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Medicine Flashcards

1
Q

How to decribe the distribution of joint that are involved in arthritis ?

A
  • Polyarticular : symmetric involvement is seen in RA , SLE, parvovirus B19 and hepatitis B.
  • Monoarticular: seen in osteoarthritis, crystal- induced arthritis (gout and pseudogout), septic arthritis (gonococcus), truma and hemarthrosis.
  • Migratory: Inflammation and pain migrate from joint to joint while the previous involved joint improve, caused by rheumatic fever, disseminated gonococal infection, and lyme disease.
  • Oligoarticular: asymmetric arthritis , with spondyloarthropathies (ankylosing spondylitis) and ostioarthritis involving the small joint of the uppper extremities.
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2
Q

What are the basic tests to run on the synovial fluid ?

A 
3 Cs: 
Cultures
Cell count 
Crystals 
\+ 
Gram stain.
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3
Q

What is the shape of crystals in synvoial fluid analysis in gout and pseudogout disease ?

A

Gout: Needle - shaped, negative birefringent

Pseudogout: rhomboid - shaped, positive birefringent.

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4
Q

Name some of the specific AntiNuclear Antibodies (ANA) and thier diseases

A
  • Anti - native dsDNA (native double stranded) —> SLE only (indicator of disease activity and lupus nephritis.
  • Anti- SM (Anti-Smith) —> SLE only 25 - 30%.
  • Anti-histone —> Drug - induced lupus.
  • Anti- Ro (SSA) Sjögren’s-syndrome-related antigen A autoantibodies —> Neonatal lupus , Sjögren’s and in the 3% of ANA- negative lupus.
  • Anti- LA (SSB) —> Sjögren.
  • Anti- centromere —> CREST
  • Anti - RNP —> 100% mixed connective tissue disease (MCTD).
  • Anti- CCP (cyclic citrullinated Peptide) —> RA
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5
Q

What is CREST syndrome ?

A 
CREST syndrome, also known as the limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder. The acronym "CREST" refers to the five main features: 
Calcinosis,
Raynaud's phenomenon,
Esophageal dysmotility, 
Sclerodactyly, and 
Telangiectasia.
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6
Q

What are Rheumatoid factors ?

A

They are autoantibodies against the Fc portion of IgG.

found in 70% of patients with RA although they are not specific for RA.

As they are not specific nor sensitive to RA diagnosis, it can help in prognosis, as patients with high titers tend to have more aggressive disease with extra-articular manifestations.

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7
Q

What are ANCAs (Anti-Neutrophil Cytoplasmic Antibodies) ?

A

They are antibodies directed against certain proteins in the cytoplasm of neutrophils.

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8
Q

In which diseases you see a positive cANCA ((Anti-Neutrophil Cytoplasmic Antibodies) ?

A

Wegener granulomatosis

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9
Q

In which diseases you see a positive pANCA ((Anti-Neutrophil Cytoplasmic Antibodies) ?

A

PAN and churg- Strauss

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10
Q

What is Antiphospholipid syndrome (lupus anticoagulant or anticardiolipin antibodies) ?

A

It is an autoimmune, hypercoagulable state, associated with a group of antibodies that are directted against phospholipids or cardiolipins. Which causes elevated PTT and false-positive RPR ( rapid plasma reagin) or VDRL (Venereal disease research laboratory).

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11
Q

In which patients we usually suspect Antiphospholipid syndrome?

A

In patients with sponataneous abortions in otherwise healthy women.

2 first- trimester spontaneous abortions suggests Antiphospholipid syndrome

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12
Q

What is rheumatoid arthritis ?

A

It is a chronic inflammatory multisystemic disease with the main target being the synovium.
The hallmark of RA is inflammatory synovitis.

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13
Q

Why is RA is very rare in patients with HIV ?

A

Because in RA, the predominant infiltrating cell is the T lymphocyte. And HIV patients has decreased T-cells.

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14
Q

What are the pro-inflammatory cytokines that mediate most of the pathogenic features of RA ?

A
  • Tumor necrosis factor alpha (TNF-a)
  • Interlukin-1 (IL-1)
  • Interlukin-6 (IL-6).
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15
Q

What are the clinical diagnostic criteria of RA ?

A

4 of the following is required to diagnose RA:

1- Morning stiffness >1 hour for 6 weeks.
2- Swelling of wrists, MCP (metacarpophalangeal joints), PIPs (proximal interphalangeal joints) for 6 weeks.
3- Swelling of 3 joints for 6 weeks
4- Symmetric joint swelling for 6 weeks.
5- RF positive or anti-cyclic citrullinated peptide.
6- CRP or ESR

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16
Q

Which joints are NEVER involved in RA ?

A
  1. DIPs (distal interphalangeal joints).

2. Joints of the lower back

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17
Q

What are the extra-articular manifestations of RA ?

A
  1. Damage to the ligaments and tendons :
    • Radial deviation of the wrist with ulnar deviation of the digits.
    • Boutonniere deformity
    • Swan neck deformity.
  2. Rheumatoid nodules:
    • Methotrexate may flare this process.
  3. Felty syndrome (RA + splenomegaly + neutropenia)
  4. Caplan syndrome (RA + pneumoconiosis).
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18
Q

Which is more specific , Anti-CCP or RF ?

