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Sven's Flashcards > 205 - Alcoholism and Hepatitis > Flashcards

205 - Alcoholism and Hepatitis Flashcards

0
Q

Apart from Hep ABCDE, what other viruses can cause acute hepatitis?

A

Epstein Barr, Cytomegalovirus, enteroviruses and herpes virus

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1
Q

What is the most common hepatitis virus in the UK and what is it worldwide?

A

UK - Hep C

Worldwide - Hep B (Highest chance of transmission on blood-blood contact)

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2
Q

what drugs can cause acute hepatitis?

A

Isoniazid
Halothane
Sulfasalazine

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3
Q

what are the possible non drug or virus causes for acute hepatitis?

A

sepsis, ischaemia, toxins

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4
Q

what are the signs and symptoms for acute hepatitis?

A

change in appetite, tiredness & weakness, fever, hepatomegaly, RUQ pain, jaundice, nausea/vomiting, weight loss

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5
Q

how could you tell whether acute hepatitis had been caused by alcohol, virus or drugs?

A
  • Transaminase levels - In alcohol low values of ~300 with AST>ALT, in viruses moderate values 100-1000 with ALT>AST, in drugs high values 100s-1000s with ALT>AST
  • Antibodies raised - Alcohol IgA, viruses IgG & IgM, drugs all IGs
  • WBCs - alcohol neutrophilia, virus leukopaenia, drugs eosinophilia
  • Marked hepatomegaly & portal HTN with alcohol and moderate hepatomegaly with virus
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6
Q

What are the stages of acute hepatitis progression, what are the symptoms and how long do they last?

A
  • pre icteric (prodrome) 3-9 days- without jaundice, flu symptoms, N&V, abdo pain, low grade fever, raised alt/ast, fatigue, headache, myalgia, anorexia
  • icteric 2-4 wks - jaundice, pale stools (low bile in stool), dark urine (high bilirubin in urine), raised alt/ast & bilirubin in blood
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7
Q

What is fulmitant hepatic failure?

A

Severe liver function impairment in a previously healthy person. Liver failure and/or encephalopathy within 8 weeks of jaundice. Also coagulopathy and multi organ failure

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8
Q

Define chronic hepatitis

A

chronic inflammation of the liver continuing without improvement for at least 6 months

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9
Q

what are the causes of chronic hepatitis?

A

drugs, viruses, autoimmune hepatitis (hepatocytes display human leukocyte antigen class II and APCs present to lymnpocytes triggered by genetics, viral infection or chemicals) and Wilson’s disease (autosomal recessive copper accumulation in tissues including kidneys and heart and seen by brown kayser fleischer rings at edge of iris)

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10
Q

what are the signs and symptoms for chronic hepatitis?

A

stigmata, jaundice, splenomegaly and portal hypertension

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11
Q

what investigations should be carried out for chronic hepatitis?

A
  • LFTs - ALT raised (mild 400) Alk phos/albumin and bilirubin often normal
  • antibodies - all Igs raised
  • liver biopsy showing necroinflammatory & fibrosis scores
  • FBC, U&Es, clotting, USS
  • Hep C - antihep C antibodies….Hep B - hepatitis antigen….autoimmune - ANA (antinuclear antibodies) and SMA (smooth muscle antibodies)…..wilsons - incr. conc of Cu in blood and decrease in caeulosplasmin (cu carrying serum proteins)
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12
Q

what causes fatty liver and can it be cured?

A

when the body turns ethanol to acetaldehyde to acetate, the NAD+ coenzyme is turned to NADH. This means fatty deposits build up due to a decr. in NAD+ causing a decr. in gluconeogenesis. It is reversible with alcohol abstinence

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13
Q

what are the transmission routes for the hepatitis viruses?

A
  • oral faecal - hep A and hep E

* parenteral - hep B, hep C, hep D (in presence of hep B)

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14
Q

what type of virus is hep C and how is it transmitted?

A
  • bloodborne RNA virus (flaviviridae)

* iv drug use, mother to child, unsafe med practice, sex, occupational exposure, blood tranfusion, infected donor organ

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15
Q

what are the signs and symptoms of hep C and what are the treatments?

A
  • often asymptomatic, malaise, weakness, anorexia. becomes chronic. cirrhosis (scaring of liver) causes portal hypertension, ascites, jaundice, easy bruising, varices, hepatic encephalopathy, liver failure
  • peg interferon and ribavirin (stops viral RNA synthesis and mRNA) and DAAs (directly acting antivirals)
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16
Q

what are the treatments for hep B?

