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Phase 2a > Liver conditions > Flashcards

Liver conditions Flashcards

1
Q

name 7 functions of the liver

A

oestrogen regulation
detoxification
metabolises carbohydrates
albumin production
clotting factor production
bilirubin regulation
immunity (kupffer cells)

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2
Q

what are 3 markers of liver function and how would they indicate liver damage

A

bilirubin- increased
albumin- decreased
prothrombin time- increased

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3
Q

the presence of which 4 enzymes indicates liver disease

A

ALT
AST
GGT
ALP

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4
Q

describe the process of liver cirrhosis

A

cirrhosis= result of chronic inflammation + damage 2 liver cells

when liver cells damaged
-replaced w. scar tissue= fibrosis
-nodules of scar tissue within liver= regenerative nodules

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5
Q

common and rarer causes of liver cirrhosis & risk factors

A

mc= ALD, NAFLD, hep B + C
rarer= haemochromatosis, A1AT def, Wilson’s disease

RFs= alcohol misuse, IVDU, unprotected sex, obesity

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6
Q

presentations of liver cirrhosis

A

hepatosplenomegaly
jaundice
ascites
HE
palmar erythma
spider naevi
caput medusae
hepatic factor (eggy breath)
xanthelasma (yellow growth on eyelids)

abdo pain
pruritis
n+v
confusion
bleeding

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7
Q

1st line + GOLD investigations for liver cirrhosis

A

1st
LFTs=
increased- bilirubin, PT/INR, AST + ALT, ammonia, GGT
decreased- albumin + glucose

FBC= anaemia, thrombocytopenia, leukopenia
U&Es= raised

GOLD= liver biopsy
-destruction of liver parenchyma, regenerative liver nodules

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8
Q

complications of liver cirrhosis

A

HCC
spont. bacterial pericarditis
oesophageal varies + portal HTN
HE
hepato-renal syndrome
ascites
bleeding

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9
Q

describe general liver failure

A

liver loses ability to regenerate/repair leading 2 decompensation

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10
Q

what is the most common cause of acute liver failure

A

paracetamol overdose

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11
Q

name 5 causes of acute liver failure

A

DRUGS- paracetamol, alcohol
VIRAL- hep A/B/E, CMV, EBV autoimmune hep
NEOPLASTIC- hepatocellular/metatstic carcinoma
METABOLLIC- Wilson’s disease, alpha 1 anti trypsin, haemochromatosis
VASCULAR- budd chiari

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12
Q

presentation of acute liver failure

A

jaundice
abnormal bleeding
hepatic encephalopathy

malaise
n + v
abdo pain

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13
Q

describe the west haven 1- 4 criteria for presentation of hepatic encephalopathy

A
  1. altered mood + sleep issues
  2. lethargy, mild confusion, asterixis (liver flap)
  3. marked confusion, quiet
  4. comatose
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14
Q

investigations for acute liver failure:
LFT,FBC,U&Es,imaging. microbiology

A

LFTs: increased- bilirubin, PT, AST + ALT, NH3
decreased- albumin + glucose

FBCs: anaemia, thrombocytopenia, leukopenia
U&Es= raised

imaging= EEG 2 grade HE
USS of abdo 2 check Budd chiari

microbiology 2 rule out infections-blood culture + urine

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15
Q

management of acute liver failure

A

ITU, ABCDE, fluids, analgesia- asses 4 liver transplant
treat underlying cause + comps
eg paracetamol overdose- give activated charcoal + N acetyl cysteine within 1hr of overdose

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16
Q

name 5 complications of acute liver failure and what you would give to treat them

A

cerebral oedema= IV mannitol
HE= lactulose
ascites= diuretics
bleeding= vit K
sepsis= sepsis 6

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17
Q

describe chronic liver failure

A

progressive liver disease over 6+ months, due 2 repeated liver abuse

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18
Q

name 3 causes of chronic liver disease

A

progression from acute liver disease
NAFLD
hep C + B

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19
Q

list 5 risk factors for chronic liver disease

A

alcohol/drugs
obesity
T2DM
inherited metabolic disease/existing autoimmunity

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20
Q

describe the progression to liver failure from hepatitis

A

hepatitis > fibrosis (reversible damage) > cirrhosis (irreversible damage) > either: compensated (some liver function) OR decompensated (end stage liver failure)

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21
Q

what is the MELD score used for

A

model for end stage liver disease
- looks at severity for transplant planning

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22
Q

what are 5 key presentations of end stage liver failure

A

jaundice
HE
coagulopathy
ascites
oesophageal varices

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23
Q

presentation of chronic liver failure (lots)

A

jaundice
ascites
abnormal bleeding
HE (symptoms)
portal hypertension + oesophageal varices
caput medusae
spider naevi
palmar erythema
gynecomastia
fector hepatic
dupuytren’s contracture

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24
Q

what is the child Pugh score used for

A

to assess prognosis + extent of treatment required for chronic liver failure

A= 100% 1yr survival
B= 80% 1 yr survival
c= 45% 1 yr survival

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25
Q

1st line investigations for chronic liver failure

A

LFTs= raised - bilirubin, PTT, AST + ALT, NH3, GGT
lowered- albumin + glucose

FBCs= anaemia, thrombocytopenia, leukopenia
U&Es= raised

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26
Q

gold standard investigation for chronic liver failure

A

liver biopsy= 2 determine extent of damage

other = ascites tap + abdo USS

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27
Q

management of chronic liver failure

A

prevent progression- lifestyle mods (no alcohol, lower BMI, low LDL + salt)
liver transplant (MELD score)
manage comps: same as acute

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28
Q

name 3 risk factors for alcoholic liver disease

A

chronic alcohol
obesity
smoking

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29
Q

describe the progression to alcoholic liver disease

A

steatosis (fatty liver) > alcoholic hepatitis > alcoholic cirrhosis

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30
Q

presentation of alcoholic liver disease

A

early stages= asymptomatic
later more severe stages= chronic liver failure symptoms + alcohol dependency

