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Phase 2a > Liver > Flashcards

Liver Flashcards

1
Q

liver faliure defornition

A

large parts of the liver become damaged beyond repair and don’t work anymore. It is liver failure without any underlying older liver disease. It has coagulopathy (derangement of clotting), and altered levels of consciousness dur to hepatic encephalopathy, and jaundice.

Chronic Liver faliure - a result of decompensation of chronic liver disease

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2
Q

liver faliure key presintations

A
  • Hepatic encephalopathy - confusion, coma, liver flap (tremor of extended wrist), drowsiness cased by aonia building up in the brian and being a neurotoxin. It cases astrocyte to clear the ammonia using glutamine which leads to an osmotic imbalance and cerebral oedema
    • Abnormal bleeding (clotting factors absent)
    • Ascites
      Jaundice
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3
Q

liver faliure viral cuases

A

Virus:
- Hep A B D E C
- Cytomegalovirus
- EBV
Herpes simplex virus

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4
Q

liver faliure dug causes

A

Drugs
- - paracetamol
- Alcohol
- Antidepressants
- NSAIDs
- Ecstasy/cocaine
Antibiotics

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5
Q

4 main causes of liver faliure

A

Hepatocellular carcinoma
Wilsons disease
drugs
virusus

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6
Q

sign and symptoms of liver faliure

A

Jaundice
Ascities
Small liver
Hepatic encephalopathy
Fetor hepaticus - foul egg smelling breath
Bruising
Clubbing cereberal osdema

Fever
Vomiting

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7
Q

tests for liver faliure

A

Bloods
- Hyperbilirubinemia
- High serum ALT and AST (hepatic enzymes tha when raised suggest liver disease)
- Low levels of coagulation factors
- Low glocuse
- High amonia

ECG
Ultrasound

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8
Q

treatment for liver faliure

A

Treat the causes - if paracetamol overdose give N-acetyl-cystine
If there is signs od ICP (intrahepatic cholestasis of pregnancy) give IV Mannitol
Liver transplant

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9
Q

complications of liver faliure

A

Malnutrition
Coagulopathy (cuase bleeding out)
Endocrine changed
Hypoglycemia

If there is advanced encephelopathy then an airway must be established

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10
Q

Alcoholic liver disease pathophysiology

A

FATTY LIVER:
Metabolism of alcohol produces fat in the liver
This means that the cells become swollen with fat
Sometimes collagen is laid down around the fat deposits which causes cirrhosis
Alcohol effects stellate cells ad turns them into collagen productid myofibroblast cells

ALCHOLIC HEPATITIS
There is an infiltration of polymorphonuclear leukocytes and hepatocyte necrosis. This inflammation can turn into cirrhosis. This causes the Prescence of mallary bodies and giant mitochondria.

ALCOHOLIC CIRRHOSIS
Micronodular type accompanying fatty change.

It is a pathway.

Reduced NAD+ and increased NADH leads to less oxidisation of fat so there is more of a build-up which leads to an accumulatino of fat.

The acetaldehyde damages the liver cell membranes.
This leads to inflammation and cirrhosis.

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11
Q

Alcoholic liver disease signs and symptoms

A

Jaundice
Hepatomegally
Ascites

Right upper quadrent pain
N&V
Diahoria

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12
Q

Alcoholic liver disease test

A

1st line test

Liver function test - GGT and ALP raised
AST and ALT - increased ratio

FBC - thrombocytosis
Hypoglyceamia
Abdominal ultrasound
CT
MRI
Liver biopsy

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13
Q

Alcoholic liver disease treat,etn

A

Alcohol abstinince -
Seizire, insomnia, cvomiign, headache, sweating, palpitations, - treat with diazepam

IV thiamine - to prevent wernike-koraskoff syndrome (B1 deficancy) the symptoms of which are confusion, ataxia, nystagmous