A

Anti-CCP (cyclic citrullinated Peptide)

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19
Q

Why does COX-2 (cyclooxygenase-2 ) inhibitors is preferred over COX-1 inhibitors in RA ?

** both are types of NSAIDs

A

because COX-2 inhibitors are selectively blocks the COX-2 enzymes at the site of inflammation and they don’t inhibit COX-1 , which is an enzyme that helps with the production of the protective stomach lining.

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20
Q

How to treat RA in general ?

A
  • NSAIDs
  • Glucocorticoids (short courses)
  • Disease - modifying anti- rheumatic drugs DMARDs.
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21
Q

What is the best initaial Disease - modifying anti- rheumatic drugs DMARDs in RA ?
and what to use next if disease is not controlled ?

A

Methotrexate

If not controlled —> Anti - Tumor necrosis factor TNF.

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22
Q

What are the adverse effect of the following DMARDs and how to screen for thier toxicity ?

  • Methotrexate:
  • Hydroxychloroquine:
A

Methotrexate:

  • Rapid onset of action
  • S/E: hepatitis, hepatic fibrosis , pneumonitis, may flare rheumatoid nodules
  • Screeing: CBC and LFT Q4-8 weeks.

Hydroxychloroquine:

  • S/E : Retinopathy
  • Screeing: Regular eye examination
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23
Q

Which screening is crucial before starting biological agents (TNF inhibitors) ?

A

TB screening

+ HCV and HBV

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24
Q

Name the 3 TNF inhibitors that are approved for the treatment of RA .

A
  1. Infliximab (Remicade)
  2. Adalimumab (Humira)
  3. Etanercept (Enbrel).
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25
Q

What are the factors of aggressive RA ?

A
  • High titers pf RF
  • Diffuse rheumatoid nodules
  • Early jointd erosions
  • Late age of onset
  • Certain subtypes of the HLA-DR4.
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26
Q

Which condition must be ruled out in patients with RA espically if they are going under an elective surgery and intubation ?

A

Atlantoaxial subluxation.

order x-ray of the cervical spine (multiple views including open mouth). Proceed to CT and MRI if needed and refer to spine surgeon if positive.

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27
Q

Which condition should be considered in RA patients with swollen painfull calf ?

A

Ruptured Baker cyst.

Baker cyst is the extension of inflammed synovium into the popliteal space.

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28
Q

What is the only enviromental factor that causes systemic lupus erythematosus flares ?

A

Ultraviolet (UV) - B light

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29
Q

What are the diagnostic criteria of SLE ?

A

you need 4 out of the following:

  1. Malar rash
  2. Discoid rash
  3. Photosensitivity
  4. Oral ulcers
  5. Arthritis
  6. Serositis (Pleuritis or pericarditis)
  7. Renal involvement
  8. Neurologic disorder ( seizures or psychosis)
  9. Hematologic disorder ( hemolytic anemia, leukopenia, thrombocytopenia).
  10. Immunologic disorder (anti-dsDNA, ani-SM, and other ANAs.
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30
Q

how to differentiate between arthritis in RA and in SLE ?

A

In SLE it’s non erosive

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31
Q

What is Libman- Sacks endocarditis ?

A

It is a noninfectious endocarditis that is occasionally seen in lupus patients.

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32
Q

What is oftenly used ti treat lupus nephritis ?

A

Mycophenolate

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33
Q

What is the most common cause of disability in patients with SLE ?

A

Lupus nephritis

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34
Q

Which antibodies should be screened in pregnant patients with SLE and why ?

A

All pregnant patients with SLE should be screened for SSA/anti-Ro antibodies, because they cross the placenta and are passively transferred to the fetus, causing neonatal lupus and heart block.

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35
Q

Name the common medications that causes drug-induced lupus.

A
  • Hydralazine
  • Isoniazid
  • Procainamide
  • Quinidine
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36
Q

What is Systemic scleroderma, or systemic sclerosis ?

A

It is a chronic rheumatoid multisystemic disease, characterized clinically by thickening of the skin caused by accumulation of connective tissue and by involvement of visceral organs (GI, lungs and kidneys).

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37
Q

What is the leading cause of death in systemic sclerosis ?

A

Pulmonary involvement

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38
Q

What is CREST syndrome?

A

It is a variant of scleroderma, now it’s called limited scleroderma or limited cutaneous systemic sclerosis.

  • Calcinosis (deposits of Ca in joints)
  • Raynaud
  • Esophageal dysfunction
  • Sclerodactyly (skin thickening affecting fingers and toes).
  • Telangictasias.
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39
Q

What is Raynaud phenomenon ?

A

It is an episodes of pallor or cynosis in response to to cold or emotional stimuli. The pallor is caused by vasoconstriction of blood vessels which results in decrease blood flow. while cyanosis is created by deoxygenation of slow- flowing blood.

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40
Q

How to treat systemic sclerosis ?

A

There is no cure.
Only symptomatic treatment:

  • D- penicillamine for skin manifestation
  • CCB (Nifedipine) in severe Raynaud phenomenon
  • ACE inhibitors for HTN
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41
Q

What is xerostomia ?

A

Dry mouth resulting from reduced or absent saliva flow.

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42
Q

What is Sjogren syndrome ?