(chronic liver failure symptoms= jaundice, hepatosplenomegaly, spider nave, dupuytren’s contracture, palmar erythema, ascites, HE, caput medusae, easy bruising)

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31
Q

describe 2 alcohol dependency questionnaires

A

CAGE=
should you Cut down?
one person Annoyed by your drinking?
feel Guilty about drinking?
do u drink in morning (Eye opener)
- 2+ means dependent

AUDIT- alcohol use disorder ID test

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32
Q

1st line investigations for alcoholic liver disease

A

LFTs= increased- GGT, AST + ALT, ALP, bilirubin
decreased- albumin
AST : ALT ratio = >2

FBC= macrolytic nonmegaloblastic anaemia

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33
Q

gold standard investigation for alcoholic liver disease

A

liver biopsy (2 confirm extent of cirrhosis)
- will see inflammation, steatosis, necrosis, MALLORY CYTOPLASMIC INCLUSION BODIES

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34
Q

management of alcoholic liver disease

A

stop alcohol- give chlordiazepoxide 4 delirium tremors

also= wt. loss, no smoking, steroids for alcoholic hepatitis (prednisolone)

liver transplant if severe- must abstain from alcohol for 3+ months first

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35
Q

list 6 complications of alcoholic liver disease and how you would treat them

A

pancreatitis
HE- lactulose
ascites- diuretics
HCC- chemo, surgery
mallory weiss tear
wernicke Korsakoff syndrome (combined B1 + alcohol withdrawl symptoms)- IV thiamine

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36
Q

what would you immediately suspect in anyone that had:
T2DM
obesity
deranged LFTs

A

non alcoholic fatty liver disease (NAFLD)

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37
Q

list 7 risk factors for NAFLD

A

obesity
hypertension
hyperlipidemia
T2DM
Family history
endocrine disorders
drugs= NSAIDs

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38
Q

presentation of NAFLD

A

typically asymptomatic
- if severe, may present w. signs of liver failure

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39
Q

investigations for NAFLD

and GOLD

A

imaging= abdo USS, fatty liver (hepatic steatosis) seen as increased echogenicity

bloods-
deranged LFTs: riased ALT= 1st indication of NAFLD
(PT increased, bilirubin increased, decreased albumin)
FBC= thrombocytopenia, hyperglycaemia

Enhanced liver fibrosis (ELF)= 1st line blood test for assessing fibrosis
10.51+, advanced fibrosis

NAFLD fibrosis score

Assess risk of fibrosis w non- invasive scoring system eg Fib-4, >2.67= advanced + refer to hepatology

GOLD= liver biopsy

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40
Q

management of NAFLD

A

wt. loss
control rfs (use statins, metformin etc)
take vit E

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41
Q

list 4 complications of NAFLD

A

HE
ascites
HCC
portal htn + oesophageal varices

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42
Q

define viral hepatitis

A

inflammation of the liver due to viral replication within hepatocytes

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43
Q

describe the pathology of viral hepatitis

A

virus infected cells undergo cytotoxic killing ( causes inflammation in liver) + apoptosis by immune system
hepatocytes undergoing apoptosis= councilman bodies

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44
Q

is hep A acute or chronic and how is it spread

A

acute
-RNA virus spread via faecal- oral route (contaminated food/water)

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45
Q

list 3 risk factors for hep A

A

living/ travelling to endemic area (Africa)
overcrowding
undercooked shellfish

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46
Q

presentation of hep A

A

prodomal phase= 1-2 weeks
- malaise
- n+v
- fever

then:
-jaundice
-dark urine + pale stools
-hepatosplenomegaly
-choleostasis
-fatigue
-headache
-pruritis
-abdo pain
-musc. aches

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47
Q

1st line investigations for hep A

A

bloods= increased- serum AST + ALT, bilirubin, ESR

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48
Q

gold standard investigations for hep A

A

HAV serology:
HAV IgM= active
HAV IgG= recovery/vaccination

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49
Q

management of hep A

A

supportive therapy- resolves by itself
- traveller vaccine available

comps= rapid liver failure

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50
Q

how is hep B spread

A

acute + chronic

enveloped DNA virus transmitted via blood + bodily fluids

50% of chronic hep B cases= under 6 yrs

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51
Q

name 4 methods of transmission of hep B

A

needles
sexual
vertical (mother 2 child)
horizontal (child 2 child)

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52
Q

list 5 risk factors for hep B

A

IVDU
healthcare worker
gay sex
unprotected sex
dialysis patients

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53
Q

presentation of hep B

A

v. similar to hep A
1-2 week prodromal phase:
-malaise
-n+v
-fever
-fatigue

then:
jaundice
dark urine + pale stools
hepatosplenomegaly
URITICARIA
ARTHRALAGIA

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54
Q

first line investigations for hep B

A

LFTs= increased ALT +AST, bilirubin, ALP

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55
Q

gold standard investigation for hep B

A

HBV DNA (direct count of viral load) + serology:

ANTIGENS=
HBsAg (HBV surface antigen)= active infection
HBcAg (core antigen in core of HBV) = active infection

HBeAg (secreted by infected cells)=
HBV replication & infectivity

ANTIBODIES=
Anti-HBc (antibodies against core antigen)- previous or ongoing contact with HBV
IgM anti-HBc= acute or excecerbation of HBV

anti-HBs (antibodies agaistn HBsAg)= recovery + immunity (vax)
anti-Hbe (antibodies against HBeAg)= low HBV replication & remission

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56
Q

management of hep B

A

SC peginterferon alpha 2 or tenofovir injection

prevention = vaccination w. HBV surface antigen (HBsAg)

