PBQ 2007

1. 5 different causes of prolonged fever

a. Autoimmune disease
b. Infection
c. Undetected cancer
d. Hypothalamus break down
e. Dengue
f. Medications/ drugs side effects
g. Fever of unknown origin
h. Skin inflammation

2. 5 relevant enquiries plus reasons

a. Describe about your fever?
o Grades & characteristics of fever
b. Did you take any medication eg: antibiotic? Have it been effective or not?
o If not, it may indicate problems regarding the immune system
c. Did you live in an area with an outbreak of disease such as dengue?
o Monitor the spread or infectivity or a disease, thus giving a clue to the most
possible infection
d. Did you have family history of cancer?
o Suggest a familial/hereditary cancer types, which is susceptible to the
nearest family member
e. Did you experience fatigue, chill, nausea?
o Check for accompanying symptoms
o Indicate certain types of infection and complication of disease

3. Mechanism of fever
a. Disruption of hypothalamic thermostat
i. CNS disease
ii. Inherited
b. High production of heat from
i. Stress
ii. Exercise
iii. Thyrotoxicosis
c. Low loss of heat
i. Heart failure
ii. Drugs that impair eating

All of these lead to failure of body to regulate temperature, thus fever.

In addition, the entrance of exogenous pyrogens into body from bacteria, viruses, and
immune complexes may produce endogenous pyrogens, (Major endogenous pyrogens
are interleukin 1  (α and β), interleukin 6  (IL-6) and  tumor necrosis factor-alpha. Minor
endogenous pyrogens include  interleukin-8,  tumor necrosis factor-α, tumor necrosis factor-
 β,  macrophage inflammatory protein-α and macrophage inflammatory protein-β as well
as interferon-α, interferon-β, and interferon-γ) which cause release of prostaglandin (PGE 2),
then, elevation of hypothalamic set point and eventually will lead to heat-creating effects to
match new temperature level, henceforth fever.

4. 3 differential diagnoses and reason based on history

a. SLE – photosensitive facial rash, hair loss, joint pain
b. Rheumatic fever – arthralgia (joint pain)
c. Scleroderma – scarring in the skin
d. Dermatomyositis- skin rash, joint pain
e. Rheumatoid arthritis – synovial joint inflammation
f. Cancer- gradual loss of apetite, lethargic, family history of breast cancer

5. 2 constitutional symptoms in this case

a. Fever
b. Loss of apetite
c. Chills
Search: http://en.wikipedia.org/wiki/Constitutional_symptoms

6. Family history of breast cancer

a. Cancer is termed malignant neoplasm, a class of diseases in which a group
of cell display uncontrolled growth through division beyond normal limits, invasion that
intrudes upon and destroys adjacent tissues, and sometimes metastasis, which
spreads the cells to other locations in the body via lymph or blood.
b. Differences between cancer and a benign growth.

Cancer Benign

Poorly differentiated Well differentiated

(anaplasia) (resembles origin)
Grow rapidly Grow slowly
Not capsulated Capsulated
Spread locally and metastasise No spread
Basement membrane invasion Basement membrane intact
Irregular shapes(poikilocytosis) Regular cell shape, sizes
and sizes (anisocytosis)
Add sarcoma for mesothelial tissue and Add suffix –oma
carcinoma for epithelial tissue Eg: lymphoma

c. Familial breast cancer oncogene – BRCA-1, BRCA-2

d. 2 main modes of metastasis and mechanism
i. Lymphatic spread
 Penetrate basement membrane of endothelium, then underlying
tissue
 Carried partly by hydrostatic pressure, partly by active movement
  Enter the drainage to the lymphatic trunk, settle and proliferate in
subcapsular sinus of lymph node
 May be important in prognosis, if not superseded by
haematogenous spread.
 common in initial spread of carcinomas
ii. Haematogenous spread
 Detach from neighbouring cells
 Invade connective tissue
 Intravasate into lumen of vessels
 Evade host defense (tumor cells in association with cells like
leukocyte, platelets, endothelial cells.. physically protected and
stabilized as platelet enriched thrombi)
 Adhere to endothelial at remote location
 Extravasate to surrounding tissue (Most common sites: lung, liver,
brain)
 Typical of all sarcomas

7. Working diagnosis +5 reasons

a. Systemic Lupus Erythematosus (SLE)
i. Tenderness and inflammation on the metacarpopharyngeal and wrist joints
ii. Alopecia
iii. Photosensitivity
iv. Facial rash
v. Thin
vi. High body temperature-fever
8. Alopecia
= hair loss
9. Cardinal signs in acute inflammation + mechanism involved
a. Rubor- redness
i. Arteriolar vasodilatation due to increase blood flow
b. Calor- heat
i. Vasodilatation causes heat loss through the skin
c. Tumor-swelling
i. Vasodilatation also increases vascular permeability, thus permit fluid
movements
d. Dolor- pain
i. Inflammatory substances and cells causes the release of mediators such as
bradykinin and prostaglandin that stimulate the nerve endings, thus pain
e. Function laesa- loss of function

10. 4 investigations to arrive definitive diagnosis + justify

a. Erythrocyte Sedimentation Rate (ESR)
i. Check for inflammatory response
b. Immunological test
i. Investigate the presence of auto-antibodies especially to the nucleus
 c. X-rays to both hands
i. Detect the causation for the occurrence of arthritis and its manifestation to
the bony structures
d. Renal profile
i. Check for any kidney abnormalities that may be due to deposition of
immune complexes and inflammation in the kidney
e. Full blood count
i. Detect abnormalities of blood such as anemia

11. ESR and C-R protein raised..why?

ESR and C-reactive protein raised, signifies the inflammatory response.
12. Urinalysis and renal profile, comment + justify
a. Urinalysis- all normal except the presence of protein (proteinuria) & erythrocyte
(hematuria). This indicates nephritis.
b. Creatinine level – low indicates deficiency of kidney filtration.

13. Conclusion from immunological test

Anti-nuclear antibody, anti-dsDNA, anti-Smith Ab shows SLE disease. Rheumatoid
factor shows positive result since joint pain is experienced by the patient.
14. Final diagnosis
SLE- due to the presence of anti-Smith, anti-dsDNA and anti- nuclear antibodies
15. Immuno-pathogenesis of this condition
a. Susceptibility genes, failure self tolerance, self reactive lymphocyte
b. Environmental triggers cellular apoptosis , nuclear protein now un-sequestered,
other self-antigen alter immune reactivity,
Activation antigen presentation cell, activation of T helper cell and B cell specific for
self-antigen, antibody production, immune complexes and auto-antibody mediated
tissue injury.
16. 4 possible complications as consequences of this disease
 Pericarditis
 Cerebral lupus
 Myocarditis
 Fibromyalgia
 Anti-phospholipid syndrome
 Pleurisy
 Vasculitis
 Microstomia
 Artherosclerosis