A

Peg interferon, entecavir and tenofovir

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17
Q

what are the types of reactions in drug metabolism in the liver?

A
  • phase I reactions - oxidative/reductive (functional groups) & hydrolytic (cleaving of esters/amides). Catalysed by hemoproteins like cytochrome P450
  • phase II reactions - products of phase I coupled with endogenous substrates like glycine, acetic acid, sulphuric acid
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18
Q

how are low and high concentrations of ethanol metabolised?

A

low conc. dealt with by 1st pass metabolism using alcohol dehydrogenase (easily saturated).
high conc. dealt with by 2nd pass metabolism using microsomal ethanol oxidising system (also used in drug metabolism = interaction)

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19
Q

describe the metabolism of bilirubin

A
  • unconjugated bilirubin (lipophilic) produced by haem-pigment breakdown and carried to liver by albumin
  • hepatocytes conjugate bilirubin making it hydrophilic which is excreted in bile salts.
  • GI bacteria break it down into urobilinogen - majority excreted in faeces and some reabsorbed in intestines and excreted in urine.
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20
Q

what are the three main causes of jaundice?

A
  • pre-hepatic - due to incr. haemolysis (haemolytic anaemia, malaria, sickle cell anaemia / thalassaemia)
  • hepatic - viral, drug, alcohol, cirrhosis, gilberts (genetic -incr in blood bilirubin), physiological jaundice of newborn (no enzymes for conjugation)
  • cholestatic - biliary obstruction due to bile stones, ca of pancreas head, ca of bileducts
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21
Q

how do you differentiate between the different causes of jaundice clinically?

A
  • pre-hepatic - incr. in conjugated and unconjugated bilirubin as more produced. normal ALT and ALP and urine
  • hepatic - incr. in conjugated bilirubin as decr. hepatic excretion and reflux into plasma. very high ALT (liver damage) and small rise in ALP (decr. in biliary excretion). dark urine (conj. bilirubin)
  • cholestatic - very high conj. bilirubin due to decr. hepatic excretion. very high ALP (decr. biliary excretion) and small incr. ALT (resulting liver damage). dark urine (conj. bilirubin), pale stools, itching
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22
Q

what investigations would be carried out in a patient with jaundice?

A

liver USS to check for dilated bile ducts - if dilated ERCP to look for and removed obstruction or if not ERCP/liver biopsy to check for inflammation/necrosis/fibrosis

23
Q

what is cirrhosis and what causes it?

A

diffuse liver disease with fibrosis and nodule formation due to regeneration causes by:
alcohol, virus, drugs, autoimmune disease, wilsons (cu), alpha 1 antitrypsin deficiency, hepatic venous outflow obstruction, prolonged cholestasis

24
Q

what are the clinical signs of cirrhosis?

A
  • stigmata - leukonychia, clubbing, palmar erythema, dupuytrens, gynaecomastia, testicular atrophy, loss of body hair
  • sometimes hepatomegaly
  • ascites & oedema - decr. osmotic pressure of blood (low albumin)
  • Portal HTN - spider naevae, caput medusa, splenomegaly
25
Q

what is decompensated cirrhosis and what are the signs and symptoms?

A

normally compensated cirrhosis tipped over the edge by minor infection causing:
encephalopathy due to toxin seen by liver flap (asterixis), fetor hepaticus (sweet faecal breath), jaundice, ascites and wasting

26
Q

what does a high haemoglobin value indicate?

A

polycythaemia - incr. RBC

27
Q

what does a low haemoglobin value indicate?

A

Anaemia - decr. RBC

  • with incr MCV - macrocytic anaemia - B12/folate (DNA production) deficiency
  • with normal MCV - normocytic anaemia - acute blood loss, renal failure, pregnancy
  • with decr MCV - microcytic anaemia - iron deficiency
28
Q

what does a high WCC indicate?

A

leukocytosis - suggest infection

29
Q

what does a low WCC indicate?

A

Leukopenia - suggests immunosuppression due to chemo/radio,infections, meds

30
Q

what causes high and low neutrophil counts?

A
  • high - bacterial infection, inflammation, steroids

* low - some viral infections

31
Q

what causes high and low lymphocyte counts?