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57
Q

How is hep c transmitted

A

RNA, transmitted via blood + bodily fluids
acute + chronic
1/4 fight off virus
3/4 become chronic

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58
Q

list 5 risk factors for hep c

A

IVDU
unsafe medical practice
unprotected sex
vertical transmission in childbirth
blood transfusion/organ transplant

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59
Q

presentation of hep C

A

-often asymptomatic in acute

chronic=
jaundice
ascites
hepatosplenomegaly
fever
n+v
malaise
pruritis
abdo pain + musc aches

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60
Q

first line investigations for hep C

A

HCV antibody enzyme immunoassay- HCV IgG
-positive indicates current infection
aminotransferases= elevated

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61
Q

gold standard investigation for hep C

A

PCR (HCV RNA test)- indicates past or current infection
-viral DNA decreasing= recovery
-viral level same= chronic

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62
Q

management of hep C

A

direct acting antivirals (ribavirin, sofosbuvir)
-no vax available

30% of cases progress 2 chronic liver failure (cirrhosis + HCC risk)

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63
Q

what does hep D need in order to survive

A

hep D= an RNA the only survives in patients that also have hep B, hep D attaches itself 2 surface antigen of hep B

spread via blood + bodily fluids

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64
Q

presentation of hep D

A

jaundice
hepatosplenomegaly
dark urine + pale stools
n+v
fever
malaise
ascites
uriticaria
arthralagia
musc aches
abdo pain

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65
Q

first line investigations for hep D

A

LFTs= increased- AST + ALT, bilirubin, ALP

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66
Q

gold standard investigation for hep D

A

serology: HDV IgM or IgG= active infection
HDV RNA in serum

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67
Q

management of hep D

A

no spec treatment
treat hep B- SC pegylated interferon alpha 2a or tenofovir

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68
Q

how is hep E spread

A

RNA spread via faecal oral route (contaminated food + water)
dogs
pigs
undercooked seafood

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69
Q

presentation of hep E

A

fever
malaise
n+v
jaundice
hepatomegaly
dark urine + pale stools
pruritis
abdo pain

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70
Q

1st line investigations for hep E

A

LFTs= increased- AST + ALT, Bilirubin, ESR

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71
Q

gold standard investigation for hep E

A

HEV serology:

HEV IgM antibodies= active infection
HEV IgG antibodies= recovery
HEV RNA= current infection

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72
Q

management of hep E

A

mild illness- no treat
self limiting within a month

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73
Q

describe autoimmune hepatitis

A

inflammation of the liver due to it being attacked by bodies own cells

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74
Q

list 4 risk factors for autoimmune hepatitis

A

female
other autoimmune conditions
viral hepatitis
HLA DR3/DR4 gene mutation

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75
Q

who is affected and which antibodies are involved in autoimmune hep type 1

A

adult women

anti-nuclear antibodies
anti-smooth musc antibodies
anti-soluble liver antigen

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76
Q

who is affected and what type of antibodies are involved in autoimmune hep type 2

A

children

anti-liver kidney microcome antibodies type 1(ALKA-1)
anti-liver cytosol antibodies type 1 (ALCA-1)

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77
Q

presentation of autoimmune hepatitis

A

25%= asymptomatic

jaundice
fatigue
malaise
fever
hepatosplenomegaly

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78
Q

1st line investigations for autoimmune hepatitis

A

LFTs- increased AST + ALT, prolonged PTH
decreased albumin

serology:
T1= ANA, ASMA,ASLA
T2= ALKM-1, ALCA-1

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79
Q

gold standard investigation for autoimmune hepatitis

A

liver biopsy

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80
Q

management of autoimmune hepatitis

A

corticosteroids (prednisolone) + immunosuppressant (azathioprine)

liver transplant if resistant to meds

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81
Q

what is hepatic encephalopathy

A

brain infection due to toxic metabolites (esp ammonia) not removed by liver due 2 liver dysfunction/cirrhosis

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82
Q

describe the pathology of hepatic encephalopathy

A

intestinal bacteria break down proteins into ammonia to be absorbed in gut

liver impairment (cirrhosis) prevents hepatocytes metabolising ammonia into harmless waste products> causing build up of ammonia in blood
>collateral vessels btwn. portal and systemic circulation mean ammonia bypasses liver + enters into systemic circulation directly

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83
Q

investigations for hepatic encephalopathy

A

serum ammonia raised
abnormal LFTs
EEG= decrease in brain wave frequency + amplitude
U&E=(maybe hyponatraemia/kalaemia)

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84
Q

management of hepatic encephalopathy

A

laxatives- LACTULOSE > promotes excretion of ammonia from gut before it is absorbed

ABxs eg rifaximin
reduces no. of intestinal bacteria that produce ammonia

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85
Q

describe Wernicke’s encephalopathy + Korsakoff syndrome + list 3 causes of it

A

caused by thiamine deficiency (B1):
alcohol (decreases thiamine levels)
malnutrition
malabsorption (IBD, stomach cancer)

wernickes= acute medical emergency- REVERISBLE stage

-b4 progressing to
Korsakoff syndrome= chronic, irreversible stage

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86
Q

pathology of wernickes encephalopathy + Korsakoff syndrome

A

thiamine def impairs glucose metabolism= decreased cellular energy
brain= vunerable 2 impaired glucose
-alcohol interfers w. conversion of thiamine 2 its active form

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87
Q

presentation of wernickes encephalopathy + Korsakoff syndrome

A

wernickes:
confusion
apathy
difficulty concentrating
opthalmoplegia weakness + paralysis of eye muscles

Korsakoff syndrome:
severe memory impairment
confabulation (makes up stories to fill in gaps)
behavioural changes

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88
Q

investigations + management of wernickes encephalopathy & Korsakoff syndrome

A

clinical diagnosis
low thiamine (B1) levels
deranged LFTs
MRI= degeneration of maxillary bodies

Tx= IV thiamine infusion (pabrinex)

