Pathology I Review 10

8/9/2019 Pathology I Review 10

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Case 1

A 56 year old female develops abdominal painand diarrhea after traveling to the Philippines.The family practitioner orders a stool culture,

which comes back positive for presence of ovaand parasites.

Which cells would you expect to be elevatedin this patient?

Which interleukins are important in mediatingthe response against this microorganisms?


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Case 2

A 32-year-old woman was admitted to the emergency departmentbecause of an abrupt onset of hives characterized by periorbital rednessand swelling, breathlessness, and wheezing. Angioedema and hypotension(90/60 mmHg) were observed. She was resuscitated by administration ofsubcutaneous epinephrine, intravenous corticosteroid, and antihistamine.

The patient was married and had delivered a baby four months previously.After abstinence from sexual intercourse for several months before andafter the delivery, she had intercourse with her husband. After coitus,during which intravaginal ejaculation occurred, she experienced an itchingsensation of the perineum and swelling of the vulva, which subsidedwithin a few hours without treatment. Her gynecologist diagnosednonspecific vaginitis, but treatment did not improve her condition. Several

days before she presented at our emergency room, she experienced anepisode of itchy hives at sites on her trunk that had been exposed tosemen. The hives subsided the next morning. On the day of her visit to theemergency room, she suffered from an itchy, swollen vulva andbreathlessness after coitus. She reported no extramarital sexual activity.She had no history of allergy and had never used contraceptives orcontraceptive devices.


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Case 2

Any thoughts?

Describe the mediators and mechanism of the

response in this patient. How is this different from the patient that

develops a rash in the vaginal area after

micturiting in the middle of the wildness and

having contact with poison ivy?


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MUST KNOW!!!

Type I immediate reaction-IgE mediated:

asthma, hay fever, hives, anaphylaxis

Type IV cell mediated delayed cytotoxicity:Hashimotos, poison ivy, tuberculosis


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Case 2 (asthma).


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Case 3


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Case 3


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Case 3

I know this might be hard, but what are your

thoughts?

Explain the mechanism for all the findings. What other conditions could result in similar

presentation?


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MUST KNOW!!

Type III immune complex deposition: serum

sickness, SLE, post-streptococcal

glomerulonephritis, polyarteritis nodosum,


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MUST KNOW!!!

The presence of certain autoantibodies have diagnostic value for SLE. The most specific tests are thosethat detect high levels of these autoantibodies. The most common and specific tests forautoantibodies and other elements of the immune system are listed first.

AntinuclearAntibody (ANA) : A screening test for ANA is standard in assessing SLE because it ispositive in close to 100% of patients with active SLE. However, it is also positive in 95% of patientswith mixed connective tissue disease, in more than 90% of patients with systemic sclerosis, in 70%of patients with primary Sjgren's syndrome, in 40-50% of patients with rheumatoid arthritis, and

in 5-10% of patients with no systemic rheumatic disease. Patients with SLE tend to have high titersof ANA.

Anti-Sm

Anti-Sm is an immunoglobulin specific against Sm, a ribonucleoprotein found in the cell nucleus.This test is highly specific for SLE; it is rarely found in patients with other rheumatic diseases.However, only 30% of patients with SLE have a positive anti-Sm test.

Anti-nDNA

Anti-nDNA is an immunoglobulin specific against native (double-stranded) DNA. This test is highlyspecific for SLE; it is not found in patients with other rheumatic diseases. Sixty to eighty percent of

patients with active SLE have a positive anti-nDNA test. For many patients with anti-nDNA, the titeris a useful measure of disease activity. The presence of anti-nDNA is associated with a greater riskof lupus nephritis.

Anti-Ro(SSA) and Anti-La(SSB)

These immunoglobulins, commonly found together, are specific against RNA proteins. Anti-Ro isfound in 30% of SLE patients and 70% of patients with primary Sjgren's syndrome. Anti-La is foundin 15% of lupus patients and 60% of patients with primary Sjgren's syndrome. Anti-Ro is highlyassociated with photosensitivity; both are associated with neonatal lupus.


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Case 4

A 51-year-old female has had fatigue, weakness, and shortness of breath (SOB) with exertion duringthe past 4-5 days. She called her primary care physician (PCP) who recommended that she had herhemoglobin checked. He called her back with the results, and told her to go to the emergency room(ER) for further treatment of severe anemia. On admission, the patient denied abdominal pain,chest pain, congestion, nausea/vomiting/diarrhea/constipation (N/V/D/C), dysuria, headache,chills, hemoptysis, neck pain, rash, or sore throat.

Her symptoms were exacerbated by activity and relieved by rest and laying supine. She also felt

palpitations intermittently.

Past Medical History (PMH)

Diabetes type 2 (DM2).

The hemoglobin (Hgb) was 4.2 mg/dL, MCV 144 fl, and reticulocyte count 41%.

