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Title: A 28YearOld Woman With Jaundice and Fever Chapter 22

1
A 28-Year-Old Woman With Jaundice and Fever
Chapter 22
Eugene G. Martin, Ph.D. Associate Professor of
Pathology Laboratory Medicine

Based upon LABORATORY MEDICINE CASEBOOK. An
introduction to clinical reasoning
Jana Raskova, MD Professor of Pathology
Laboratory MedicineStephen Shea, MD
Professor of Pathology Laboratory
MedicineFrederick Skvara, MD Associate
Professor of Pathology Laboratory MedicineNagy
Mikhail, MD Assistant Professor of Pathology
Laboratory MedicineUMDNJ-Robert Wood Johnson
Medical SchoolPiscataway, NJ

2
History and Presentation

28 y.o ? known to be HIV for 6 years
Admitted to hospital because of jaundice and a
fever of 102o F
Contracted HIV from an old boyfriend who
subsequently died. Husband refused to be tested
Previously treated with anti-retroviral drugs
poorly tolerated
Developed Progressive Wasting Syndrome and
anemia. Previous fever treated with antibiotics.
Current problems Progressive Liver Failure with
? liver enzymes and jaundice occuring during the
past five days accompanied by fever.
Physical Exam
Cachectic ?, oriented
Temp. 101.8 oF
BP 100/40
HR 88 bpm and regular
Skin and sclerae were icteric. No
lymphadenopathy. Chest clear.
Ascites. Liver and spleen markedly enlarged.
Lower extremities were edematous

3
What is Progressive Wasting Syndrome? Is
HIV-related anemia related to CD4 or viral load?
Progressive Wasting Syndrome
HIV Anemia

Clinical syndrome in which an individual has lost
more than 10 of his or her body weight in the
absence of active infections or any other
identifiable cause of weight loss.
One of the most common symptoms of HIV infection
Associated with malnutrition, which may
contribute to increased immune suppression
http//www.aidsmap.com/treatments/ixdata/english/C
EFC89BA-7146-4966-8F39-701651DD559D.htm

Anemia is associated with HIV disease
progression, independent of CD4 count and viral
load. Most common in patients with CD4
Common causes of HIV-related anemia
Infections e.g. B19 parovirus
cancers of the bone marrow
drugs which suppress the bone marrow as a
side-effect of therapy
AZT, foscarnet, ganciclovir, co-trimoxazole (at
the high doses used to treat PCP anaemia is
rare at the doses used for PCP prophylaxis) and
dapsone
Bleeding most common reason in HIV-negative m

4
Is HIV anemia related to CD4 count?

Anemia is associated with HIV disease
progression, independent of CD4 count and viral
load. Most common in patients with CD4
Common causes of HIV-related anemia
Infections e.g. B19 parovirus
cancers of the bone marrow
drugs which suppress the bone marrow as a
side-effect of therapy
AZT, foscarnet, ganciclovir, co-trimoxazole (at
the high doses used to treat PCP anaemia is
rare at the doses used for PCP prophylaxis) and
dapsone
Bleeding most common reason in HIV-negative
patients

5
HEMATOLOGY
6
CHEMISTRY
7
Why was Alk. Phosphatase Increased?

Alk. Phosphatase
Sources
Liver hepatocytes and biliary tract mucosal
cells
Bone
Intest. Mucosa
Placenta
Normal adolesc. 3-5x adult values (bone growth)
Greater sensitive to biliary tract obstruction
whether intra or extrahepatic. Does increase with
liver cell acute injury

Hepatic ALP Elevation
Extrahepatic bil. Tract obstruct.
Intrahepatic bil. Tract obstruct.
Liver cell acute injury
Liver passive congestion
Drug-induced liver cell dysfunction
Space occupying lesions
Primary biliary cirrhosis
Sepsis
Dont forget bone or placental origin

8
Why do you think AST is increased so modestly
(1.3 x Upper Range Normal (URN)

AST

Sources

Liver

Heart

Sk. Musc.

RBCs

Diseases with mild moderate abnormality
(

Acute hepatitis resolving phase

Chronic hepatitis

Active cirrhosis

Liver passive congestion

Drug induced liver dysfunction

Metastic liver tumor

Bile duct obstruction

CMV, inf. Mono

In extrahepatic obstruction there usually is no
elevation unless secondary parenchymal acute
injury occurs
AST/ALT ratio is elevated (1) in active
alcoholic cirrhosis, liver congestion and
metastatic tumor to the liver
Etiologies for AST Elevation)
Heart MI, Pericarditis
Sk. Mus. Inflammation, MD, recent surgery, DTs
Kidney Acute injury or damage, Renal infarct
Other Intest. Infarct., Cholecystitis, shock,
acute panreatitis, hypoparathyroidism

9
GGTP

GGTP has equal to or greater sensitivity than ALP
in obstructive liver disease and greater
sensitivity in hepatocellular injury (16x URN)
Etiologies for GGT Elevation
Liver, space-occupying lesion (M-H)
Alcoholic active liver disease M)
Common bile duct obstruction (M)
Intrahepatic cholestatis (M-H)
CMV infection, Mono infection (S/M)
Tylenol overdose (S/M)
Severe liver congestion (S)
Reyes syndrome (S)
S small, Mmedium, Hhigh