A

It is a chronic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands, resulting in xerostomia and dry eyes.
It can be primary or secondary (with other autoimmune diseases).

As the syndrome progresses, it becomes a systemic disease involving major organs and may cause lymphoproliferative disease ( malignant lymphoma).

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43
Q

What are the clinical manifestations of Sjogren syndrome?

A
  • Itchy eyes with a sandy feeling (Keratoconjunctivitis sicca.
  • Difficulty swallowing food.
  • Increase in dental carries.
  • Parotid enlargement
  • Schirmer’s test show decreased tear production and rose bengal stain.
  • ANAs positive : Anti-Ro (SSA), Anti-La (SSB).
  • Lymphocytic infiltration of the salivary glands on biopsy
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44
Q

What is the ttreatment of Sjogren syndrome?

A

symptomatic only:

  • Artificial tears.
  • Pilocarpine and Cevimeline —> increases acetylcholine and increases tear and saliva production.
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45
Q

Name the Seronegative arthropathiesm spondyloarthropathies.

A
  1. Ankylosing spondylitis.
  2. Reactive arthritis.
  3. Psoriatic arthritis.
  4. Enteropathic arthropathy.
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46
Q

In which group age and gender does Ankylosing spondylitis usually occurs ?

A

In young men in thier 20s - 30s

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47
Q

What is the characteristics of Ankylosing spondylitis ?

A
  • 90% of patients has positive HLA B-27.
  • presents with lower back pain in young men. The giveaway in the morning stiffness lasting for at least 1 hour that improves with exercise.
  • Evidence of decresed spine mobility, on PEx: positive Schober test.
  • possible obliteration of the lumbar lordosis.
  • X-rays: evidence of sacroilitis + fusing of the sacroiliac joint.

Chronic spine inflammation will cause bamboo spine and squaring of vertebral bodies.

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48
Q

What are the extraarticular manifestations in Ankylosing spondylitis ?

A
  • Anterior uveitis.

- Aortic insufficiency that may cause CHF and 3rd-degree heart block .

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49
Q

What is the treatment of Ankylosing spondylitis ?

A
  • NSAIDs
  • Physical therapy
  • Excercise.
  • TNF blockers (infliximab, adalimumab, etanercept) –> recommended in axial disease.
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50
Q

What is reactive arthritis ?

A

It is a seronegative arthropathy that occurs as a complication from an infection.

- Reiter syndrome: occurs after a nongonococcal urethrritis (Chlamydia or ureaplasma).
Mucocutaneous manifestations: 
   * Keratoderma
   * Blennorrhagica
   * Circinate balanitis 
   * Oral or genital ulcers
   * conjunctivits 
   * arthritis
  • Infectious diarrhea (enteroinvasive diarrheas) : Campylobacter (most common), shigella, or salmonella
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51
Q

What is the treatment of reactive arthritis ?

A

Same as ankylosing sponylitis:

  • NSAIDs
  • Physical therapy
  • Excercise.
  • TNF blockers (infliximab, adalimumab, etanercept) –> recommended in axial disease.

+
- In Reiter syndrome caused by chlamydia: Prolonged Tetracycline use ( 3 weeks) could accelrate recovery.

  • Antiretroviral medications in HIV patients could improve the aggressive skin manifestations.
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52
Q

What is the leading cause of disability in elderly ?

A

Knee osteoarthritis.

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53
Q

What is the most common and the second common joint affected by osteoarthritis?

A

1st : knees

2nd : thumb

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54
Q

What is the clinical presentation of osteoarthritis ?

A
  • Oligoarticular, asymmetric or monoarticular pattern
  • Very slow, progressive and irreversible
  • Joint pain increases with excercise and improves with rest.
  • Morning stiffness is always < 20 - 30 mins.
  • Crepetations of joint may occour.
  • No systemic manifestations
  • It’s not an inflammatory disease, so CRP and ESR is always normal.
  • Osteophytes (spurs) , called Bouchard’s nodes in PIPs and Heberden’s nodes in DIPs.
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55
Q

What is the treatment of osteoarthritis ?

A

There is no cure, only palliative therapy.

  • Focus on maintaining mobility and reducing pain.
  • Reduce joint loading with correction of poor posture and weight loss.
  • Physical therapy, excercise programs which maintain range of motion, strengthen periarticular muscles and improve physical fitness.
  • Use acetaminopthen then NSAIDs for pain improvement
  • Use Capsaicin cream.
  • Intraarticular injection of hyaluronic acid.
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56
Q

What is crystal - induced arthropathies ?

A
  • MSU : monosodiuam Urate
  • CPPD: Calcium pyrophospahte
  • CaOx: Calcium oxalate
  • HA: Calcium hydroxyapatite.

are caused by micro-crystal deposition in joints and they all present with same clinical presentation. It only can be distinguished by synovial fluid analysis.

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57
Q

What is gout and what is its clinical presentation ?

A

It is a type of inflammatory arthritis that is caused by high levels of uric acid in the blood.

  • affects middle aged men and postmenopause women

Presentation:

  • Acute monoarthritis
  • Metatarsophalangeal join of first toe in commonly affected (podagra).
  • First episode usually ocurs at night with severe joint pain waking the patient from sleep, the joint rapidly becomes warm, red and tender (looks exactly like cellulitis).
  • Spontaneuos resolvement occurs without meds within 3- 14 days.
58
Q

What are the precipitating factors of gout disease ?