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89
Q

define spontaneous bacterial pericarditis & give the m.c cause + 3 risk factors

A

bacterial infection of ascitic fluid (mc. infection in liver cirrhosis)

mc. caused by E.coli - gram neg
other = staph. aureus - gram pos

RFs= cirrhosis, liver failure, GI bleeding

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90
Q

presentation of spontaneous bacterial pericarditis

A

severe abdo pain w. shock & collapse
fever
ascites
guarding- rigidity helps w. paim
hypotension
n+v
confusion
tachycardia

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91
Q

investigations for spontaneous bacterial pericarditis

inlcudingGOLD

A

1st:
FBC= leucocytosis, anaemia, raised CRP/ESR

blood cultures + ascitic tap= shows causative microorgansim

hCG test (exclude pregnancy)
abdo x-ray (exclude bowel obstruction)

GOLD= ascitic fluid neutrophil count (ANC) >250 cells/mm3

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92
Q

management of spontaneous bacterial pericarditis

A

IV ABxs= piperacillin/tazobactam
cephalosporins can also be used (cefotaxime)

peritoneal lavage- surgical cleaning of peritoneal cavity

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93
Q

define jaundice

A

also called ‘icterus’
yellowing of skin + eyes due to accumulation of conjugated/unconjugated bilirubin

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94
Q

describe the pathway of RBC breakdown to excretion of unwanted components

A

RBCs= broken down by reticuloendothelial macrophages @ spleen
haemoglobin> haem + globin
haem> Fe2+ & biliverdin
biliverdin converted to unconjugated bilirubin by biliverdin reductase
unconjugated bilirubin= insoluble - travels in blood bound to albumin
@liver UGT conjugates bilirubin (now H20 soluble)
conjugated bilirubin stored @ gall bladder + excreted into small intestine as bile
conjugated bilirubin is converted to urobiligen via colonic bacteria
urobiligen converted either:
1. stercobilin (poo)
2. urobilin (oxidised by kidneys, wee)
3. recycled in enterophepatic circulation

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95
Q

describe pre-hepatic jaundice

A

unconjugated hyperbilirubinemia
-due 2 increased RBC breakdown, overwhelming livers ability to conjugate bilirubin

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96
Q

causes of pre-hepatic jaundice

A

HAEMOLYTIC ANAEMIA:
sickle cell anaemia
G6PDH deficiency
autoimmune haemolytic anaemia
thalassemia
malaria

GILBERT’S SYNDROME
CRIGGLER NAJJAR SYNDROME

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97
Q

describe intra-hepatic jaundice

A

dysfunction of hepatic cells- liver loses ability to conjugate bilirubin= mix of conjugated + unconjugated in blood

98
Q

causes of intra-hepatic jaundice

A

alcoholic liver disease
hepatitis
HCC
hepatotoxic medications

99
Q

describe post-hepatic jaundice

A

conjugated hyperbilirubinemia
-due to obstruction in biliary drainage

100
Q

list 4 causes of post-hepatic jaundice

A

gallstones
pancreatic cancer
cholangiocarcinoma
mirizzi syndrome

101
Q

presentation of all 3 types of jaundice

A

prehepatic= norm urine + stool
intrahepatic= dark urine + norm stool
post-hepatic= dark urine + pale stool

102
Q

what is Courvoisier’s sign and what does it indicate

A

painless jaundice + palpable gallbladder= mc. pancreatic cancer

103
Q

what does jaundice, RUQ pain and fever indicate for Charcot’s triad

A

ascending cholangitis
(can also use Reynold’s pentad w. altered mental status & sepsis)

104
Q

what will a LFT show for pre-hepatic jaundice

A

norm conjugated bilirubin
increased unconjugated bilirubin
increased urobilinogen

norm ASP +ALT +ALP
no conjugated bilirubin in urine

105
Q

what will a LFT show for intra-hepatic jaundice

A

increased conjugated bilirubin
increased unconjugated bilirubin
decreased urobilinogen

increased ALP, AST + ALT

conjugated bilirubin= present in urine

106
Q

other investigations for jaundice

A

FBCs
coagulation studies
liver screen
abdo USS

107
Q

describe hepatocellular carcinoma (HCC)

A

cancer arising from hepatocytes in predominantly cirrhotic liver

90% of all liver cancers

108
Q

risk factors for HCC

A

chronic hep virus- C+B
Cirrhosis from ALD/NAFLD

109
Q

describe how HCCs metastasise

A

haematogenous spread- via hepatic/portal veins
spreads 2 lymph nodes, bones & lungs

110
Q

presentation of HCC

A

signs of decompensated liver failure:
-jaundice
-ascites
-HE
-hepatomegaly

signs of cancer:
unexplained weight loss
tired all the time (TATT)
RUQ pain

111
Q

1st line investigations for HCC

A

LFT= increased serum AFP (HCC tumour marker)

imaging= abdo USS

112
Q

gold standard investigation for HCC

A

CT scan
-biopsy usually avoided to prevent tumour spread

113
Q

management of HCCs

A

surgical resection of tumour
liver transplant

prevention= HBV vax

114
Q

describe cholangiocarcinoma

A

bile duct cancer- usually adenocarcinomas
10% of liver cancers
poor prognosis

115
Q

list 5 risk factors for cholangiocarcinoma

A

under 50
parasitic flukeworms
biliary cysts
IBD
primary sclerosing cholangitis

116
Q

presentation of a cholangiocarcinoma

A

jaundice
weight loss
abdo pain
pruritis
fever
malaise
courvoiser’s sign (painless jaundice + palpable gall bladder- also common in pancreatic cancer