10
Questions

Discuss the status of the patients liver
Hyperbilirubinemia Impaired hepatic excretion
of conjugated bilirubin. This is not of hemolytic
origin ? unconjugated bilirubin
Hypoalbuminemia and ? protein impaired hepatic
synthesis and malnutrition
? Calcium as a consequence of ? albumin
50 of total Ca is ionized, the remainder
protein bound.
A ? in serum albumin will ? ? total serum Ca
Only hepatitis marker HBsAb. Consistent with
Immunization
Long ago exposure and recovery with loss of HBcAb
No active infection (No HBeAg). No Carrier state
(No HBsAg HBcAb)
Transaminases (AST, ALT) are only modestly
elevated
Ascites and splenomegaly common in patients
with portal hypertension
What is the significance of the depressed amylase
level?
Amylase is typically elevated in pancreatitis, in
biliary tract disease (cholecystitis, tumor,
spasm of sphincter of Oddi). In this instance it
is low
Pancreatitis can occur in association with HIV
therapy (DDI) or more commonly in alcoholic
patients
Because in requires good renal function to clear,
serum amylase is sometimes elevated in renal
failure.
Pancreatic enzymes are important in the digestion
of carbohydrates. In a patient losing weight it
may be helpful to rule/out a digestive disorder

11
What are the 3 stages of HIV infection?

Acute
3-6 weeks after initial infection
Non-specific symptoms resolves spontaenously
Fever
Rash
Myalgia
Middle
Clinical latency patient asymptomatic, mild
constitutional symptoms, lymphadenopathy
Crisis
Immune system breakdown
Fever
Loss of Weight
Diarrhea
Opportunistic infections and secondary neoplasms

12
Urinalysis
13
Miscellaneous Tests
14
T Lymphocyte Subsets
15
CHEMISTRY
16
HEMATOLOGY
17
Clinical Course

Treatment
Treated empirically for CMV and mycobacterium
intracellulaire
Diuretics and salt-poor albumin for ascites
Liver function continued to deteriorate
Patient developed electrolyte imbalance that
reqd. correction
Cytopenia worsened reqd transfusion of several
units of packed red blood cells
Blood and urine culture negative
One week later oral and esophageal lesions
Grim prognosis discussed. Patient died at home 2
days later.
Antemortem stool culture positive for acid fast
organisms

18
Autopsy results
19
Liver Biopsy HE x120
Poorly defined granuloma composed of
epitheliodcells
20
Liver Biopsy Acid Fast x120
Numerous filamentousacid-fast organismsconsisten
t with Mycobacteriumavium intracellulare.
21
Impact of HIV on acquisition, activation and
outcome of TB?

Acquisition 113 x higher risk of being infected
than a person with no risk factors
Mechanism HIV infects helper-T-cells leading to
a decrease in cell-mediated immunity. Absence of
immunity ?development or activation of the
disease
37 of HIV-infected individuals develop TB within
5 months of exposure as compared to 5 of
patients with normal immune system
Assessment PPD in HIV ONLY 30-50 of TB
infected HIV patients will respond with an
induration 10mm. THUS induration 5mm is
considered

22
HIV Positive Patient. What do you do?

Ordinarily INH daily for 12 months
Some recommend INH for life since eventual
failure of the immune system will allow infection
to progress to active disease
If drug-resistant strain start on two drug
regimen INH and EMB or INH and cipro for
preventive therapy
If an HIV-infected patient develops
drug-resistant TB the chances of dying from the
disease are between 72-89, even with aggressive
therapy!!
AIDS patients progress to MDR-TB immediately
after infection and die within 4-19 weeks

23
Esophagus

HE x 31
Esophagus covered by adherent grey-white membrane
Note numerous fungal organisms as bluish wavy
band across bottom of iimage
Inflammatory cells, necrotic debris and
collections of bacteria near lumen at top
Gomori silver stain x100
Fungi, numerous yeast and pseudohyphal forms are
present consistent with Candida species

24
Lymph node HE x12

Atrophic lymph node
Marked depletion of lymphocytes in both mantal
and germinal centers
Germinal centers are small and show signs of
hyalinization

25
Organization of spleen

Marginal zone - assortment of mononuclear cells
Principal function of the marginal zone is
antigen trapping.
SECONDARY LYMPHOID ORGANS, Art Anderson's
Immunology Lecture Notes

26
Spleen

Patient
Lymphoid depletion of the spleen severe
White pullp is nearly devoid of lymphocytes
Normal
White pulp containing numerous lymphocytes
Clearly delineated from the surrounding red pulp

27
Case Summary

Final Diagnosis
AIDS
Liver Failure
Mycobacterium Avium intracellulare infection
Esophageal Candidiasis

28
References

Prog. Wasting Syndrome -http//www.aidsmap.com/tre
atments/ixdata/english/CEFC89BA-7146-4966-8F39-701
651DD559D.htm
HIV anemia - http//www.aidsmap.com/treatments/ixd
ata/english/4B95EF8B-A38A-4FFB-BD5B-4D87339162B4.h
tm
Splleen
SECONDARY LYMPHOID ORGANS, Art Anderson's
Immunology Lecture Notes