A
  1. Excessive alcohol ingestion
  2. Red meat intake
  3. Truma
  4. Surgery
  5. surgery
  6. Steriods withdrawl
  7. Drugs:
    • Diuretics: hydochlorothiazide and Furosemide
    • Anti-TB: Pyrazinamide and ethambutol
  8. Serious medical illness.
59
Q

How to diagnose gout ?

A

By synovial fluid analysis which shows:

  • MSU (monosodium urate) crystals are negative birefringent
  • Needle shaped

And WBC count from 5000- 50,000

x-ray in multiple gouty attacks may show erosive calcifications.

60
Q

What is the treatment and the goal of treatment in acute/chronic gouty arthritis ?

A 
Acute gouty arthritis: 
Goal: 
- Decrease inflammation 
- Prevent erosion and joint destruction 
- Avoid fluctuations in serum uric acid level.

Tx:

  • NSAIDs
  • Steriod oral (intraarticular in elderly patients who can’t tolerate NSAIDs / has renal impairment).
  • Colchicine (rarely used).

Chronic gouty arthritis:
Goal:
- Decreased uric acid levels, which may help to follow the effect of hypouricemic Tx.

Tx:

  • Allopurinol ( can be used in pts with renal failure and kidney stones).
  • Febuxostat (2nd line)
  • Pegloticase : dissolves uric acid - used in refractory disease.
  • Prebenecid: Rarely used.
61
Q

How to diagnose and treat pseudogout ?

A

Dx:
Synovial fluid analysis: Typical, rectangular, rhomboid, positive birefringent crystals.

x-rays: linear radiodense deposits in joint menisci or articular cartilage (chondrocalcinosis)

Tx:
same as gout
+ Colchicine low doses may be considered to prevent frequent recurrences.

62
Q

What is the most common cause of septic arthririts ?

and whats the Tx:

A
  • In young females : gonorrhea —> Ceftriaxone
  • In elderly patients with RA or with preexisitng joint destruction from other rheumatic disease: Staphylococcus aureus. —–> Nafcillin or Vancomycin.
63
Q

What is Wegener Granulomatosis ?

+ clinical presentation, Dx and Tx?

A
  • It is a small vessels vasculitis.
  • Presentation:
  • Typically affect respiratory tract (sinuses, nose, trachea, and lungs) and kidneys
  • Sx if there is a respiratory tract involvement: sinusitis, rhinitis, nasala ulcers. usually chronic rhinitis occur and it will not response to usuall Tx and become worse.
  • Sx if lung ivolvement occured: cough, hemoptysis and dyspnea.
  • Kidney involvement is the major cause of morbidity and mortality.
  • Arthritis may occur
  • Dx:
  • Antineutrophil cytoplasmic antibodies (C-ANCA) support Dx but it’s NOT diagnostic
  • Confirmative test: tissue biopsy which shows vasculitis and granulomas.
  • Tx:
  • combination between Glucocorticoids + immunosuppresive agents (cyclophosphamide).
64
Q

What is Polyarteritis Nodosa ?
Presentation ?
Dx?
Tx?

A

It is a multisystem disease which presents with:

  • Nonspecific Sx: malaise, fever, weight loss, anorexia, abdominal pain.
  • All systems are involved EXCEPT lungs.
  • Peripheral neuropathies: tingling , numbness, pain in hand, legs or foot, and mononeuritis.
  • GI manifestations: pain , GI bleed.
  • Active HBV.

Dx:

  • Biopsy of involved organ (usually skin) : pathological changes in medium- size arteries.
  • angiogram og abdominal vessels could show aneurysms affecting kidneys and GI tract.

Tx:
- High doses of corticosteriods and immunosuppressive drugs (cyclophophamide

  • if not treated it’s fatal (by kidney, heart or GI complications)
65
Q

What is Churg- Strauss syndrome ?

A

PAN (polyarteritis in an asthmatic patient)

  • involve small and medium sized arteries. and any orgns

Cardinal maifestations:

  • Asthma
  • Eosinophilia
  • lung involvement

Dx:

  • Biopsy
  • CXR: transient pumonary infiltrates

Tx:
Prednisone + cytotoxic agents

66
Q

What is temporal arteritis (Gaint cell arteritis)?

A

It is a vasculitis affecting large areties that supplies the head, eyes and optic nerve.

67
Q

What Sx makes you suspect temporal arteritis (Gaint cell arteritis)?

A

In patints wiht new -onset of headache who are aged > 50 - 60. years.

68
Q

What happens if temporal arteritis (Gaint cell arteritis) is untreated ?

A

Permanent vision loss.

69
Q

What are the Sx of temporal arteritis (Gaint cell arteritis)?

A
  • Headache and pain in one or both temples (most common).
  • Scalp tenderness (pain when combing hair)
  • Jaw caludication (pain when chewing)
  • Decreased vision or blurry vision
  • Tongue numbness
  • Sudden vision loss
  • Proximal stiffness (nexk, arms and hips) due to polymayalgia rheumatica a coexisitng condition
70
Q

How to diagnose and treat temporal arteritis (Gaint cell arteritis)?