117
Q

1st line investigations for a cholangiocarcinoma

A

increased CA19-9 (tumour marker for cholangiocarcinoma) + increased CEA

LFTs= increased bilirubin, increased ALP
imaging= abdo USS + CT

118
Q

gold standard investigation for a cholangiocarcinoma

A

ERCP (endoscopic retrograde cholangiopancreatography)- invasive BUT:
- can stent structures in biliary tree (therapeutic)
-can obtain sample for biopsy (diagnostic)

119
Q

management of a cholangiocarcinoma

A

majority of cases= inoperable bc. patients present v. late- sometimes surgical resection/ ERCP to stent bile duct that cancer is compressing

120
Q

name 2 primary, benign liver tumours

A

haemangioma (mc. seen on infants as strawberry mark in 1st few weeks of life)

hepatic adenoma

121
Q

where do secondary liver tumour most commonly metastasise from

A

breasts, GIT, lungs (bronchial)

122
Q

1st line investigations for benign liver tumours

A

LFT- increased serum ALP
imaging= abdo USS

123
Q

gold standard investigation for benign liver tumours

A

CT/MRI for staging + primary tumour location

124
Q

management of benign liver tumours

A

surgical resection of primary/hepatic tumour if possible + chemo

125
Q

what type of tumour is 99% of pancreatic cancer and which part of the pancreas does it normally affect

A

adenocarcinoma of exocrine pancreas of ductal origin
-usually affects head + neck

126
Q

list 6 risk factors for pancreatic cancer

A

male, 60+
chronic pancreatitis
smoking
alcohol
diabetes
FHx

127
Q

presentation of pancreatic cancer

A

Courvoisier’s sign (palpable gallbladder + painless jaundice)
pale stool + dark urine
pruritis
weight loss
trousseau sign of malignancy (blood clots felt as small lumps under skin)

128
Q

1st line investigations for pancreatic cancer

A

abdo USS (pancreatic mass, dilated bile ducts)

129
Q

gold standard investigation for pancreatic cancer

which tumour marker is present

A

pancreatic CT protocol
Ca19-9 tumour marker positive

130
Q

management of pancreatic cancer

A

v. poor prognosis- 5yr survival= 3%
surgical resection + post op chemo if no mets
palliative care

131
Q

describe gallstones

what is biliary colic pain

A

cholesterol stones in gallbladder formed from bile (bile= cholesterol + bile pigment + phospholipids)

biliary colic= pain caused by gallstones blocking gallbladder drainage

132
Q

what are 5Fs risk factors for biliary tract diseases (gallstones, cholecystitis, ascending cholangitis)

A

Fat (BMI +30)
Female
Forty (40+ yrs)
Fertile (preggo/many kids)
Fair

133
Q

presentation of gallstone pain

A

severe colicky RUQ pain- come & goes (lasts >30mins)-worse after fatty meal
n+v

134
Q

1st line investigations for gallstones

A

LFTs- increased ALP + bilirubin (If gstone blocking bile duct)
normal FBC + CRP

135
Q

gold standard investigation for gallstones

A

abdo USS
1. identify stones
2. gb thickness- inflammation
3. duct dilation

136
Q

management of gallstones

A

1st= NSAIDs + analgesia
then- elective laparoscopic cholecystectomy (removal of gb)

ERCP- bile duct clearance if stones

137
Q

describe cholecystitis

A

inflammation of gb due 2 blockage of cystic duct- preventing it from draining eg gallstone
bile build up distends gb- can reduce vascular supply- therefore inflammation

138
Q

presentation of cholecystitis

A

RUQ- may radiate to R shoulder (phrenic)
fever + fatigue
tender Gb/ RUQ tenderness
Murphy’s sign positive (press on gb + ask patient to inhale- they will wince + stop inspiring)

139
Q

initial investigations for cholecystitis

A

positive Murphy’s sign
FBC= increased WCC + CRP
LFTs= norm

140
Q

gold standard investigation for cholecystitis

A

abdo USS
- shows thickened gb wall >3cm + fluid around gb

141
Q

management of cholecystitis

A

IV fluids + abxs + analgesia

best= cholecystectomy surgery within 24hrs of symptoms
ERCP if gallstones in bileduct

142
Q

describe ascending cholangitis

A

infection + inflammation of bile ducts
-this is due to prolonged blockage of bile duct by gallstones/bacteria infection from ERCP procedure
- bile isn’t ‘flushing out ducts’- bacteria migrate from GI tract + cause infection in biliary tree

143
Q

presentation of ascending cholangitis (Charcot’s triad)

A

charcot’s triad:
-RUQ pain
-fever
-jaundice

144
Q

1st line investigations for ascending cholangitis

A

FBC= increased WCC + CRP, leukocytosis
LFT= increased ALP + unconjugated hyperbilirubenia

abdo USS for gb dilation + gallstones

145
Q

gold standard investigation for ascending cholangitis

A

ERCP

146
Q

management of ascending cholangitis

A

Iv fluids + Abxs
ERCP then laparoscopic cholecystectomy

gallstone > cholecystitis > cholangitis > sepsis

147
Q

define primary biliary cirrhosis/cholangitis (PBC)

A

autoimmune disease where T cells attack cells of small bile ducts- causes inflammation

148
Q

list 5 risk factors for PBC

A

female
40-50 yrs
smoking
other autoimmune conditions
rheumatoid diseases

149
Q

pathology of PBC

A
  1. immune system attacks small intralobular bile ducts in the liver- obstructs bile flow (cholestasis)
  2. bile acids (itching + bilirubin (jaundice) + cholesterol (deposits in skin + blood vessels)
  3. back pressure of bile obstruction> fibrosis + cirrhosis + liver failure
150
Q

presentation of PBC

A

-often initially aysmpto

pruritis + fatigue (earlier onset)
jaundice
hepatomegaly + xanthelsma (yellow cholesterol deposits around eyes)
joint pain + abdo pain
signs of cirrhosis

151
Q

1st line investigations for PBC

A

LFTs- increased- bilirubin, ALP, GGT
decreased albumin
abdo USS (2 exclude extra hepatic cholestasis)