The patient was admitted to a regular medical floor and a hematology consult was called. Thedirect Coombs' test was reported as positive.

TheCX

R andC

T scans were negative for neoplastic disease.


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Case 4


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Case 4

Can you explain the mechanism by which this

patient developed the symptoms?


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Case 5

A healthy 19 year old African American man presented with shortness of breathfor two weeks duration associated with subjective fever, chills and non productivecough. He was recently seen by his primary care provider with the abovesymptoms and was prescribed a two weeks course of Azithromycin with no clinicalimprovement.

On arrival to Emergency Department, he was found in mild respiratory distress

with respiratory rate of 30 per minute. He was alert and able to answer allquestions in full sentences. Rest of the vitals included temperature of 101.8 F (38.8C), blood pressure of 120/60 mm Hg, heart rate of 100 beats per minutes, andpulse oximetery of 93%-98% on 40% oxygen. Head and neck examination wereunremarkable. Chest auscultation revealed good air entry bilaterally withoccasional bibasilar crackles and few scattered wheeze. Cardiovascular, abdominal,neurological examinations were within normal limits.

Laboratory work up was remarkable for leukocytosis, otherwise was non-

contributory. Arterial blood gas was remarkable for hypoxia. (PaO2-71 mm of Hg).A chest x ray and chest CT were performed. (See figure 1 and 2). The patient'scondition steadily deteriorated and was eventually intubated and ventilatedrequiring high peak end-expiratory pressure (PEEP). All cultures were negative.


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Case 5

Vascuilitic and autoimmune screening was foundto be negative on initial laboratory investigation.Lung tissue biopsy was performed via video-

assisted thoracoscopic approach (VATS) whichshowed acute lung injury characterized byinterstitial and intra-alveolar organization, intra-alveolar fibrin deposition, squamous metaplasia

of bronchiolar epithelium and rare fibrin thrombi.These changes were associated with focalalveolar hemorrhage and capillaritis.


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Case 5

An X-ray of the chest and a renal biopsy were

obtained and showed the following:


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Case 5

Which test would you order to confirm your

diagnosis?

Can you explain the mechanism for thepresentation of the previously described

patient?


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MUST KNOW!!!

Type II direct cytotoxic antibodies:

autoimmune hemolytic anemia, ITP,

Goodpastures disease (anti-BM), Graves

(anti-TSHR), ANCA + diseases, myasthenia

gravis, incompatible blood transfusion


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Case 6

An 18-year-old Asian male was admitted to hospital 7with a four week history oflethargy, weight loss, palpitations and excessive sweating. He had tachycardia,sweating, tremors, mild tenderness in the region of the thyroid gland. TSH wasundetectable and free T4 was 97 pmol/l (1222 pmol/l). Anti thyroid peroxidaseantibody was >600 IU/ml (034). Haemoglobin was 10 g/dl, total white cell count1.32 with a neutrophil count of 0.8, and a platelet count of 137. His CRP was 187

mg/l. He was commenced on propranolol, prednisolone 30 mg and carbimazole 20 mg

and he showed rapid clinical improvement with a normal full blood count after 4days. Prednisolone was stopped and he was discharged on carbimazole andpropranolol.

He was readmitted 3 weeks later with a sore throat and a white cell count of 0.8,neutrophil count of 0.04 and platelet count of 119. His TSH was 14.8 mU/l with afree T4 of 5.7. Neutropenic sepsis secondary to carbimazole was diagnosed and

carbimazole and propranolol were stopped. Two weeks later he was stillneutropenic with a white cell count of 1.53, neutrophil count of 0.6 and plateletcount of 86, and clinically hypothyroid with a TSH of 52.7 (5.0-50.0 mU/L )and afree T4 of 10.4 (1222 pmol/l). He was commenced on thyroxine.


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Case 6

Explain the whole mechanism behind all

stages of the presentations.


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Case 6


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Case 6

Type II direct cytotoxic antibodies:

autoimmune hemolytic anemia, ITP,

Goodpastures disease (anti-BM), Graves

(anti-TSHR), ANCA + diseases, myasthenia

gravis, incompatible blood transfusion

Type IV cell mediated delayed cytotoxicity:

Hashimotos, poison ivy, tuberculosis


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Case 7

A 26 year old African American patientpresents to the OB/GYN ward afterexperiencing continuous contractions that

have been increasing in intensity. The patientis prepared for a natural delivery, but thenurse reports that the monitor cannot detectthe babys heart beat. This patient had a

spontaneous abortion 2 years ago. Thefollowing is the picture of the expired babythat was delivered after 3 hours of labor.


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Case 7


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Case 7

Can you reason the mechanism by which this

unfortunate event took place?

What approach would you prefer in order toavoid future abortions or fetal deaths in this

patient?

If this pregnancy was in fact completed, the

most likely complication would have been?


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MUST KNOW!!!

Pathology I Review 10

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