemesis
syndrome - Cause - vomiting - usually alcoholism of bulimia
- Risk for Boerhaave syndrome

Boerhaave - Esophageal rupture leading to air in mediastinum and
syndrome subcutaneous emphysema (crepitis)

Esophageal varices
Definition - Dilated submucosal veins in lower esophagus due to portal hypertension

Anatomy - Esogpageal vein is connected to portal vein via left gastric vein
Epidemiology - Most common cause of death in cirrosis pt
Presentation - Asymptomatic or present as painless hematemesis

Achalasia - Disordered esophageal motility with inability to relax lower esophageal sphincter
Definition (LES) due to damage of ganglion cells in myenteric plexus

Etiologies - Chagas disease (HY)
- Idiopathic
Clinical
features - Dysphagia of solid and liquid food
- Putrid breath (rotting)
- High LES pressure on esophageal manometry
- Bird beak sign on X-ray

GI Page 3.2

Complicatio - Increased risk for squamous cell carcinoma
n

Gastroesophageal reflux disease (GERD)

Definition - Reflux of stomach acid due to reduced LES tone

Risk factor - Hiatal hernia
- EtOH, tobacco
- Obesity, fat rick diet
- Caffeine

Clinical features - Heartburn (mimics cardiac chest pain)
- Asthma (adult-onset) and cough
- Damage to enamel of teeth

Complication - Barret esophagus (in 10% of pt with GERD) and strictures

Barret's esohagus

Definition - Metaplasia in lower esophageal mucosa from stratified squamous epithelium to
columnar epithelium with goblet cells

Complicatio - May progress to adenocarcinoma
n

Histology

Fig: squamous epithelia on left, columnar epithelia with goblet cells (right) - barret's
esophagus

Esophageal carcinoma Squamous cell carcinoma

Adenocarcinoma - Most common esophageal cancer
worldwide
Epidemiolo - Most common esophageal cancer in western
gy world (classically seen in lower 1/3rd of - EtOH and tobacco (most common
cause)
esophagus) - Achalasia
- Esophageal web (ex- Plummer-
Risk factor - Barret esophagus Vinson synd)

GI Page 3.3

Vinson synd)
- Esophageal injury (ex - lye
ingestion)
- Very hot tea

Prognosis - Poor (both type presents late)
Presentation
- Progressive dysphagia of solid and liquid food
Lymph node - Weight loss, pain
involvement - Hematemesis
- SCC may have hoarse voice (recurrent laryngeal nerve involvement) and
cough (tracheal involvement) (HY)

If cancer in upper 1/3rd of Cervical nodes
esophagus
Middle 1/3rd Mediastinal or tracheobronchial
nodes
Lower 1/3rd Celiac and gastric nodes

GI Page 3.4

10.4 Stomach

Sections of stomach

Gastroschisis and Omphalocele (schisis = break; omphalo = navel; cele = swelling)
Gastroschisis - Absence of anterior abdominal wall and exposure of abdominal contents outside
Omphalocele - Persistent herniation of bowel into umbilical cord
- Due to failure of herniated intestines to return to body cavity, contents are covered by peritoneum and amnion
of umbilical cord

Fig: omphalocele (middle), gastroschisis (right)
Pyloric stenosis

Definition - Congenital hypertrophy of pyloric smooth muscle
Epidemology - M>F

- Presents after 2 weeks of birth
Presentation - Visible peristalsis and projectile non-bilious (non-green) vomiting after eating

- Olive like mass on abdomen

Fig: visible peristalsis after eating in a kid with pyloric stenosis
Treatment - Myotomy (cut open pyloric sphincter
Acute and chronic gastritis

GI Page 4.1

Acute and chronic gastritis Chronic gastritis
Acute gastritis
- Chronic inflammation of stomach mucosa that leads to intestinal
Definition - Acidic damage to stomach mucosa metaplasia

Defense - Mucin produced by foveolar cells
against - Bicarb secretion
acid - Normal blood supply (provides nutrition
and picks up acid

Fig: intestinal metaplasia seen in chronic gastritis

Etiologies - Severe burn (aka Curling ulcer) - due to - Chronic autoimmune gastritis
loss of blood supply due to hypovolemia - Chronic H. Pylori gastritis
- Increased intracranial pressure (aka
Cushing ulcer) - causes increased
stimulation of vagus nerve and increased
acid production
- NSAIDs - decrease PGE2 (PEG2 decreases
acid production, stimulate mucus, bicarb
production and increases blood flow)
- Chemotherapy
- Shock
- Heavy alcohol consumption

Differentiate chronic autoimmune gastritis and chronic H pylori gastritis.

