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Reasoning Report

Pathophysiology problem-based learning case 1

Group A members : 侯宗佑、莊凱舟、廖庭偉、李季恆、周延、林家興、顏寧、陳柏


翰、廖尉凱、許雅鈞、余沛修、鄭朝允

Mr. Liu, a 30-year-old salesman came to our hospital for consultation


as he had developed an intermittent fever over the last month. His
armpit temperature lied between 37.8 and 38.5 ℃ while he felt
febrile. The fever occurred mostly between afternoon and early
evening. Occasionally, fever was accompanied by a mild chill.

Obviously, the chief complaint of Mr. Liu is fever. To deal with this
symptom encountered frequently, the origin of the condition is set
up to be our first “Need to know”. With regard of detailed
description about the characteristics of patient’s fever, we obtained
our first group learning objective : What is the possible etiology
and pathophysiology of intermittent fever?

Therefore, we find out something essential in this case, discovering


how the homeostasis of our body temperature is disturbed in
diseased situations.

As shown above, during a febrile illness, the body temperature


homeostasis is usually maintained but at higher, febrile levels. The
“set point” is elevated by several causes. Common causes include
microbe infection, autoimmune disease , CNS disease (head trauma)
and malignancy, especially lymphoma, leukemia, renal cell
carcinoma, primary or metastatic liver cancer. Less common causes,
which should not be overlooked, include cardiovascular disease
(myocardial infarction, thrombophlebitis, pulmonary embolism),
gastrointestinal disease (inflammatory bowel disease, alcoholic
hepatitis, granulomatous hepatitis) and miscellaneous conditions
(drug fever, tissue injury, hematoma).

Physical Examination findings offered us more useful information.


Focus on abnormal findings: higher body temperature, white
patches and ulcers in oral cavity, painful masses and not painful
lymph nodules, interstitial infiltrations in the upper lung both sides
shown by CXR.

Oral cavity smear and culture data provide an important evidence :


candidiasis, an opportunistic infection strongly indicating
immunocompromised condition of the host immune response.

History taking allows us to know the patient’s bisexual preference


with several sex partners without protection of condoms, which is a
hint that he’s at higher risk of sexually transmitted infectious
diseases like HIV.

After biopsy examination and HIV test, we confirmed our hypotheses


of his condition of AIDS resulting from HIV infection. Evidences of
Mycobacterium infection are found and then culture of sputum and
lymph node tissue confirmed the diagnosis of Tuberculosis.

To review our collective reasoning of the case, we trace the final


diagnosis back to the very beginning of patient’s fever complaint.
We establish the probably most significant learning objective in this
case: The clinical manifestations of TB in HIV-infected
patients. Looking at the disease development course of HIV
infected individuals:
The clinical manifestations of TB in HIV-infected patients are quite
varied and generally show different patterns as a function of the
CD4 T cell count.

CD4+ T Cell >300 <200 130


counts(cells/m (early (late HIV)
m3 ) HIV)
pattern Like Like -
reactivati progressive
on of primary
tuberculo tuberculosis
sis
Findings Apical No Granulomat
disease granuloma, ous
with cavitaion inflammatio
cavitatio Extrapulmon n
n Intermittent
ary
involvement fever 
arise systemic TB
Sputum smear Often Often Sputum: +
and tuberculin positive negative Culture: +

In patients with relatively high CD4 T cell counts, the typical pattern
of pulmonary reactivation occurs in which patients present with
fever, cough, dyspnea on exertion, weight loss, night sweats, and a
CXR revealing cavitary apical disease of the upper lobes.

In patients with lower CD4 T cell counts, disseminated disease is


more common. In these patients the CXR may reveal diffuse or
lower lobe bilateral reticulonodular infiltrates consistent with miliary
spread, pleural effusions, and hilar and/or mediastinal adenopathy.
Infection may be present in bone, brain, meninges,
gastrointestinaltract, lymph nodes (particularly cervical lymph
nodes), and viscera.

However, our case seems to show manifestations from both


categories above. Most of the manifestations including fever,
cough,weight loss, night sweats, and upper lobe lung lesions in CXR
indicates that the patient still have relatively high CD4 T cell counts.
Extrapulmonary involvement like cervical lymph nodes involvement
in our case, which typically emerges from patients with lower CD4 T
cell counts, is somehow not coherent to the categorization of
manifestations.

References:
1. Gandhi, NR, Moll, A, Sturm, AW, et al. Extensively drug-
resistant tuberculosis as a cause of death in patients co-
infected with tuberculosis and HIV in a rural area of South
Africa. Lancet 2006; 368:1575.
2. Alexander J. McAdam, Arlene H. Sharpe; infectious disease;
Vinay Kumar, Abul K. Abbas, Nelson Fausto, Jon Aster; Robbins
& Cotran Pathologic Basis of Disease 8th edition; Philadelphia,
Saunders, 2010; 366-372
3. World Health Organization; TB/HIV: a Clinical Manual, Second
Edition, November 2003
4. AIDS pathology, The Internet Pathology Laboratory
for Medical Education; The University of Utah Eccles Health
Sciences
Library(http://library.med.utah.edu/WebPath/TUTORIAL/AIDS/AI
DS.html)
5. Pathology of tuberculosis, The Internet Pathology Laboratory
for Medical Education; The University of Utah Eccles Health
Sciences
Library(http://library.med.utah.edu/WebPath/TUTORIAL/MTB/M
TB.html )
6. Gary Maartens, C Fordham von Reyn, Barbara H McGovern;
Clinical features and diagnosis of tuberculosis in HIV-infected
patients; UpToDate online, 2010
7. HIV In Site; University of California, San Francisco.
(http://hivinsite.ucsf.edu/InSite )
8. CENTERS FOR DISEASE CONTROL AND PREVENTION: HIV/AIDS
Surveillance Report, 2002;14, 2003. Available at
http://www.cdc.gov/hiv/stats/hasrlink.HTM

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