152
Q

gold standard investigation for PBC

A

serology- AMA (antimicrobial antibodies) present

other= liver biopsy for bile duct lesions + granuloma formation

153
Q

management of PBC

A

1st= URSODEOXYCHOLIC ACID ( bile analogue, reduces intestinal absorption of cholesterol)

for pruritis- cholestyramine

vit ADEK supplements
consider liver transplant

154
Q

describe primary sclerosing cholangitis (PSC)

A

inflammation + fibrosis of intra + extra hepatic ducts- results in strictured ‘beading’ appearance of bile ducts + narrowing of bile ducts

155
Q

list 3 risk factors for PSC

A

male
40-50 yrs
strong link 2 IBD (esp UC)

156
Q

pathology of PSC

A

same path as PBC, but affects more ducts

157
Q

presentation of PSC

A

pruritis + fatigue
jaundice
charcot’s triad
hepatosplenomegaly
IBD

158
Q

1st line investigations for PSC

A

LFTs- increased: bilirubin, AST, ALT, ALP, GGT
decreased albumin

serology;
AMAs positive
HBVsAg/HCVAB positive
pANCA positive in 33-88%

159
Q

gold standard investigation for PSC

A

imaging- MCRP (magnetic resonance cholangiopancreatography)
-will see bile ducts strictures or lesions

160
Q

management of PSC

A

treat symptoms (ursodeoxycholic acid doesnt work)

pruritis- cholestyramine
fat soluble ADEK
consider liver transplantation

161
Q

describe acute pancreatitis and its 3 main causes

A

sudden + rapid onset inflammation of the pancreas

  1. gallstones
  2. alcohol
  3. post ERCP
162
Q

list all the causes of acute pancreatitis using I GET SMASHED

A

Idiotpathic

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion venom/ spider bite
Hypercalcaemia/hyprelipidemia
ERCP
Drugs (azathioprine, NSAIDs, ACE-i)

163
Q

describe the pathology of acute pancreatitis

A

gallstones obstruct flow of pancreatic secretions into duodenum- causes accumulation of digestive enzymes + reflux of bile= inflammation

host defences= overwhelmed - therefore auto digestion- inflammation + enzymes leak into blood

164
Q

presentation of acute pancreatitis

A

sudden, severe epigastric pain radiating to back
jaundice
fever
steathorrea
Grey Turner sign (flank bruising)
Cullen sign (periumbilical bruising)
hypocalcaemia
vomiting
signs of hypovolemia + pleural effusion

165
Q

investigations for pancreatitis

A

bloods= increased serum amylase (x3 times upper level) + increased serum lipase

FBC=
leukocytosis w. L shifts (increase in immature vs mature WBCs)
increased haemocrit, CRP, urea
decreased calcium

imaging= chest x-ray, abdo USS (gallstones, CT scan (inflammation, necrosis, effusions)

166
Q

what does an acute pancreatitis diagnosis require

A

needs out of 3 of:
1. acute abdo pain
2. increased pancreatic enzymes (amylase/lipase)
3. abnormal imaging

167
Q

list the Glasgow score and what it Is for

A

assessing severity of acute pancreatitis (after 48hrs)

PANCREAS
PaO2 low
Age 55+
Neutrophils raised
Calcium low
uRea raised
Enzymes raised
Albumin low
Sugar raised

use APACHE 2 - assess severity within 24hrs

168
Q

management of acute pancreatitis

A

ABCDE
IV fluids
analgesia
nil by mouth
O2
antibiotics
electrolyte replacement

169
Q

define chronic pancreatitis

A

persistant chronic inflammation (3+ months) = irreversible fibrosis and reduced pancreas function

170
Q

list 5 causes of pancreatitis

A

alcohol (mc)
trauma
CKD
progression from acute
CF

171
Q

list 6 presentations of pancreatitis

A

severe epigastric pain radiating to back
jaundice
loss of exocrine function (no lipase secreted in GI tract)
loss of endocrine function (lack of insulin> T2DM)
wt. loss
n + v

172
Q

1st line investigations for pancreatitis

A

bloods= low/no amylase + lipase
faecal- elastase 1 (low)
faecal fat (high)
pancreatic function tests (decreased function)
ERCP for visualisation of ducts

173
Q

gold standard investigation for pancreatitis

A

x-ray/CT/MRI= shows calcification of pancreas + dilated bile ducts

174
Q

management of pancreatitis

A

control risk factors- (no alcohol + smoking + decreased BMI)
control pain (analgesia + NSAIDs)
pancreatic supplements eg lipase
insulin for T2DM
ERCP
surgery 2 drain bile ducts

175
Q

what is portal hypertension a complication of and what does it lead to

A

portal HTN= comp of cirrhosis
- increases BP in portal vein

176
Q

list the causes of pre-hepatic, intra-hepatic and post-hepatic portal hypertension

A

pre-hepatic- portal vein obstruction (thrombus)

intra-hepatic- cirrhosis (mc.), sarcoidosis , schistosomiasis (caused by blood flukes aka worms)

post-hepatic= R sided heart failure, constructive pericarditis, budd chiari

177
Q

what is the normal venous pressure in the portal vein

A

5-8mmHg

178
Q

describe the pathology of portal HTN

A

cirrhosis> causes venous blood to accumulate in portal system- pressure increases (+8mmHg)

causes formation of portosystemic shunts- blood directed into systemic veins

liver therefore receives less blood- liver function + detoxification decrease

therefore toxic products in blood eg NH3 (can cross BBB + causes HE) increase

increase of portosystemic shunts @ oesophagus- causes oesophageal varices @ cardia + lower oesophagus- these can rupture + cause GI bleed

179
Q

presentation of portal HTN

A

asymptomatic until comps. occur:

ascites
caput medusae
GI bleeding from oesophageal varices
haemoptysis
malaena
jaundice
HE symptoms

