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phase 2a mine > liver middle tier > Flashcards

liver middle tier Flashcards

1
Q

acute vs chronic hepatitis time-wise

A 
acute = <6m
chronic = 6m +
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2
Q

signs and symptoms of acute hepatitis

A
  • none/few
  • malaise
  • lethargy
  • myalgia
  • GU/ abdom pain - RUQ
  • jaundice (pale stool, dark urine, itch)
  • ascites
  • tender hepatosplenomegaly
  • bleeding
  • encephalopathy
  • high bilirubin
  • high ALT/AST
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3
Q

signs and symptoms of chronic hepatitis

A
  • none/few
  • clubbing
  • palmar erythema
  • spide naevi
  • signs of decompensated liver
  • – coagulopathy, jaundice, low albumin, ascites, encephalopathy
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4
Q

causes of hepatitis

- split into acute and chronic

A

ACUTE
infectious
- hepatitis A,B,C,D,E (c= less so, more chronic)
- herpes, EBV, CMV, VZV
- non viral - toxoplasmosis, coxiella, leptospirosis
non infectious
- alcohol, drugs
- toxins / poisons
- pregnancy
- autoimmune
- metabolic, heridatry - Wilsons, A1AT def

CHRONIC
infectious
- hepatitis B,C,D (A+ E= acute only)
non infectious 
- alcohol, drugs
- autoimmune
- metabolic, heridatry - Wilsons, A1AT def
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5
Q

hepatitis LFTs

hepatitis complications

A

may be normal! may be high in acute

hepatocellular carcinoma
portal hypertension
– varices, bleeding, ascites

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6
Q

hep A epidemiology

  • where
  • commonness
A

LIC, poor sanitation (Africa, S america)

most common Hep worldwide

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7
Q

hep A risk factors

A 
travel
food handler
sexual
shellfish
poor sanitation, overcrowding
drug use, lick needle first
household contacts of infected
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8
Q

hep A pathophysiology

  • spread
  • incubation
  • virus
  • acute/ chronic
  • other features
A
  • faeco-oral spread
  • short incubation period - 2-6w
  • RNA
  • self limiting, ONLY acute. + 100% immune once had
  • rarely results in liver failure
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9
Q

hep A diagnosis

A 
anti HAV antibodies 
IgM - acute marker
I gG = marker of past infection / vaccine + immunity
\+ billirubinuria
\+ nausea
\+ fever
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10
Q

hep A management / prevention

A
  • good prognosis
  • supportive treatment
  • – close contacts –> vaccine, immunoglobulins
  • – avoid alcohol
  • – monitor liver function
  • notify public health
  • hygiene inc boil water
  • vaccine
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11
Q

hep E epidemiology

  • age
  • gender
  • where
  • mortality
A

indonesia
endemic in UK
older men
mortality high in preg

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12
Q

hep E pathophysiology

  • spread
  • incubation
  • virus
  • acute/ chronic
  • other features
A
  • two strands. GT1/2 spread in contaminated food/water (faecooral). GT3/4 spread in undercooked meat, pigs, rodents, dogs
  • RNA virus
  • self limiting - only chronic in immunosuppressed and GT3/4. 100% immune after infection
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13
Q

hep E diagnosis

A

anti HEV antibodies
IgM - acute marker
I gG = marker of past infection / vaccine + immunity
+ neurological manifestations

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14
Q

hep E management/ prevention

A
  • supportive treatment
  • – close contacts –> vaccine, immunoglobulins
  • – avoid alcohol
  • – monitor liver function
  • notify public health

vaccine
thorough meat cooking, sanitation/hygiene
dont be immunocomprimised

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15
Q

hep B epidemiology

A

worldwide - esp Africa, mediterranean, Far East, common

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16
Q

hep B pathophysiology

  • spread
  • incubation
  • virus
  • acute/ chronic
  • other features
A
  • very infectious
  • blood
    — sex esp MSM
    — needle (needle stick , IV drug use, dialysis, tattoos)
    — vertical (mum to baby)
    + semen/saliva
  • incubation period 1-6m
  • DNA!! only one not rna
  • can cause acute + chronic (most resolves alone though)
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17
Q

hep B AND D risk factors

A 
healthcare/ emergency proffesion
dialysis - CKD
travellesrs
tattoo lads
MSM
IV drug use
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18
Q

Hep B diagnosis

A

anti HBV antibodies
IgM - acute marker
I gG = marker of chronic infection/ previous infection (may not be resolved)
+ HBsAG (hep B surface antigen - produced by hepatocytes)
+ rashes
+ anorexia

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19
Q

hep B AND D management/ prevention

A
  • supportive treatment
    — close contacts –> vaccine, immunoglobulins
    vaccine for hep B. (NO vaccine for hep D)
    — sex contacts/ preg mum –> vaccine
    — avoid alcohol
    — monitor liver function
  • notify public health

pegylated interferon subcut if chronic
nucleotide analogues - inhibit viral replication

