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?

A

10%

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
Q

what is the incubation period for Hep A, B, C, D, E F. G?

A
WEEKS
A 2-6
B 8-32
C 8-16
D 2-12
E 6-8
F and G unknown
26
Q

What is the acute mortality rate for Hep A, B, C, D, E F. G?

A
A 0.1%
B 1%
C less than 1%
D 10-20%
E 1-2%
F and G uknown
27
Q

what is the morbidity rate for Hep A, B, C, D, E F. G?

A
A V low
B 20%
C 80%
D 90%
E low
f and G unknown
28
Q

Is there a Carrier state for all the hep viruses?

A

A No
B, C, D yes
E, No
F and G unknown

29
Q

is there are vaccine available for the hep viruses?

A

A B D yes

C, E, F, G No

30
Q

What are the denral implications of hepatitis?

A

Liveer function impaired: Bleeding, metaoblism of drugs and liver cancer
assoicated diseases: HIV
Curretn medications
Liver trabsplant issues

31
Q

What is CJD?

A

a prion disease

32
Q

What are prions?

A

proteinacous infections particles

33
Q

What are the size of prions?

A

less than 30nm

34
Q

T/F prions are unifomly distributed amongst the tissues once infected?

A

F

35
Q

T/F PRIONS ARE not resistant to chemical and physical destructon?

A

F

they are resistant

36
Q

What can prions cause?

A

TSE

Transmissible Soingiform Encephalopathies

37
Q

What is TSE?

A

groups is diseases which lead to spongiform cahnge in CNS

38
Q

Where were TSE’s first seen?

A

sheep

39
Q

where are TSE more recently seen in?q

A

cattle

mad cow diseease

40
Q

What are the human forms of TSE?

A
  1. Kuru
  2. Sporadia CJD
  3. Familial CJD including fatal familila insomnia and gertsmann-strausller-scheinker
  4. Iatrogenic CJD
  5. variant CJD
41
Q

WHat are the three types of CJD recognised

A
  1. Sporadia CJD 85%
  2. Familial CJD including fatal familila insomnia and gertsmann-strausller-scheinker 10%
  3. variant CJD
42
Q

Which type of CJD is linked with BSE?

A

Variant

43
Q

How is iatrogenic CJD caused?

A

by any of the three recognised CJD when they are transmistted directly.

44
Q

How many cases of iatrogenic CJD are there per year?

A

accounts for 1%

45
Q

What are the clinical features of vCJD?

A

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
Q

How can varian CJD be transmitted?

A
human to human via
dural and corneal grafts
infected blood produtct
poorly sterilised equip
human GH and gonadotrophin
Ritual cannabilsm
47
Q

Since what year has BSE been out of the food chain since?

A

1996

48
Q

WHat agents are effective against TSE? and are they guranteed to be effective?

A

sodium hypocholoite
sodium hydroxide
Non porous load steam steriliser

NO GUARANTEE

49
Q

What concentration of sodium hypochlorite is needed to be effective agsint TSE agents?

A

20 000ppm 1 hour

50
Q

What concentration of sodium hydroxide is needed to be effective agsint TSE agents?

A

2M 1 hour

51
Q

How long must you sterlise for and at what temp to be effective against TSE agents?

A

134=137 degrees for 18 mins holding time of 6 cycles of 3 mins each

52
Q

How can we prevent trasmission of TSE?

A

good infection and control

for instuments dealing with CNS tissue, sngle use eg endo files