Diet high in vitamins and protines
Liver transplant

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14
Q

Alcoholic liver disease compliations

A

Cirrhosis
Faliure
Encephalopathy

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15
Q

non alcoholic fatty liver disease causes

A

Affects individuls awoth metabolic syndromes:
* obesity
* Htn
* Diabeties
* Hyperlpidemia
hypertriglyceridemia

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16
Q

pathophysiology and types of non alcoholic fatty liver disease

A

There is a fat accumulation in the liver
There are two types:

* NAFL - steatosis (fat inflatration) without inflamation 
* NASH - non alcoholic steatohepatisis - teatosis wit hepatic inflammation, this is indistinguishable firm alcoholic version. This is worse than NAFL. NASH leads to cryptogenic cirrhosis which impairs liver function. You need a biopsy to distinguish between the two
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17
Q

non alcoholic fatty liver disease symptoms

A

Asymptomatic
Sometimes a liver ache
Fatigue and malaise
RUP pain
Jaundice
Hepatomegaly
Ascities

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18
Q

non alcoholic fatty liver disease tests

A

LFT - elevated, raised ALT and AST due to destruction of the liver
Ultrasoud
CT
MRI
Liver biopsy

rule out other causes and then it can lead to a diagnosis with teh LFT

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19
Q

non alcoholic fatty liver disease tx

A

Weight loss
Avoid a fatty diet
Statins

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20
Q

out of teh 5 viral hepatitis, are they DNA or RNA, and are they acute or chronic?

A

A
RNA virus
Only acute.
This is notifiable disease!!!!!

B
DNA Virus
Acute and chronic

C
RNA flavivirus
acute and chronic

D
Incomplete RNA
Acute and chronic
Requires B for assembly

E
RNA virus
Acute only apart form sometime chronic in immunosuppressed

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21
Q

hep a pathophysiology

A

It is a picornavirus
It replicates in the liver and is excreted in the bile and faeces for 2 weeks before clinical illness and 7 days after
Its maximally infections just before onset of jaundice
2-6 week incubation period
ACTUTE HEP only

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22
Q

hep a key presintations

A

Key presentations

There are tow stages:
- Pre-icteric - constitutional symptoms (feelings of beieng genrally unwell such as fever, fatigue, anorexia, night sweate, malaise) and abdominal pain
- Icteric - jaundice, hepatomegally, RUQ pain, priutus

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23
Q

hep a tests

A

Tests

  • Antibody test - initial one is anti-HAV IgM, and then Anti-HAV IgGis made
  • Raised serum bilirubin
  • Bloods - reduced WBC
  • Raised ESR - erythrocyte sedimentation rate faster sinkage means higher levels of inflamation
  • Serum transaminases will be elevated
  • Raised urea and creatine
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24
Q

hep a differential

A

Differential diagnosis

Other causes of jaundice
Viral and drug induced hepatitis

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25
Q

hep a manegemtn

A

Management
Initial
Secondary

  • Supportive treatment and monitoring
  • Moniter liver function tests
  • Peimary prevention - Hep A vaccination
  • Management fo close contacts with the HNIG vaccine
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26
Q

Hep B causes

A

Semen and saliva so sexually transmitter
Blood bore as well
Needle stick, tatoos
Sexual
IV drig users
Vertical transmission mother to child

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27
Q

Hep B pathophysiology

A

DNA virus which has an inner core and outer antigens

It can lead to chric infectio which can cuases cirrhosis and cancer!

There is a relase of IgM antibody first and then

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28
Q

Hep B key presintations

A

It is commonly asymptomaic
Hepatomegally
Ascities
Fever
Jaundice
Malaise
N&V
RUQ pain

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29
Q

Hep B tests

A

Antibody tests - Hep B surface antigen HBsAg present 1-6 months after exposure.
HBsAg oprescne for more than 6 onths implies that theyre a carrier
Anti-HBs - antibodues to Hep B

LFTs - elevated ALT and AST due to damage, low albumin levels

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30
Q

Hep B treatment

A

Acute - Supportive -
* moniter LFTs
* Tenofovir, entecarvir (antivirals) (Interferon alpha, nucleoside reverse transcriptase inhibitors (NRTI)
* Mangae the contacts of the person