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20
Q

hep D epidemiology

where

A

E europe, N africa

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21
Q

hep D pathophysiology

  • spread
  • incubation
  • virus
  • acute/ chronic
  • other features
A
  • blood borne (sex, needles, vertical)
  • RNA (but incomplete)
  • needs hep B to be present to exist (activation, assembly, replication)- so acquired with hep b
  • can be acute or chronic
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22
Q

hep B and D - coinfection/ superinfection

A

coinfection = hep b acute + hep D

  • indistinguishable from hep b acute
  • igM present got anti HBV and HDV

superinfection = hep B chronic + hep D

  • severe - risk of fulmiant hepatitis –> liver failure
  • fibrosis
  • high AST/ALT
  • secondary acute hep
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23
Q

hep C epidemiology

-where

A

Egypt

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24
Q

hep c risk factors (inc transmission type)

A
  • blood : IV drug users, blood transfusion before 1991 (before blood product screening),
  • limited sex transfusion but MSM more severe infection
  • alcohol –> more severe infection
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25
Q

hep c pathophysiology

  • spread
  • virus
  • acute/ chronic
  • other features
A
  • blood transmission,
    limited sex transmission
    rare vertical transmission
  • RNA
  • majoirty = chronic –> cirrhosis, hepatocellular carcinoma, liver failure
    minority= acute , resolves alone
  • doesn’t stimulate v good immune response
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26
Q

hep c diagnosis

A

acute – HCV RNA

chronic / was infected – HCV IgG

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27
Q

hep c treatment / prevention

A

prevention

  • no vaccine! (C, D don’t have)
  • reduce risk factors (needles, blood screening etc)

destroy virus :
- pegylated interferon subcut if chronic
nucleotide analogues - inhibit viral replication
- antiviral

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28
Q

diarrhea red flags

A 
blood in stool
family history of cancer
chronic
weight loss
old
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29
Q

diarrhea onset if cause is worms

A

slower

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30
Q

what is the most common cause of infective diarrhea in uk

A

viral

norovirus - anyone, epidemics as v contagious

rotavirus - childen, vaccine given to baby

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31
Q

travellers diarrhea

  • relation to travel
  • main cause
  • symtoms
A
  • from trip start up to 10 days after return
  • bacteria mainly - ecoli
  • diarrhea
  • naus/vom
  • fever
  • cramps
  • bloody stool
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32
Q

enterotoxin mediated bacteria diarrhea

  • affects where
  • pathophys
  • effect
  • eg
A
  • upper bowel
  • bacteria –> enterotoxins –> increase intracellular AMP–> cells secrete fluid–> watery, voluminous diarrhoea
  • dehydration
  • cholera, c.diff
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33
Q

invasive bacteria diarrhea

  • affects where
  • pathophys
  • effect
  • eg
A
  • large bowel
  • penetrate intestinal mucosa
  • bloody stool
  • shigella, salmonella
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34
Q

infective diarrhea risk factors

A
  • travel
  • low hygiene person/ workplace etc
  • children who attend preschool
  • health workers
  • immunocomprimised
  • hobbies/ occupation (fresh water swimming, chef)
  • food/drink (street foot, sea food)
  • contact with animals
  • taken antibiotics (wipe gut flora out so bad bacteria more able to flourish)
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35
Q

infective diarrhea investigation

A

history inc pain where

Stool sampleS

  • Microscope
  • Culture
  • blood/pus/eggs (ova)
  • Toxin detection -toxin positive = infectious

Bloods

  • Inflammatory markers
  • Blood cultures
36
Q

what is faecal transplant used to treat

A

C.diff

to replenish bacteria

37
Q

cholera treatment

A

doxycycline

38
Q

infective diarrhea general treatment

A
  • Hydrate inc electrolytes
  • Wait - normally self limiting
  • Sometimes antibiotics
  • Sometimes need to notify public health
  • Sometimes barrier – + their family etc
39
Q

non-infective causes of diarrhea

A 
hormonal
neoplasm
inflammatory
irritable bowel
chemical 
radiation
anatomical
40
Q

bristol stool chart- which end is which

A

1 (hard) -7 (liquid)

41
Q

dys/meta/neoplastic

A

meta –> dys –> neo

meta= reversible replacement of one differentiated cell type with another
dys= appear abnormal but not cancer
neo = tumour (benign/malignant)
42
Q

enteric fever aka typhoid fever

  • where in world
  • cause
  • spread
  • symptoms
  • treatment
  • complications
A
  • S Asia, poor sanitation
  • salmonella typhoid
  • faeco-oral
  • high fever
  • general/ RLQ pain
  • headache
  • myalgia
  • bradycardia
  • rose spots
  • constipation
  • antibiotics
  • surgery - emergency
  • vaccine
  • GI bleed,
  • abscesses
  • myocarditis
43
Q

haemochromatosis causes

A

Genetic:

  • C282Y mutation and H63D mutation on the HFE gene, recessive (low penetrance so screening not advised)
  • this causes deficiency of iron regulation hormone = hepcidin
  • rarely not genetic, but guess these thing may precipitate/ worsen:
  • high iron intake (ascrobic acid, )
  • blood transfusion needs iron chelation
  • alcoholic
44
Q

haemochromatosis

  • race
  • gender
A

m>f (menstruation protective)

C282Y mutation more common if white

45
Q

wilsons cause/ risk factor

A

mutation in ATP7B (needed to remove excess copper) , recessive

consanginuity

46
Q

wilsons

  • commonness
  • age
A
  • rare

- 20-30

47
Q

A1AT deficiency more common in what race

cause

A

white populations

genetic

48
Q

haemochromatosis pathophysioogy

A
  • low levels of hepcidin (regulating hormone)
  • high iron uptake due to increased intestinal uptake
  • exceeds binding capacity of transferring
  • iron is deposited in liver, heart, pancreas –> fibrosis
49
Q

A1AT deficiency pathophysiology

A
  • alpha-1-antitrypsin deficiency
50
Q

heamochromatosis symptoms

A
  • Not many
  • Fatigue , weakness
  • Weight loss
  • Joint pain- arthropathy from psuedogout
  • Heart problems
  • Erectile dysfunction (hypogonadism)
  • absent/irregular periods (hypogonadism)
  • Bronzed/grey skin
  • Diabetes (iron deposited in pancreas :/ )
  • splenomegaly/ hepatomegaly
  • cirrhosis –> failure due to deposition here
51
Q

haemochromatosis investigations

A
  • Screening not advised as v low penetrance
  • Genotyping (look at genetic make up of them)
  • Liver biopsy
  • Bloods
  • – Raised serum ferritin/iron
  • – transferrin saturation ratio raised (total iron binding capacity reduced)
  • MRI - can detect iron overload
  • ECHO/ECG if cardiomyoptahy is suspected
52
Q

haemochromatosis treatment

A
  • Phlebotomy / venesection- removing blood regularly for a lifetime - excess iron then used to make new rbc, reducing excess . and can monitor levels during that time
  • Chelation if they cant tolerate that - desferrioxamine
  • Testosterone replacement
  • Diet: Iron low diet (high in tea,coffee, red wine) and avoid fruit juice, avoid alcohol and uncooked seafood
  • Liver transplant if severe
  • Insulin (treat diabetes)
  • Screen first degree relatives (or not as it is low penetrance)
53
Q

wilsons pathophysiology

A
  • disorder of copper billiary excretion. unable to move it across out of hepatocyte membranes so it accumulates
  • so copper builds up in the liver and CNS
54
Q

normal copper physiology

A
  • copper absorbed from diet
  • transported by albumin
  • incorporated into ceruloplasmin glycoprotein
  • rest is excreted in bile
55
Q

wilsons signs/symptoms

A
  • Kayser fleischer ring on eyes = bronze/greenish brown ring on cornea
  • Sunflower cataracts
  • These are able to be seen with a slit lamp
  • acute liver disease / hepatitis/ asterixis
  • CNS problems:
    • Reduced memory
    • Low mood
    • Behavioural problems
    • Tremor
    • Slowed speech = dysarthria
    • involuntary movements
    • dementia
56
Q

wilson investgations

A
  • Slit lamp - to detect kayser-fleischer rings and sunflower catarcats
  • Low serum caeruloplasmin (what copper is supposed to be converted into without pathology)
  • Serum copper can be low/ normal
  • High copper in urine
  • Liver biopsy
  • MRI can see CNS degeneration
57
Q

wilsons management

A
  • Avoid alcohol, reduce copper intake
  • Prevent copper absorption in gut
  • – Zinc / penicillamine used as a chelating agent
  • – Zinc salts - inhibits copper absorption
  • Liver transplant mebs
  • Neuro - deep brain stimulation
58
Q

A1AT deficiency pathophsyiology

A
  • A1AT deficiency = Can’t export alpha1 antitrypsin from liver, so it accumulates in hepatocutes and is low in serum
  • A1AT role = inhibits the proteolytic enzyme neutrophil elastase
  • neutrophil elastase enzymes lose their inhibition from A1AT. so can break down elastase excessively in liver (cirrhosis, hepatocellular cancer ) and lungs (emphysema)
59
Q

A1AT def management

A

No treatment cure

Liver

  • stop drinking
  • Treat liver disease
  • possible liver transplant - if decompensation