A
  • ESR is always high (100% sensitive)
  • Biopsy of temporal arteries show giant cells.

Tx: Corticosteroids

If temporal arteritis (Gaint cell arteritis) is suspected —–> ESR , if high start Prednisone immediately, before Bx.

71
Q

Which feature differentiate inflammatory myopathies from myasthenia gravis and Eaton - lambert syndrome ?

A

Ocular muscles are NEVER involved in inflammatory myopathies.

72
Q

Name the inflammatory myopathies.

A
  • Polymyositis
  • Dermatomyositis
  • Inclusion body myositis.
73
Q

What is the presentation of Dermatomyositis

A
  • Heliotrope rash is a purple - lilac discoloration of the face, eyelids and sun-exposed areas of the body.
  • Gottron’s papules are the scaly lesions seen over the knuckles.
74
Q

What are the lab findings in patients with inflammatory myopathies.

A
  • High muscle enzymes: Creatinine- phosphokinase CPK and aldolase.
  • Autoantibodies (Anti-Jo-1) support the Dx.
75
Q

How to Dx inflammatory myopathies ?

A
  • Electromyography: short duration, low amplitude units.

- Muscle Bx : confirmation

76
Q

sHow to Tx inflammatory myopathies ?

A
  • Polymyositis and Dermatomyositis : Steriods

- Inclusion body myositis : resistant to immunosuppressive therapy.

77
Q

What is achalasia ? and what are the causes ?

A

It is the failure of the lower esophageal sphincter to relax and decreased peristalsis.

It is caused by degenertion of the myenteric plexus with loss of the normal inhibitory neural structure of the LES.

Etiology is unknown, but could be from :

  • Chagas disease.
  • Gastric carcinoma
  • lymphoma.
78
Q

What is the clinical presentation of achalasia ? and how to diagnos it ?

A

Clinical pressentation:

  • Progressive dysphagia to both soilds and liquids.
  • Regurgitation several hours after eating.
  • weight loss.
  • Not related to smoking or alcohol consumption

Dx:
- Heme - positive stool , Sx more than 6 months and weight loss will guide to diagnosis.

start with this order:

  1. Barium swallow: dilation of the proximal esophaguswhich narrows into (bird’s- beak).
  2. Esophageal manometry: GOLD STANDARD, showes increased LES resting pressure.
  3. Upper Endoscopy: to rule out adenocarcinoma (pseudoachalasia).
79
Q

What is the treatment of achalasia ?

A
  • First line : Pneumatic dilation
  • Second line: Botulinum toxin injections, relive Sx for 6 months.
  • Third line: CCB and nitrates.
80
Q

Which type of cancer is found in each part of the esophagus?

A

Proximal 2/3 : Squamous cell cancer

Distal 1/3: Adenocarcinoma.

81
Q

What is the clinical presentation, Dx and Tx of esopahgeal cancer ?

A

Clinical presentation:

  • Progressive dysphagia first for solid food then for liquids.
  • Wight loss
  • Halitosis (bad breath)
  • Regurgitation
  • Hoarseness
  • Hypercalcemia.

Dx:

  • Barium swallow
  • Upper endoscopy: mandatory as it gets tissue biopsy.
  • CT scan to detect degree of local spread
  • Bronchoscopy detect asymptomatic spread into the bronchi.
  • Endoscopic U/S for staging.

Tx:

  • Surgical resection (25% only are operable).
  • Chemotherapy with 5-fluorouracil- based - chemotherapy is combined with radiation to control locally metastatic disease.
82
Q

How to Dx and Tx patients with scleroderma that has esophageal Sx ?

A

Dx:
- Motility study, as in scleroderma the LES will neither contract nor relax, it basically an immobile open tube.

Tx:

  • PPI : omeprazole
  • Metoclopramise: promotility agents.
83
Q

Name the esophageal spastic diorders.

A

Diffuse esophageal spam and Nutcracker esophagus.

84
Q

What is the clinical presentation, Dx and Tx of esophageal spastic diorders ?

A

Clinical presentation:

  • Intermittent chest pain
  • Dysphagia
  • Pain can be same as MI but has no relationship with exertion.
  • Pain is precipitated by cold liquids.

Dx:

  • Barium study : Corkscrew.
  • MAnometric study: more accurate. show high-intensity, disorganized contractions.

Tx:
- CCC, e.g : Nifedipine or nitrate.

85
Q

What is the most common etiology of infectious esophagitis ?

A
  1. Candida albicans
  2. Herpes simplex
  3. Cytomegalovirus
  4. Aphthous ulcers.
86
Q

In which patients does candida albicans esophagitis occurs ?

A

HIV positive with CD4 count < 200/mm (often < 100/mm).

87
Q

What is the clinical presentation of esophagitis ?

A

Progressive odynophagia (pain only on swallowing.

Food is still able to pass (until the disease is extremely advanced).

88
Q

How to treat esophagitis?

A

If patient is HIV positive, assume candida and start Fluconazole. If Sx improved, diagnosis is confirmed. If not, do endoscopy and biopsy.

89
Q

Name the common pills that can cause esophagitis.

And how to prevent esophagitis from occurring while taking those pills ?