180
Q

1st line investigations for portal HTN (4)

A

liver USS (nodules= cirrhosis)
CT/MRI (ascites, cirrhosis, splenomegaly)
endoscopy (oesophageal varices)
Labs (FBC, LFT, serology)

181
Q

gold standard investigation for portal HTN

A

hepatic venous blood pressure against gradient measurement (diff in pressure between IVC & portal vein)

182
Q

management of portal HTN

A

beta blockers 2 reduce portal venous pressure
treat comps

183
Q

what are oesophageal varices and what are they a direct complication of

A

enlarged + fragile oesophageal veins that can easily rupture- direct comp of portal HTN + liver cirrhosis

184
Q

what are 4 presentations of oesophageal varices

A

upper GI bleeding:
-haematemesis
-melaena
-haematochezia (fresh blood in poo)
-splenomegaly

185
Q

1st line and gold standard investigation for oesophageal varices + other tests

A

oesophagogastroduodenoscopy (presence of varices)

other=
FBC- anaemia, thrombocytopenia
LFTs= increased AST, ALD, ALT, bilirubin
U&Es= hyponatremia

186
Q

how would you stop bleeding when managing oesophageal varices

A
  1. IV trelipressin
  2. vatical banding
  3. balloon tamponade
  4. TiPPS- (trans- jugular intrahepatic portosystemic shunt)> decreases portal pressure by diverting blood 2 other larger veins
187
Q

how would you prevent bleeding when managing oesophageal varices

A

Beta blockers (non-selective eg propranolol) + nitrates
repeat vatical banding
last resort= liver transplant (decompensated cirrhosis)

188
Q

describe ascites

A

collection of fluid in peritoneal cavity

poor liver function= decreased albumin> decreased blood oncotic pressure> fluid loss into peritoneal cavity

189
Q

list 3 categories of conditions causing ascites

A

local inflammation=
peritonitis, TB, abdo cancer

low protein= nephrotic syndrome, hypoalbumenia (liver failure)

flow stasis (build up causes leakage) = cirrhosis, budd chiari, congestive heart failure, constrictive pericarditis

190
Q

presentation of ascites

A

distended abdo
shifting dullness
may have jaundice + pruritis

191
Q

how would you check for shifting dullness in ascites

A
  1. tap on central abdo when supine
  2. tap on flanks- dull due 2 fluid
  3. ask patient to lie on side and tap top flank- resonant (fluid has shifted 2 otherside + bowel floated here)
192
Q

1st line investigations for ascites

A

shifting dullness on examination
ascites tap (peritocentesis of 10-20ml of fluid)

193
Q

describe an ascites tap

A

peritocentesis of 10-20ml of fluid

1.cytology (WCC)
2. protein measurement:

  • Transudate fluid proteins= <25g/L, serum ascites-albumin gradient= <11g/L
    clear fluid due to hydrostatic pressure
    increase in hydrostatic pressure due 2 cirrhosis, heart failure, portal HTN, budd chiari

-Exudate fluid proteins= >25g/L, serum ascites-albumin gradient= >11g/L
cloudy fluid due to decreased oncotic pressure
decrease in oncotic pressure due to malignancy, peritonitis, TB, nephrotic syndrome

194
Q

gold standard investigation for ascites

A

abdo USS

195
Q

management of ascites

A

treat underlying cause

diuretic (spironolactone, furosemide) 2 increase Na+ excretion, therefore more fluid flushed out

lower Na+ in diet

paracentesis

liver transplant

196
Q

what is peritonitis

A

inflammation of peritoneal cavity

197
Q

name 2 primary causes of peritonitis

A

ascites
spontaneous bacterial peritonitis (infection)

-

bacterial causes:
gram neg- e.coli, klebsiella
gram pos- staph aureaus

198
Q

what is a secondary cause of peritonitis

A

underlying cause eg bile, malignancy

199
Q

presentation of peritonitis

A

sudden onset + severe abdo pain
then> collapse + septic shock

fever
rigidity helps pain (guarding etc)
poorly localised to well localised
usually +/- ascites

200
Q

investigations for ascites

A

ascites tap- shows neutrophilia
cultures show causative organism
increased ESR + CRP
exclude pregnancy + bowel obstructions as causes
chest x-ray- shows air under diaphragm

201
Q

management of ascites

A

A-E assessment
treat underlying cause; IV fluids + IV abxs
surgery= peritoneal lavage (cleaning out of peritoneum)

comps= sepsis if not treated early

202
Q

what happens in haemochromatosis

A

body absorbs too much Fe= increase in total body Fe + Fe deposition in tissues
-can poison tissues (liver, pancreas, heart, pituitary)

203
Q

which mutation causes haemochromatosis and what does it cause

A

auto recessive mutation of HFE gene on chromosome 6

causes increased iron absorption, xtra iron= Organ damage via free radical production

204
Q

name 3 risk factors for haemochromatosis

A

male (women lose Fe in menstruation)
50+
family history

205
Q

presentation of haemochromatosis

A

chronic tiredness
joint pain
pigmentation (bronze/slate discolouration)
hair loss
hypogonadism (due 2 a. pit damage)
liver cirrhosis symptoms
erectile dysfunction
heart failure
cog symptoms- memory + mood disturbance

206
Q

1st line investigations for haemochromatosis

A

Fe studies:
increased- serum Fe, transferrin saturation, ferritin
decreased- TIBC (total iron binding capacity- don’t want to bind more Fe)

LFTs= increased aminotransferases

other= genetic test (HFE)