Lungs

  • Manage emphysema : Bronchodilators for lung
  • treat infection
  • No smoking
60
Q

ATA1 def investigations

A

Serum levels of A1AT

Liver biopsy

61
Q

A1AT def symptoms

A

liver:
- Neonatal jaundice
- Liver disease presentation esp in children
- Possible cirrhosis/ failure

lungs:

  • COPD-like symptoms, emphysema esp in adults
  • Dysnopea, cough, wheeze
62
Q

hepatocellular carcinoma

  • gender
  • commonnes
  • where
A

men>women
Common
China

63
Q

secondary liver tumour

- commonness

A

common, even more common than hepatocellular carcinoma

64
Q

pancreatic adenocarcinoma

  • gender
  • age
A

males>females

Increase with age (rare below 40, typically 60+)

65
Q

risk factors for hepatocellular carcinoma

A

HBV, HCV carriers- high likelihood
Cirrhosis
- Alcohol
- Haemochromatosis

66
Q

cholangiocarcinoma risk factors

A

Parasitic worms
Biliary cysts
Inflammatory bowel disease - UC (ulcerative colitis) and Crohns

67
Q

haemangioma risk factors

A

Oral contraceptives
Anabolic steroids
Pregnancy

68
Q

pancreatic adenocarcinoma risk factors

A 
Smoking
Excess alcohol/coffee/aspirin
Diabetes
Pancreatitis
Family history 
Genetic predisposition
69
Q

what cancers are esp likely to spread to liver

A

GI tract, bronchus, breast

70
Q

hepatocellular carcinoma

  • what type of cancer
  • single or mutliple nodes
  • cells resemble?
  • metastases?
A
  • primary liver tumour
  • single/ multiple nodules in liver
  • Cells resemble hepatocytes
  • Can metastasize to lymph, bones, lungs via hepatic/portal veins
71
Q

secondary liver tumour

- single or multiple nodes

A

normally multiple (As with all secondary tumours)

72
Q

cholangiocarcinoma
= cancer of where?
- fast/slow

A

= biliary tree cancer

Slow growing

73
Q

pancreatic adenocarcinoma

  • where
  • metasases?
  • when does is present
A
  • In epithelium, most in pancreatic head. Majority in exocrine part (releases pancreatic juice)
  • Metastasise early
  • Present late
74
Q

hemiangioma

  • where
  • benign/malignant
  • size
  • single/ multiple nodes
A
  • liver
  • benign
  • small and singular normally (but can be multiple /large ones)
75
Q

symptoms and signs of hepatocellular carcinoma

A
  • jaundice
  • Fever
  • Enlarged, irregular, tender liver
  • Ascites
  • Liver disease decompensation
  • Weight loss, anorexia
  • R hypochondrium ache
  • Abdominal pain
  • Fatigue
76
Q

symptoms and signs of secondary liver tumour

A
  • Hepatomegaly
  • Jaundice sometimes
  • Malaise
  • Upper abdom pain
77
Q

symptoms and signs of pancreatic adencarcinoma

A
  • Anorexia, weight loss
  • Change in bowel habit
  • Pain if body/tail and radiates to back . No pain if head
  • Acute pancreatitis
  • Jaundice - if head of pancreas (+stool, urine etc). No jaundice if body/tail
78
Q

symptoms and signs of cholangiocarcinoma

A
  • Fever
  • Malaise
  • Abdominal pain
  • jaundice
  • ascites
79
Q

hepatocellular carcinoma investigations

A
  • Examination of liver
  • Biopsy confirms diagnosis
  • CT/ultrasound
  • bloods - bilirubin (jaundice), raised LFTs -alkaline phosphate
80
Q

pancreatic adencarcinoma investgations

A
  • bloods - jaundice,
  • CT/MRI/ ultrasound
  • biopsy
81
Q

cholangiocarcinoma investigations

A
  • bloods - bilirubin (jaundice), raised alkaline phosphate

-

82
Q

secondary liver cancer investigations

A
  • CT/MRI/ultrasound

- alkaline phosphate is raised

83
Q

hepatocellular carcinoma treatment

A

Chemo
Transplant
Surgical Resection /local ablation

84
Q

secondary liver cancer treatment

A

Depends on where primary is
Sometimes chemo
Sometimes surgery

85
Q

cholangiocarcinoma treatment

A

Surgical resection and transplant are NOT good ideas

86
Q

haemangioma treatment

A

Need no treatment

Surgery only if symptomatic (intraperitoneal bleeding , abdominal pain)

87
Q

pancreatic adenocarcinoma treatment

A
  • Low prognosis
  • Surgery -pancreatoduodectomy
  • – If fit
  • – High post - op morbidity
  • – Post-op chemo good idea
  • Palliative care
  • – Jaundice stenting
  • – Opiates
  • – Nutritional supplements

phase 2a mine (38 decks)

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