Chronic -
* Peginterferon alfa-2a - aform of recombinant interferon used as part of combination therapy to treat chronic Hepatitis by decreasin gteh levels of the virus in the body, there are side effects lie autoimmune diseases, mental helath problems, low WBC and platelts
* Nucleoside analogues – tenofovir, entecavir, thes are lifelong antivirals to reduce the levels

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31
Q

Hep B and C complications

A

Liver cirrhosis, hepatocellular carcinoma,

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32
Q

Hep C causes

A

There are 7 genotypes, and there is rapod mutaiot which makes it hatrd ot make a vaccine

Vhronic hepatitis makes it hard to make a vaccine.
It is incubated for 6-7 week sbut tehn is a liflong infection

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33
Q

Hep C key presintations

A
  • constitutional symptoms
  • jaundice
  • ascites
    signs of hepatic encephalopathy
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34
Q

Hep C test

A
  • HCV antibody test - if not detected they’ve not had it, if detetced they have been exposed at some pint
  • HCV RNA - if detected they have the cirus currently, if not it is not current
  • LFT - raised ALT and AST
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35
Q

Hep C treatment

A
  • Interferon alpha - ribavirin
  • Ther eis no HVC vaccine available!!!
  • Liver transplant in the case of liver failure
  • Direct oral acting antivirals (DAAs) Daklinza, Exviera, Harvoni, Olysio, Sovaldi and Viekirax
  • NS5A (-asvir), NS5B (-buvir) and NS3/4A protease (-previr) inhibitors

A previous c infection doent mean immunity

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36
Q

Hep D pathophysiology

A

It is unable to reproduce on its own but is actiatedy HepB
If there is a coinfection it incraess the severity og the infection
It is clinically indistuinguishable

There is coinfection where they are acquired at the same time - leads to bad acute stage and prescent oc bother IhM anti-HDV

Superinfection - when someone with chronic HBV gets Hdv - it cuases a secondary acute hepatitus which an incrased rate of liver fibrosis pregression

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37
Q

Hep D risk factors

A

Blood bone
Healthcare
Dialysis #
Grug
Travellers

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38
Q

Hep D symptoms

A

It is commonly asymptomaic
Hepatomegally
Ascities
Fever
Jaundice
Malaise
N&V
RUQ pain

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39
Q

Hep D test

A

Antibody test - if the antibod is positive test for HDV RNA to see if it’s a curret infection.

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40
Q

Hep D treatment

A

pegylated interferon-α (future: Myrcludex B)
HBV vaccine

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41
Q

Hep E causes

A

Feacooral route
In uncooked pork

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42
Q

Hep E symptoms

A
  • Maily asymptomatic
  • Ususlaly self limiting
  • Fulminant hepatasis - severe liver imparement cuases hepatic coma, liver necrosis
  • Sometimes extrahepatic symptos - neurological
  • When chronic there is rapid pregression to cirrhosis and fibrosis
  • Constitutional symptoms
    Fatty stools, dark urine, jaundice
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43
Q

Hep E test

A

Serology – HEV antibodies
Nucleic acid amplification test
LFT - ALT and AST increased

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44
Q

Hep E treatmetn

A

Supportive manegment
* If they develop fuliment hepatitis, ribavrin and liver transplant

Hronic infection - reverse immunospupression if positble (steriods), if HEV RNA prescence persists treat with RIBA ( an antiviral)

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45
Q

autoimmune hepatitis types

A

ƒ Type 1: 80% of cases
ƒ Type 2: most common in young
biologically-female individuals
ƒ Type 3: different antibodies but presents as
Type 1
ƒ Type 4: no detectable antibodies

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46
Q

autoimmune hepatitis key presintations

A

Wide specturm presintation raging from asynmptomatic to cirrhosis and liver faliure
Common moderate symptoms - fever, jaundice, hepatosplenomegally
Chronic diseases symptoms:
Hashimotos thyroiditis, graves disease