A
  • NSAIDS
  • Iron sulphate
  • potassium chloride
  • Alendronate
  • Quinine
  • Risedronate
  • Vitamin C
  • Doxycycline

Swallow pill in the upright position and drink enough water to flush them into the stomach.

90
Q

How to treat Eosinophilic esophagitis?

A

Swallow Fluticasone or budesonide.

If biopsy shows eosinophils, give PPIs before oral steroids

91
Q

What is the definition of Zenker Diverticulum ?

A

It is the outpocketing of the posterior pharyngeal constrictor muscles at the back of the pharynx.

92
Q

What is the clinical presentation of Zenker Diverticulum ?

A
  • Bad breath
  • Difficulty in intiating swallowing (due to proximal lesion)
  • Need to repeatdly clear the throat.
  • Waking up with undigested, regurgitated food on the pillow.
93
Q
  1. How to diagnose Zenker Diverticulum ?
  2. What are the contraindicated procedures if Zenker Diverticulum is suspected ?
  3. Tx ?
A
  1. Barium study is confirmative
  2. NGT and endoscopy as there is a risk of pharyngeal perforation.
  3. Surgical resection.
94
Q
  1. Define Mallory- weiss syndrome.
  2. Clinical presentation
  3. Dx
  4. Tx ?
A

1, It’s a nontransmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting.

  1. Painless upper GI bleeding - Melena if bleeding is > 100 mL - Hematemesis if there is continued vomiting.
  2. Direct visualization on upper endoscopy.
  3. Resolves spontaneously. May be you need to inject with epinephrine or perform cauterization.
95
Q

What are the factors that can cause decreased tone or loosening of the LES , and therefore could cause GERD ?

A
  • Nicotine
  • Alcohol
  • Caffeine
  • Anticholinergics
  • CCB
  • Nitrates
96
Q

What is the clinical presentation of GERD ?

A
  • Heartburn
  • Metal-like taste in mouth
  • Sore throat
  • hoarsness
  • cough
  • Wheezing
  • Pain in the substernal area that worsens after a meal or when lying flat.
97
Q

What is the most accurate diagnostic test for GERD ?

A

A 24 hour pH monitor

98
Q

How to approach GERD ?

A
  • Initiate PPI.
  • If no improvement, increase PPI to 2X daily for 4-8 weeks (make sure its taken the right way: 30-60 mins before meal).
  • If no improvement, do EGD:
    • Esophagitis : confirm GERD, 24 hour pH monitoring is NOT needed.
    • If EGD in normal: do 24 hour pH monitoring (while off PPI).
  • If GERD confirmed : Do Nissen fundoplication.
99
Q

Name PPI medications.

A
  • Omeprazole
  • Esomeprazole
  • Pantoprazole
  • lansoprazole
  • Rabeprazole
100
Q

What are the side effects of PPI ?

A
  • Increases risk of C.difficile infection
  • aspiration pneumonia
  • osteoporosis
  • Hip fracture.
101
Q
  1. What is Barrett esophagus ?

2. Tx?

A
  1. It is a complication of long-standing reflux disese. the epithelium of the lower esophagus undergoes histologic change from a normal squamous epithelium to a columnar epithelium.
  2. PPI
102
Q

Who should be screened for Barrett esophagus ?

A 
Men age > 50 years with chronic GERD (5 + years ).
and additional risk factors: 
- Nocturnal symptoms
- Hiatal hernia 
- obese 
- smokers
103
Q

How frequent should patients with Barrett esophagus repeat endoscopy ?

A

Q 3-5 years.

  • If low - grade dysplasia : repeat endoscopy 6-12 months.
  • If high - grade dysplasia : do radiofrequency ablation, photodynamic therapy, endoscopic mucosal resection.
104
Q

What are the stimulants that produces acid from the parietal cells of the stomach?

A
  • Gastrin
  • Acetylcholine
  • Histamine
105
Q

What is Zollinger - Ellison syndrome ?

A

It is hypergastrinemia caused by cancer of the gastrin-producing cells.

(It is the excessive production and release of gastrin from the pancreas).

106
Q

What are the most common causes of ulcer disease ?

A
  • H.pylori
  • NSAIDs.
  • Idiopathic.
107
Q

What are the tests used to diagnose H.pylori ?

A
  • Urea breath testing.
  • Stool antigen testing
  • Biopsy with histology.
  • Rapid urease testing.
108
Q

Before performing H.pylori tests , you should make sure that the patient is off which medications and for how long?

A

make sure that the patient is off :

  • PPI for 2 weeks.
  • Antibiotics for 4 weeks.
109
Q

Triad medication of H.pylori infection ?

A
  • PPI
  • Clarithromycin
  • Amoxicillin

for 10 - 14 days.

110
Q

When to give PPI for prophylaxis ?

A
  • History of PUD or GI bleed.
  • Age 65 years or older
  • Chronic comorbid illness.
  • High - dose NSAIDs use.
  • Concomitant use of aspirin, anticoagulants, glucocorticoids.
111
Q

What are the indications of surgery in PUD?

A
  1. UGI bleed not amenable to endoscopic procedures.
  2. Perforation
  3. Refractory ulcers.
  4. Gastric outlet obstruction.
112
Q

What are the types of gasteritis ?