Chronic autoimmune gastritis Chornic H pylori gastritis

Defn - T cell mediated damage to gastric parietal cells (type 4 - H pylori produces urease to create basic environment; and

hypersensitivity) protease damages mucosal defense - acidic damage to

stomach

Epi. - Most common cause of gastritis (90%)
- Antrum is most common site

Cli. - Atrophy of mucosa and intestinal metaplasia (stomach - Intestinal metaplasia - high risk of intestinal type
Feat.
biopsy looks like intestine) - high risk of stomach adenocarcinoma of stomach

adenocarcinoma - Epigastric abdominal pain

- Achlorhydria (low acid) with increased gastrin levels - Increased risk of ulceration

and antral G cell hyperplasia

- Megaloblastic anemia (pernicious anemia) due to lack

of IF

Lab - see Ab against parietal cells and/or intrinsic factor (IF) - +ve urea breath test
- Stool antigen seen

Treat. - Triple therapy (PPI + marcolide (clarithromycin) + amoxicillin
- Intestinal metaplasia, gastritis and ulcer goes away after
treatment

Comp. Increased risk of gastric adenocarcinoma (intestinal Increased risk of adenocarcinoma (intestinal type) and
type) MALToma

GI Page 4.2

type) MALToma

Peptic ulcer disease

Definition - Solitary mucosal ulcer involving proximal duodenum (90% of cases) or distal stomach (10%)

Differenc Duodenal ulcer Gastric ulcer
es
- 95% due to H. pylori - 75% due to H. pylori
Cause - Rarely due to Zolinger Ellision (ZE) syndrome - NSAID use
- Bile reflux

Present. - Epigastric pain that improves with meal - Epigastric ulcer that worsens with
meal

Location - Mostly in anterior duodenum. - Mostly in lesser curvature of
antrum

Risk - If ulcer in posterior duodenum, rupture may lead to bleeding - Risk of bleeding from left gastric

from gastroduodenal artery or pancreatitis artery

Biopsy - Ulcer with hypertrophy of Brunner glands

Risk of - Duodenal ulcers almost never malignant (duodenal carcinoma - May be caused by gastric

carcinoma extremely rare) carcinoma (intestinal subtype)

How do you differentiate if gastric ulcer is due to gastric carcinoma or not?

Benign gastric peptic ulcer Malignant gastric peptic ulcers (intestinal type)

- Usually small (<3cm), sharply demarcated (punched out), and - Usually large and irregular with heaped up margins
surrounded by radiating folds of mucosa (biopsy is needed for
definitive diagnosis)

Gastric carcinoma (adenocarcinoma)

Classes - Intestinal type (more common)
- Diffuse type

Presentatio - Presents late with weight loss, abdominal pain, anemia and early satiety
n - Rarely presents as acanthosis nigricans (hyperplasia and darkening of epidermis) and Leser-Trelat sign (lots of

seborrheic keratosis)

Metastasis - Liver (most common)

- Periumbilical region (sister mary joseph nodule) Intestinal type

GI Page 4.3

- Bilateral ovary (Kukenberg tumor) Diffuse type

Differentiate intestinal and diffuse type of gastric carcinoma

Intestinal type Diffuse type

Epid More common

Presentati - Large irregular ulcer with - Prominent desmoplasia and thick stomach wall (linitis plastica)
on heaped up margin

Location - Lesser curvature of gastric
antrum (similar to gastric ulcer)

Risk - Intestinal metaplasia ( H. pylori - Not associated with any of the previous
factor and autoimmune gastritis)
- Nitrosamine (present in
smoked food- japan has high
rates)
- Blood type A

Histology - Signet ring cells that diffusely infiltrate the gastric mucosa - nucleus pushed to
edge as tumor cell produces lots of mucin - looks like ring

GI Page 4.4

Mets - Periumbilical region (sister - Bilateral ovary (Kukenberg tumor)
mary joseph nodule)

GI Page 4.5

10.5 Small Bowel, 10.6 Appendix

Duodenal atresia
Defn - Failure of duodenum to canalize
Association - Down syndrome
Clinical features - Bilious vomiting
- Polyhydramnios
- Distension of stomach and blind loop of duodenum (double bubble sign)

