Case Study - Mariana Flashcards

(35 cards)

1
Q

What is relevance of her travel history

A

Tattoo, potential unprotected sex, heavy drinking - Hep. B/C
Length of stay in high TB prevalence areas.
Jungle travel, exposure to mosquitoes - dengue fever, malaria.
Possible exposure to contaminated water - leptospirosis.
Repeated food poisoning/poor diet - Iron, B12, folate deficiency, anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is relevance of Asian ethnicity

A

TB - more common in Asian’s.
Hep. B - more common in Asian’s.
G6PD deficiency - more common in Asian’s.
Ethnicity doesn’t cause symptoms but can influence disease susceptibility, diagnostic considerations and risk factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is ruled out in initial testing?

A
  • Acute bacterial infection as normal WBC and no sign of inflammatory response
  • Acute malaria - platelet count is normal.
  • Sever parasitic infections - no eosinophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why test a faeces sample, although there was no mention of diarrhoea.

A
  • Detecting parasitic infections.
  • Checking for gastrointestinal bleeding (F. occult blood test)
  • Liver and bilary infections from raw fish and contaminated water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What conclusiosn from initial haem and clinical chem results?

A
  • TB possible, as mild anaemia, weight loss, fatigue.
  • Hep B/C possible, as fatigue, weight loss, mild anaemia, prolonged APTT.
  • Chronic GI infection possible.
  • Liver failure possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What tests do we reccommed for Mariana after the initial testing?

A

Liver function tests - for chronic infection
Clotting screen - repeat APTT with coagulation profile, to investigate clotting time.
FBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2nd visit to GP symptoms

A

pale orange urine, tenderness of lower abdomen and a number of bruises on her leg (mentioned she bruises easily)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Liver Function Tests results

A

Bilirubin - raised.
ALP - highly raised
AST - v. highly raised.
ALT - v. highly raised.
Albumin - normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2nd visit. Which results are abnormal.

A
  • high lymphocytes
  • low platelets
  • high PT
  • high serum bilirubin
  • v. high ALP
  • v. high AST
  • v. high ALT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

2nd visit. Differential diagnosis

A

Damage to liver - as 10x higher AST and ALT levels. also AST:ALT is <1, indicates hep.-causing virus.
Clinical jaundice - slight yellow in eye and hyperbilirumia (high bilirubin levels)
Possible viral cause - high lymphocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain link between liver inflammation and elevated lymphocytes

A

viral infections like hep a/b, cause a lymphatic response and therefore reflects body’s system immune system reacting to a viral pathogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain link between low platelets (thrombocytopenia)

A

so liver produces thrombopoietin (hormone that regulates platelet productions.
in liver inflammation, thrombopoietin production reduces so therefore platelet count reduces too.
also explains her bruising as platelets help with clotting and reduced levels can cause easy bruising/bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain link between liver inflammation and prolonged PT

A

PT = measure of how fast blood clots.
the liver synthesises clotting factors (e.g. II, VII, IX) and if inflamed it can’t make enough of them and reduces clotting.
Also why bruising occurs, impaird coagulation due to your dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Narrowed differential diagnosis:

A
  1. Acute viral hep.
  2. Drug/toxin-induced hep.
  3. Autoimmune hep.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What further investigations after the 2nd trip is needed?

A

Hep. B serology screening.
Assessing for HBsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the method for assessing for HBsAg, IgM Anti-HBc, Anti-HBc, Anti-HBs

17
Q

What does HBsAg indicate if +ve

A

active infection (>6mths)

18
Q

What does a +ve Anti-HBs test indicate

A

immunity from past infection/vacc.

19
Q

What does a +ve Anti-HBc test indicate?

A

Previous/current infection

20
Q

What does a +ve IgM anti-HBc test indicate?

A

acute/recent infection. (>6mths)

21
Q

What were Mariana’s ELISA results

A

HBsAg= +ve, Hep. B surface Ag present and therefore has current HBV infection
IgM Anti-HBc = borderline, possible early acute infection or flare of chronic HBV
Anti-HBc = +ve, has been exposed to virus (past/current)
Anti-HBs = -ve, has no protective immunity yet, no vacc./recovered.

22
Q

Treatment for acute hepatitis vs chronic

A

Acute:
close monitoring to see whether infection resolves/becomes chronic.
repeat HBsAg, ALT, AST every 3 mths for next 6-12. no immediate cantiviral therapy unless ALT remains elevated/develops worsening liver function
Chronic:
antiviral therapy.
monitor for cirrhosis - screen with ultrasound & AFP every 6mths.

23
Q

H&E Stain:
Difference in healthy liver tissue and diseased liver tissue

A

Hepatocytes - H(uniform, blue central nuclei, pink eosinophillic cytoplasm). D(ballooned, degenerate, ground glass appearance. Less nuclei and more pink cytoplasm).
Lobular structure = H(preserved, clear arrangement around central veins and portal triads), D(disrupted, fibrous septa.). Necrosis/fibrosis = H(none). D(spotty N, councilman bodies, varying degrees of F, depending on stage).

24
Q

Other special stains

A

Orecin, Masson’s Trichrome, Reticulin, PAS+/- Diastase, Prussian Blue, Rhodanine, IHC

25
Orecin
for HBsAg detection. brown granular deposits in hepatocytes.
26
Masson's trichrome
Fibrosis detection, blue/green fibrous bands.
27
PAS +/- Diastrase
For glycogen and A1AT deficiency. Magenta cytoplasmic inclusions.
28
Prussian blue
Iron overload, blue iron granules
29
Rhodanine
Cu detection (in Wilson's disease), orange/brown periportal Cu deposits,
30
IHC
for HBsAg and HBeAg, brown staining when antigens are present.
31
Long term complications of development of chronic Hep. B with respect to liver - CHRONIC INFLAMMATION
1. Chronic inflammation and hepatocyte damage. Persistent inflamm leads to hepatocyte injury and necrosis. 2. Liver Fibrosis leads to CIRRHOSIS. = end stage fibrosis (build of scar tissue). Decreased liver function, portal hypertension (increase pressure in liver circulation), splenomegaly (enlarged spleen), ascites (fluid in abdomen), variceal bleeding (esp. form eosophagus), hepatic encephalopathy (brain dysfunction due to toxin buildup)
32
Long term complications of development of chronic Hep. B with respect to liver - CIRRHOSIS
2. Liver Fibrosis leads to CIRRHOSIS. = end stage fibrosis (build of scar tissue). Decreased liver function, portal hypertension (increase pressure in liver circulation), splenomegaly (enlarged spleen), ascites (fluid in abdomen), variceal bleeding (esp. form eosophagus), hepatic encephalopathy (brain dysfunction due to toxin buildup).
33
Long term complications of development of chronic Hep. B with respect to liver - HEPATOCELLULAR CARCINOMA (HCC)
HBV can integrate its DNA into host hepatocytes, triggering mutation that promote malignancy.
34
Long term complications of development of chronic Hep. B with respect to liver - ALL
1. Chronic Inflammation. 2. Cirrhosis 3. Hepatocellular Carcinoma (HCC)
35