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47
Q

autoimmune hepatitis tests

A
  • Type 1 – anti-nuclear antibody (ANA), anti-smooth muscle antibody (ASMA)
  • Type 2 – anti-LKM-1 or anti-liver cytosolic-1 (anti-LC-1) antibodies
  • Liver biopsy
    LTF - raised ALT and AST, low albumin
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48
Q

autoimmune hepatitis treatment

A

mmunisurpresants

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49
Q

cirrhosis defornition

A

Not a specific disease but it’s the end stage of all progressive chronic liver disease which when fully developed is irreversible and has signs of portal hypertension and liver failure. There is loss of normal hepatic architecture, nodular regeneration and bridging fibrosis.

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50
Q

cirrhosis causes

A

Most common:
* Chronic alcohol abuse
* Non-alcoholic fatty liver disease
* Hep B&D
* Hep C

  • Primary biliary cirrhosis
  • Autoimmune hepatitis – presents as high ALT
  • Hereditary haemochromatosis (iron overload)
  • Wilson’s disease
  • Alpha-Antitrypsin deficiency
  • Drugs e.g. amiodarone and methotrexate
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51
Q

cirrhosis risk factors

A

Viral hepatitis
Chronic alcohol abuse
Obesity

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52
Q

cirrhosis pathophysiology

A

Chronic liver results in inflammation, matric depostion necrosis and angiogenesis and fibrosis

The necrosed cell release cell contents and the stellate cells release cytokines which attracft neutrophills and macrophage sto the lver which causes further inflamation and fibrosis
There is a severee reduction in liver function as fibrosis is non functioning

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53
Q

cirrhosis types

A

Two types of cirrhosis:
* Micronodular - regenerating nodules <3mm in size with uniform involvement, often caused bu alcohol or billarary tract infections
* Macronodular - nodules of varying size, and normal acini may be seen in larger nodules - causes by viral hepatitis!

There is also compensated and decompensated.
* Compensated - asymptomatic, non-specific such as weight loss, fatigue and weakness.
* Decompensated - jaundice, Prituis, Abdominal pain, Ascites

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54
Q

cirrhosis signs

A
  • Bruising
  • Leukonychia - white discoleration on the naile due ot hypoalbumineamia
  • Clubbing of the fingers
  • Palmar erythema - red plams of the hands
  • Spider naevi - small clusters of blood vessles that show up
  • Dupuytresn contracture
  • Xanthelasma - yellow fat deposits under skin usually around eyelids
  • Ascites
  • Jaundice
    Oedema due to decreased albumin
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55
Q

cirrhosis test

A

Liver biopsy
LFT - serum albumin, increased PT time, raised billirubin, asperate amino transferase, alanine aminotransferase
Liver biochemistry
FBC - low plateltes (loss of thrombopoeitin)
Abdominal CT and mRI
Upper GI edocscopy

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56
Q

cirrhosis treatment

A

Treat the cause : Alcohol abstinance
Antoviral for hep B
Spiralactone for ascities
Liver transplant
Good nutrition
6 month ultrasound for hepotocellular carcinoma

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57
Q

cirrhosis complications

A

Fall in clotting factors
Encephalopathy - liver flap when amonia causes problems in the brain
Thrombocytopenia
Hepatocellular carcinoma
Hypoalbunineamia
Portal hypertension
Ascities
Oesophageal varacies

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58
Q

what is decompensated liver

A

Decompensated liver cirrhosis:

Jaundice
Ascites
Variceal haemorrhage secondary to portal hypertension
Hepatic encephalopathy

Treatment: treat the symptoms for mannitol, liver transplant

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59
Q

what is prehepatic jaundice

A

Prehepatic
* There is an incrased breakdown of Hb leading to unconjugated billirubin
* There is increased unconjugated billirubin
* Normal stools and urine
There is mre heamolysis due to aneamia