Fig: bilious vomit (left), double bubble sign (right)

Merkel diverticulum (MOST COMMON CONGENITAL GI ANOMALY)

Defn - Outpouching of all three layers of bowel wall (true diverticulum) due to failure of vitelline
duct to involute (partial involution)

Anatomy - Developing midgut receives nutrients through vitelline duct from yolk sack
- Vitelline duct forms in 4th week and involutes in 7th week

Partial involution of vitelline duct Merkel diverticulum

No involution Meconium comes out through umbilicus

Rule of 2 - Seen in 2% of population
- 2 inches long
- 2 feet away from ileocecal valve
- Presents within first 2 year of life

Presentation - Most cases are asymptomatic
- Bleeding due to heterotopic gastric mucosa
- Volvulus, intussuception (telescoping) or obstruction (CAN MIMIC APPENDICITIS)

Volvulus and intussuception

Volvulus Intussusception

Defn - Twisting of bowel along its - Telescoping of proximal bowel forward into distal segment
mesentery - Results in obstruction and infraction
- Results in obstruction and
ischemia

GI Page 5.1

ischemia

Cause - Associated with leading edge (focus of traction)
• In kids, most common cause is rotavirus related
Pres - Most common location are lymphoid hyperplasia - mostly occurs in terminal ileum
sigmoid colon (elderly), leading to intussuception into cecum
cecum (young adult) • In adults most common cause is tumor

- See currant jelly stool

Small bowel infraction

Feature - Small bowel highly susceptible to infraction
- Abdominal pain, bloody diarrhea and decreased bowel sounds

Types Cause

Transmural - Thrombosis/embolism of SMA (a-fib, vasculitis) or thrombosis of
infraction mesenteric vein (polycythemia vera, lupus)

Mucosal - Hypotension
infraction

Lactose intolerance

Defn - Hypofunction of lactase enzyme found in brush-border of enterocytes. Enzyme breaks
lactose into glucose and galactose

Presentation - Lactose osmotically active (abdominal distension and diarrhea after eating milk products)

Cause - Congenital - autosomal recessive
- Acquired - develops in late childhood
- Temporary - after infection (lactase is highly susceptible to injury)

Celiac disease

Defn - Immune mediated damage to small bowel villi due to gluten exposure
- Damage most prominent in duodenum (Fe deficiency)

Genetics - Related to HLA DQ2 and HLA DQ8

Pathophys - Gliadin pathogenic component in gluten. After absorption, its deamidated by tissue
transglutaminase (tTG). Deamidated gliadin is presented by APC. CD4 T cells mediate tissue
damage.

Presentati - Chlidren present with failure to thrive, abdominal distention diarrhea
on - Adults present with chronic diarrhea and bloating

- Dermatitis herpetiformis - small, herpes like vesicles on skin due to IgA deposition on
dermal papillae

GI Page 5.2

Lab dermal papillae
findings - IgA deficiency may be seen
- All symptoms resolve with gluten free diet
Biopsy
- IgA against endomysium, tTG, or gliadin
- IgG against those antigens if pt have IgA deficiency

- Flattening of villi, hyperplasia of crypts, increased intraepithelial lymphocytes

Fig - Flattened villi with crypt hyperplasia in Celiac (left) and normal villi (right)

Complicati - Small bowel carcinoma and T cell lymphoma despite good dietary control
on

Tropical sprue

Defn - Damage to small bowel villi due to unknown organism (disease responds to
antibiotics) resulting in malabsorption
- Biopsy finding similar to Celiac?

Difference from - Damage most prominent in jejunum and ileum (Vit B12 and folate deficiency - I fuck

celiac bitches in France) - In Celiac, damage is mostly in duodenum

- Arises after infectious diarrhea and responds to antibiotics

- Occurs in tropical regions - ex-Caribbean

Whipple disease

Defn - Systemic tissue damage due to macrophages loaded with Tropheryma whippelii

Presentati - Classic damage is done in small intestine lamina propria
on • Macrophages compress lacteal and interfere with chylomicron transport from
enterocytes - fat malabsorption and steatorrhea

- Other sites include joints (arthritis), cardiac valves, lymph nodes and CNS

Biopsy - Foamy macrophages in lamina propria of small intestine
- Tropheryma whipplii stain PAS +ve inside the lysosome of macrophage (mucin also PAS
+ve)

GI Page 5.3