A

Type A:

  • Caused by atrophy of the gastric mucosa.
  • Associated with an autoimmune process : Vitamin B12 deficiency.
  • Associated with diminshed gastric acid production and achlorhydria.
  • All patient with achlorhydria will have markedly elevated gastrin because acid inhibit gastrin release from G cells.

Type B (most common):

  • Caused by: NSAIDs , alcohol, Helicobacter, head trauma, burns, and mechanical ventilation.
  • Associated with increased gastric acid production.
113
Q

How to initialy diagnose and confirm the diagnosis of pernicious anemia ?

A

Initially: Increased methylmalonic acid.
Confirmed: presence of antiparietal cell antibodies and anti-intrinsic factor antibodies.

114
Q

Where is the common sites of Zollinger - Ellison syndrome ?

A
  • 50% in duodenum.
  • 25% in pancreas.
  • <20% multiple endocrine neoplasia - 1 (MEN-1) or parathyroid, pituitary and pancreatic tumor.
115
Q

What is the clinical presentation of Zollinger- Ellison syndrome ?

A
  • Ulcers that are recurrent after therapy, multiple in number, occur in the distal portion of the duodenum, or resistant to routine therapy.
  • Diarrhea (ordinary water diarrhea, or steatorrhea due to inactivated lipase from large volume of acid passed into the duodenum.
116
Q

Why does all patient on H2 blockers or PPI have elevated gastrin levels ?

A

Because the main stimulus to the suppression of gastrin release is acid.
If acid production in suppressed, then gastrin goes up.

117
Q

What are the causes of increased gastrin production ?

A
  • Zollinger- Ellison syndrome
  • Pernicious anemia
  • Chronic gasteritis
  • Renal failure
  • Hyperthyroidism.
118
Q

How to Tx Zollinger- Ellison syndrome ?

A
  • locallized : Surgically removed.

- Metastatic: Suppressed only by PPIs.

119
Q

What are the test used to detect Zollinger- Ellison syndrome metastasis ?

A
  • U/S , CT and MRI : specific to prove the presence of tumor if positive but not sensitive enough to safely exclude the disease if negative.
  • Nuclear test, somatostatin - receptor scintigraphy is 90% sensitive for detection of mets.
  • Endoscopic U/S is the single most sensitive test.
120
Q

What is gastroparesis ?

What are the causes of it ?

A

Delayed gastric emptying.

Caused by DM and electrolytes imbalence.

121
Q

Clinical presentation of gastroparesis ?

A
  • Early satiety.
  • Postprandial nasuea.
  • General sense of increased abdominal fullness.
  • Abdominal pain
  • Bloating.
122
Q

Risk factors of gastroparesis ?

A
  • Long standing history of DM.
  • Long standing history of poor glycemic control
  • retinopthy
  • Neuropathy
  • Nephropathy
  • Scleroderma
  • Hypothyroidism
  • Anti-cholinergic use
  • Narcotic use.
123
Q

How to Dx gastroparesis ?

A
  • It is a clinical diagnosis.

- Gastric- emptying study is confirmatory.

124
Q

How to Tx gastroparesis ?

A
  • Agents that increases motility of the stomach:
    Erythromycin or Metoclopramide.
  • Smaller, more frequent portions of food are recommended.
125
Q

Crohn’s disease Vs. Ulcerative colitis:

  1. Common site.
  2. Sx.
  3. Thickness of inflammation.
  4. Distribution.
  5. Smoking
  6. Dx
  7. antibodies ?
A
  1. Crohn’s disease: Terminal ilieum
    Ulcerative colitis: rectum
  2. Both: fever, abdominal pain, weight loss, bloating.
    Crohn’s disease: fistulas, strictures.
    Ulcerative colitis: bloody diarrhea

3.
Crohn’s disease: Transmural
Ulcerative colitis: Submucosa or mucosa

  1. Crohn’s disease: skip lesions , entire GIT
    Ulcerative colitis: continuous , limited to large bowel
  2. Crohn’s disease: smoking is a risk factor
    Ulcerative colitis: smoking improves Sx.
  3. Both with endoscopy and barium study
    Crohn’s : has cobblestones appearance.
  4. Crohn’s disease: ASCA +ve (Anti-Saccharomyces cerevisiae antibodies).
    Ulcerative colitis: ANCA +ve (Anti-Neutrophil cytoplasmic antibody)
126
Q

Why in Crohn’s disease we find prothrombin time is prolongated ?
and why kidney stones are common ?

A

prothrombin time is prolongated becuase of Vitamin K malabsorption.

kidney stones becasue of fat malabsorption caused by reduced calcium and increased absorption of oxalate.

127
Q

How to treat calcium oxalate stones ?

A

By using cholestyramine

128
Q

What are the Sx in mild , moderate and severe in Crohn’s disease?

A 
Mild: non specific
Moderate: 
- Fever 
- Weight loss
- anemia 
- abdominal pain 
- nausea and vomiting.

Severe to fulminant:

  • hight fever
  • vomiting
  • rebound obstruction.
129
Q

What are the Sx in mild , moderate and severe in ulcerative colitis ?

A

Mild:

  • 4 bowel movements / day
  • mild bleeding
  • normal labs.

Moderate:
4-6 bowel movements/day

severe:
>6 bowel movement/day

130
Q

How to treat Crohn’s disease and Ulcerative colitis ?

