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Dental Implications of managing pt with systemic disease Flashcards

1
Q

What is hepatitis?

A

inflammation of liver

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2
Q

What are the causes of hepatitis?

A 
Acute: 
infection: bacterial or viral
Drugs: alcohol, statins, street drugs, paracetemol 
Pregnancy
Chronic:
Viral 
Alcohol,
AI: primary sclerosimg cholangits
Genetic: wilsons ans haematochoromais
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3
Q

What are the complications of hep?

A 
cirrhosis
clotting defect
Hepatocellular carcinoma
chromic glomernephrits
carrier state
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4
Q

What are the hep B antibodies?

A

HepB surface antigen: infected acute or chronic
HepB surface antibody: recovery from natrual or vaccine infection

HepBe antigen: infected at some time
HebBeantibody: recovery from natrua, or vaccine

HepB core antobody: igM test for core antibody but this is not protective. This indicates previous or ongoing infection
DNA polymerase

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5
Q

Which hep B markers are present in early incubation of hepatitis?

A

HBs Ag and HBeAg

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6
Q

Which Hep B markers are present during acute hepatitis? And how do you treat it?

A

HBsAG , HBcAg HBe Ag and AntiHbcAg

LA
Lamuvidine
Adenosine

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7
Q

Which hep B markers are repsent in recovery phase and immunity?

A

AntiHBsAg
antiHBeA
AntiHBcAg

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8
Q

Which Hep B markers are present in healthy carrers with low risk of infectivity?

A

HBsAg
Anti HBEAg
AntiiHBcAg

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9
Q

Which Hep markers are present in chronic carriers wth high risk of infectiveity?

A

HBsAg
HBeAg
AntiHBcAg

More than 6 months

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10
Q

WHat does Hep D do?

A

this rides on the back of HBV and replicates only in presence og HepB

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11
Q

Hep D is what type of virus?

A

incomplete RNA

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12
Q

Which Hep virus is usally seen post transfusion?

A

Hep C 90% of cases

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13
Q

How is Hep C transmitted usually?

A

paraenteral, IVDU, rarely sexual and vertical and sailva seen in animals

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14
Q

How do you diagnose Hep C?

A

dectection of anti HCV antibody

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15
Q

How long does seroconversion on Hep C take?

A

may take sevreal months

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16
Q

How can you diagnose acute HCV infection?

A

use PCR techniques to amplify HCV RNA

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17
Q

t/F there is a higher incidence of developing HCC with Hep B then with Hep C?

A

False

other way round

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18
Q

T/F there is a vaccine for Hep C?

A

false

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19
Q

How do you treat Hep C?

A

interforn alpha

ribavarin: which has been shown to reduce serum levels of HCV RNA

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20
Q

what percentage of people using interforn alpha for the treatment of HCV regress after 6 months?

A

50-80%

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21
Q

WHat is the incidence fpr Hep B?

A

most prevelane: 15-44 years
peak incidence 25-34 years
M:F 1.5:1

22
Q

What is the incidence for hep c?

A

most prevelant 25-44

M:F 2:1

23
Q

What is the risk of seroconversion following a needle stick injury in a HEp C pos pt?

24
Q

How is Hep A, B, C, D, E F. G transmitted?

A 
A: Faceo-oral
B: IV.Sex. Vertical
C: IV/Sex/Verical
D: With Hep B
E: faeco oral
F: IV
G: IV
25
what is the incubation period for Hep A, B, C, D, E F. G?
``` WEEKS A 2-6 B 8-32 C 8-16 D 2-12 E 6-8 F and G unknown ```
26
What is the acute mortality rate for Hep A, B, C, D, E F. G?
``` A 0.1% B 1% C less than 1% D 10-20% E 1-2% F and G uknown ```
27
what is the morbidity rate for Hep A, B, C, D, E F. G?
``` A V low B 20% C 80% D 90% E low f and G unknown ```
28
Is there a Carrier state for all the hep viruses?
A No B, C, D yes E, No F and G unknown
29
is there are vaccine available for the hep viruses?
A B D yes | C, E, F, G No
30
What are the denral implications of hepatitis?
Liveer function impaired: Bleeding, metaoblism of drugs and liver cancer assoicated diseases: HIV Curretn medications Liver trabsplant issues
31
What is CJD?
a prion disease
32
What are prions?
proteinacous infections particles
33
What are the size of prions?
less than 30nm
34
T/F prions are unifomly distributed amongst the tissues once infected?
F
35
T/F PRIONS ARE not resistant to chemical and physical destructon?
F | they are resistant
36
What can prions cause?
TSE | Transmissible Soingiform Encephalopathies
37
What is TSE?
groups is diseases which lead to spongiform cahnge in CNS
38
Where were TSE's first seen?
sheep
39
where are TSE more recently seen in?q
cattle | mad cow diseease
40
What are the human forms of TSE?
1. Kuru 2. Sporadia CJD 3. Familial CJD including fatal familila insomnia and gertsmann-strausller-scheinker 4. Iatrogenic CJD 5. variant CJD
41
WHat are the three types of CJD recognised
2. Sporadia CJD 85% 3. Familial CJD including fatal familila insomnia and gertsmann-strausller-scheinker 10% 5. variant CJD
42
Which type of CJD is linked with BSE?
Variant
43
How is iatrogenic CJD caused?
by any of the three recognised CJD when they are transmistted directly.
44
How many cases of iatrogenic CJD are there per year?
accounts for 1%
45
What are the clinical features of vCJD?
lower age of onset: 20 instead of 60yrs Longer duratio of illness> 14 months vs 5 months Earlier psychilatric changes and sensrory and cerebellar signs
46
How can varian CJD be transmitted?
``` human to human via dural and corneal grafts infected blood produtct poorly sterilised equip human GH and gonadotrophin Ritual cannabilsm ```
47
Since what year has BSE been out of the food chain since?
1996
48
WHat agents are effective against TSE? and are they guranteed to be effective?
sodium hypocholoite sodium hydroxide Non porous load steam steriliser NO GUARANTEE
49
What concentration of sodium hypochlorite is needed to be effective agsint TSE agents?
20 000ppm 1 hour
50
What concentration of sodium hydroxide is needed to be effective agsint TSE agents?
2M 1 hour
51
How long must you sterlise for and at what temp to be effective against TSE agents?
134=137 degrees for 18 mins holding time of 6 cycles of 3 mins each
52
How can we prevent trasmission of TSE?
good infection and control | for instuments dealing with CNS tissue, sngle use eg endo files

Oral Med (31 decks)

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