A
  • high - viral infections, EBV (affects B cells and incr T cells to attack them), come chronic bac. infections, leukaemia
  • low - steroids
32
Q

what causes a high eosinophil count?

A

helminth infections, allergies, drug reactions

33
Q

what causes high monocyte counts?

A

post chemo/radio, chronic infection

34
Q

what do high basophil counts indicate?

A

myeloproliferative diseases, Ig E, viral infection, inflammation

35
Q

what does a high and low platelet count indicate?

A
  • high - thrombocytosis - myeloproliferative diseases, inflammation, surgery
  • low - thrombocytopenia - DIC, ideopathic thrombocytic purpura, B12/folate dificiency
36
Q

what do high levels of alkaline phosphatase indicate?

A

biliary obstruction - ALP secreted in bile from liver

37
Q

what does an increase PTT indicate with regards to the liver and why?

A

liver dysfunction as clotting factors produced by liver (not specific to liver however)

38
Q

how does alcohol affect inhibitory and excitatory pathways?

A
  • potentiates inhibitory pathways (gaba receptors)
  • reduces excitatory pathways (glutamate receptors). inhibits NMDA receptor activity causing memory loss
  • inhibits calcium channel flow
39
Q

what causes chronic tolerance to a drug?

A

incr. in number and activity of enzymes used in metabolism

40
Q

how does acute tolerance affect motor function in alcohol intoxication?

A

motor function lost at a level of blood alcohol conc. but returns at a higher level than it was lost

41
Q

what is himmelsbach hypothesis?

A

acute alcohol affect is counteracted by adaptation to produce alcohol tolerance. when alcohol is removed this adaptation still remains causing withdrawal syndrome (hangover) until an alcohol free state is achieved

42
Q

name some symptoms of withdrawal syndrome and a clinical treatment

A

motor agitation, anxiety, insomnia, reduction in seizure threshold and delirium tremens (hallucinations, tremors)

treatment - benzodiazepines

43
Q

what combination of treatments are available for alcoholism?

A
  • naltrexone & nalmefene (opioid receptor antagonists to counter endogenous opioids
  • acamprosate - nmda receptor antagonist)
  • behavioural therapy
44
Q

what is replacement therapy?

A

fast acting drug (addictive) replacedwith a slow acting one like nicotine, opioids, benzodiazepine

45
Q

what is the reward circuit?

A

dopamine produced by the ventral tegmental area and moves to the nucleus accumbens. Rewards stimulate dopamine release through release of endogenous opioids and act as a learning signal. The prefrontal lobe can override this circuit by the executive function

46
Q

how do nicotine, opioids, psychostimulants and alcohol affect the release of dopamine?

A

alcohol and nicotine activate neurones which release dopamine
opioids inhibit dopamine inhibition
pschostimulants reverse dopamine transporters

47
Q

what are the main functions of the liver?

A
  • detoxifies blood from gut - drugs and toxins
  • fat metabolism
  • glucose storage as glycogen
  • breaking down haem pigments and production of bile
  • production of clotting factors
48
Q

describe the blood supply and drainage of the liver?

A
  • hepatic artery 33% high o2 high P
  • portal vein - from Superior and inferior mesenteric veins and splenic vein 66% low o2 low P

*hepatic vein - drains into IVC

49
Q

what do liver lobules contain?

A
  • portal tracts -branch of hepatic artery, branch of portal vein, tributary of biliary ducts
  • central vein - drains processed blood
50
Q

what do sinusoids do?

A

fenestrated capillary like tubes lined with epithelium that drain blood from hepatic artery/portal vein, pass it to hepatocytes and drain back to central vein. Contain kuppfer cells (macrophages) and lymphoid cells (NK cells)

51
Q

what is the space of disse

A

space between sinusoids and hepatocytes. Contain stellate cells which are fibroblasts for repair

52
Q

what does the red pulp of the spleen do?

A

destruction of old RBC (>120 days old)
recycle iron to liver
send haem products to liver

53
Q

what does the white pulp of the spleen do?

A

immune defence - blood enters germinal centres and diffuses through lymphocytes then encapsulated organisms are opsonised

54
Q

what causes splenommegaly?

A 
infection
congestion due to portal hypotension backing up
hemolytic anaemia
autoimmune diseases
haematological malignancy

Sven's Flashcards (32 decks)

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