207
Q

gold standard investigation for haemochromatosis

A

liver biopsy- Prussian blue stain= brown spots of Fe deposited in hepatocytes

208
Q

management of haemochromatosis

A

1st= phlebotomy/venesection to decreased serum Fe- done weekly

2nd= iron chelation (desferrioxamine) + lifestyle mods

209
Q

what is Wilson’s disease

A

excessive accumulation of copper in body + tissues- can lead to tissue damage

210
Q

name 2 risk factors for Wilson’s diseaes

A

under 20
family history

211
Q

what mutation occurs in Wilson’s disease

A

auto recessive defecit of ATP7B copper-binding protein- leads to copper build up in hepatocyest + production of free radicals

212
Q

presentations of Wilson’s disease for:
liver, neuro, psych, eyes

A

liver: hepatitis, cirrhosis

neuro:
parkinsonism (tremor, bradykinesia, rigidity)
dysarthria (speech difficulties)
concentration + coord difficulty
dementia

psych: depression, psychosis

eyes: kayser-fleischer rings in cornea (brown rings of copper deposits in Descemet’s membrane)

213
Q

1st line investigations for Wilson’s disease

A

serum copper + ceruloplasmin reduced (copper in tissues, not blood)
24hr urinary copper excretion= high
LFTs= abnormal

214
Q

gold standard investigation for Wilson’s disease + others

A

liver biopsy= increased copper + hepatitis

other= silt lamp examination (4 Kayser-fleischer rings)
genetic testing

215
Q

management of Wilson’s disease (1st line & second line)

A

1st line= copper chelation with penicillamine

2nd line= zinc salts, decreased copper diet (less chocolate, nuts, mushrooms, shellfish)

cirrhosis= consider liver transplant

216
Q

describe acute anti trypsin deficiency

A

genetic abnormality of protein alpha 1 anti trypsin

-alpha 1 antitrypsin= normally inactivates elastase (breaks down elastin)
-therefore A1AT deficiency= elastase breaks down elastin unchecked

217
Q

where is A1AT produced

A

in the liver

218
Q

what dose A1AT deficiency cause in the lungs

A

protease enzymes attack connective tissue in lungs > damages alveoli causing emphysema + bronchitis

219
Q

presentations of A1AT in the lungs

A

young/middle aged with COPD like symptoms
dyspnoea
chronic cough
wheeze
emphysema

220
Q

presentations of A1AT in the liver

A

jaundice
cirrhosis (+comps)
hepatitis
hepatosplenomegaly

221
Q

investigations for A1AT

A

decreased serum A1AT
reduced pulmonary function tests (spirometry obstruction FEV:FVC <0.7)
Chest x-ray= barrel chest (hyper inflated lungs)
CT= panacinar emphysema
LFTS= increased- bilirubin, aminotransferase ALP
liver biopsy- cirrhosis + periodic acid schiff staining A1AT mutant globules
genetic test= positive for PI mutation

222
Q

management of A1AT

A

no treatment= curative

no smoking
manage emphysema eg inhalers
A1AT infusions
consider decompensation patients for liver transplantation

223
Q

how many mg/kg of paracetamol over a 24hr period is considered toxic

A

> 200mg/kg in 24hr period

224
Q

what is the max dose of paracetamol for adults in 24hr

A

4g

225
Q

what happens in a paracetamol overdose

A

not enough glutathione stores to inactivate NAPQI
-causes build of toxic NAPQI > damages liver

226
Q

presentation of a paracetamol overdose

A

acute, severe RUQ pain
severe n+v

227
Q

investigations for a paracetamol overdose

A

serum paracetamol concentration= increased
LFT= increased ALT + PTT
hypoglycaemia

228
Q

management of a paracetamol overdose

A

N-acetylcysteine + activated charcoal within 1hr of digestion

N-acetylcysteine increases availability of glutathione

229
Q

describe Gilbert’s syndrome

A

auto recessive condition - mc. of hereditary jaundice- causes mild unconjugated hyperbilirubenia due 2 deficient/abnoraml UGT

230
Q

presentation of Gilbert’s and crigier najjar

A

gilbert’s= short episodes of jaundice- asymptomatic in-between

crigier najjar= more severe jaundice- treat w. phototherapy (breaks down unconjugated bilirubin)

231
Q

what is a hernia

A

protrusion of an organ thru. defect in wall of its cavity- typically bowel

232
Q

name 3 kinds of hernias

A

reducible- able to ‘push back into place’

irreducible
-obstructed (intestinal obstruction)
-strangulated (intestinal ischaemia)

incarcerated- contents are fixed in sac

233
Q

describe rolling and sliding hiatal hernias

A

hiatal hernia= herniation of stomach thru diaphragm hiatus

rolling= gastroesophageal junction stays in abdo, part of fundus rolls into thorax

sliding= stomach + gastroesophageal junc slide up through diaphragmp

234
Q

presentations and investigations for a hiatal hernia

A

SXs=
GORD
dysphagia
dyspepsia

Dx=
Chest x-ray
barium swallow (diagnosis)
endoscopy
oesophageal manometry

235
Q

describe an inguinal hernia and its risk factors

A

protrusion of abdo contents thru inguinal canal
-spermatic cord herniates thru inguinal canal in males

RFs= male, heavy lifting, past abdo surgery, chronic cough

236
Q

describe direct and indirect inguinal hernias

A

direct= into hesselbach’s triangle 2 inferior epigastric arteries

indirect= bowel herniates thru inguinal canal

237
Q

presentation and investigations for inguinal hernias

A

painful swelling in groin- pointing along groin Margin
+/- reducible

investigations=
usually clinical diagnosis, if unsure use abdo USS/CT/MRI

238
Q

describe a femoral hernia and its risk factors

A

bowel goes thru femoral cord- v. likely to strangulate due 2 rigid femoral canal borders

RFs= female, mid-old age

239
Q

presentations and investigations for a femoral hernia

A

swelling in upper thigh- pointing down

investigations= usually clinical, USS of abdo/pelvis if unsure

240
Q

how would you treat all kinds of hernias

A

surgery

Phase 2a (12 decks)

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