A

Crohn’s disease:

  1. If mild:
    - Active: Prednisone
    - Maintenance: Azathioprine and 6-mercaptopurine.
  2. If moderate:
    - Active: steroids
    - Maintenance: Azathioprine and 6-mercaptopurine. OR methotrexate.
    - For remission: anti-TNF antibodies.
  3. Severe to fulminant (acute exacerbations):
    - IV steroids OR anti-TNF

Ulcerative colitis:
1. If mild:
Mesalamine OR sulfasalazine

  1. If moderate:
    - Active: Prednisone
    - Remission: Budesonide
    - long term maintenance: Azathioprine and 6-mercaptopurine
  2. Severe:
    - For acute exacerbations: Steroids , if fail, IV steroids then anti TNF-alfa (infliximab - adalimumab - golimumab)
    - For maintenance: Azathioprine and 6-mercaptopurine, if failed IV steroids then anti TNF-alfa (infliximab - adalimumab - golimumab).
131
Q

What is the side effect of sulfasalazine (used to treat ulcerative colitis) ?

A
  • causes reversible infertility in men

- Leukopenia.

132
Q

What is the side effect of 6-mercaptopurine (used to treat IBD)?

A

associated with drug - induced pancreatitis.

133
Q

What is the rule of surgery in IBD ?

A

Crohn’s disease:

  • Not effective
  • Disease tend to reoccur at the site of anastomosis.

Ulcerative colitis:

  • Curative
  • 60 % of patients will reqiure surgery within 5 years
134
Q

When to screen for colonoscopy in IBD ?

A

In both UC and CD,

  • start screening colonoscopy 8-10 years after diagnosis.
  • Repeat Q 1-2 years
135
Q

What is the most common cause of bacterial diarrhea ?

A
  • Campylobacter and Salmonella.

espicially in patients with sickle cell and achlorhydria

136
Q

What are the clues to the diagnosis of the following infectious diarrhea causitive agents prior to the results of the culture :

  • Bacillus cereus
  • Campylobacter
  • cryptosporidia, isospora
A

Bacillus cereus:

  • Ingestion of refried chinase food and the spores fron Bacillus that it contains.
  • Vomiting is prominant
  • Blood in NEVER present.
  • short incubation period (1-6 hours).

Campylobacter :

  • most common cause of bacterial gastroenteritis
  • Reactive arthritis
  • Guillain - Barre syndrome.

Cryptosporidia, isospora:

  • in HIV patients with <100/mm3 CD4 cells.
  • Isospora Tx : TMP-SMX
137
Q

What are the clues to the diagnosis of the following infectious diarrhea causitive agents prior to the results of the culture :

  • E.coli
  • Giardia
  • Salmonella
A

E.coli:
- Ingestion of contaminated hamburger meat, organism release Shiga toxin, which provokes hemolytic uremic syndrome.

Giardia:

  • ingestion of unfiltered water
  • Blooe is NEVER present.
  • If not eradicated, it will stimulate celiac disease and casues fat and vitamin malabsorption.
  • Diagnosis best by: ELISA stool antigen test.
  • Tx: Metronidazole

Salmonella:
- Ingestion of chicken , eggs amd dairy products.

138
Q

Why does antibiotics are contraindicated in E.coli diarrhea with hemolytic uremic syndrome ?

A

Because hemolytic uremic syndrome happens when organism dies, that is why ABx are contraindicated.

139
Q

What are the clues to the diagnosis of the following infectious diarrhea causitive agents prior to the results of the culture :

  • Scombroid
  • Shigella, Yersinia
  • Vibrio parahaemolyticus
  • Vibrio vulnificus
  • Staphylococcus aureus
  • Ciguatera - toxin
A

Scombroid:

  • Ingestion of contaminated fish
  • Immediate vomiting, diarrhea, flushing and wheezing.
  • Tx: Antihistamine ( diphenhydramine).

Shigella, Yersinia:

  • No clue
  • Yersinia could memic appendicitis.

Vibrio parahaemolyticus:
- Ingestion of raw shellfish

Vibrio vulnificus:

  • Ingestion of raw shellfish
  • Skin bullae
  • Tx: Doxycycline

Staphylococcus aureus:

  • Ingestion od dairy products, eggs and salads
  • Upper GI Sx: nausea and vomiting
  • Short incubation period (1-6 hours).

Ciguatera - toxin :

  • Ingestion of large reef fish
  • 2-6 hours of ingestion
  • Neurological Sx leading to paresthesia, weakness, reversal of hot/cold.
140
Q

When to use antibiotics in diarrhea ? and which antibiotics are used ?

A

If there is abdominal pain , blood in the stool and fever > 7 days.

Abx is always empiric because decision is made before culture results.
Best empiric Tx:
- Ciprofloxacin OR other fluoroquinolones +/- metronidazole.

141
Q

In which patient s does microscopic colitis is considered ? and how to diagnoe it treat it ?

A
  • In Women aged 45 - 60 ,
  • that has diarrhea not related to food (nocturnal diarrhea)
  • No abdominal pain
  • No weight loss
  • Normal colonoscopy

Dx:
Biopsy

Tx:

  • Stop PPI and NSAIDs
  • Loperamide , Bismuth or budesonide.

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