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60
Q

what hepatic jaundice

A

Hepatic
* Faliure of the hepatocytes to take up and metabolise the billirubin
* Dark urine and pale stools
* Hepatitis,m drugs, alcohol cirrhosis

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61
Q

what is post hepatic juandice

A

Posthepatic
* Obstruction in the billary sytem (gallstone)
* Increased conjugated billirubin
* Dark urin and pale stools
* Gallsotnes, pancreatitis (the head blocks the CBD)

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62
Q

what are teh investigations for jaundice

A

Investigations
* History
Dark urine, pale stools, itching?
Symptoms
Biliary pain
Rigors – shivering
Abdomen swelling
Weight loss
Past history
Biliary disease/intervention
Malignancy
HF
Blood products
Autoimmune disease
Drug history – drugs/herbs started recently
Social history
Alcohol
Potential hepatitis contact
Irregular sex
IVDU
Exotic travel
Certain foods
Family history/system review – rarely helpful
* Liver enzymes - very high AST/ALT suggests liver disease (some exceptions)
* Biliary obstruction – 90% have dilated intrahepatic bile ducts on ultrasound
* Further imaging
○ CT
○ Magnetic resonance cholangiogram (MRCP)
○ Endoscopic retrograde cholangiogram (ERCP)

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63
Q

Wernicke’s encephalopathy defornition

A

Acute deficiency of thiamine in a susceptible host, there are neuropsychiatric manifestations such as consciousness, eye movement, gait and balance. Three is mental status chane and gait and occular motor dysfunction.

If it is not treated it will turn into korsakiff syndorem which is chronic.

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64
Q

Wernicke’s encephalopathy risk factors

A

Conditions that prediposose malnutrition - aids, cnace, d&V

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65
Q

Wernicke’s encephalopathy key presintations

A

Mental slowing
Impaired concentration, apathy
Frank confusion
Ocular motor finding

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66
Q

Wernicke’s encephalopathy tests

A

Theraputic trial of parenteral thiamine
Finger prick glicse
FBC
Serum electrolytes
CT f the brain
MRI of the brain

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67
Q

what is teh mnumonic for wernikes and korsakoff

A

COAT RACK

wernickes is COAT
Confusion
Opthaalomoplegia
Ataxia
thiamine deficancy

Korsikoff is RACK
Retrograde amnesia
anterograde amnesia
confabulation
korsacoff syndrome!

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68
Q

Wernicke’s encephalopathy manegemtnet

A

B1 - injectino of pabrinex

they will pfen present as hypoglyceamic but you MUST give pabrinex first otherwise they will die!!!

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69
Q

Hepatic encephalopathy defornition

A

Neuropsychiatic syndrome cuased b acute or chronic helpatic insurficancy

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70
Q

Hepatic encephalopathy pathophysiology

A

There is impareid amonia clearance due to damage in eh liver. This cuases amonia to cross the blood brain barrier leading to glutimate to all be used up causeign the brain to malfunction

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71
Q

Hepatic encephalopathy key presintations

A

Liver flap
Sleep dosturbancs
Ataxia
Motor distrubances
Jaundice
Peripheral oedema
Heaptomegal
Spider angiomatea
Palmar erthythrma

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72
Q

Hepatic encephalopathy tests

A

LFTs
Serum glucose
U and Es
FBC
Blood alcohol level
Blood amonia level
Potenitally a head CT

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73
Q

hepatic encephalopathy treatment

A

Treat the cause - what is casing the liver faliure- alcohol, paracetamol hypovolemia, infections.

Prtoien resticed diet

Lactulose - a laxative which draws amonia from the blood into the colon to be excreted

Rifaximin

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74
Q

Korsakoff syndrome defonition

A

A memory diorder that results form vit B1 deficentcy and is associated ith alcoholism. It damages the cells in the brain.

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75
Q

Korsakoff syndrome key presintations

A

Amnesia
Tremor
Coma
Disorientation
Vision problems

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76
Q

Korsakoff syndrome treatment

A

B1

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77
Q

Pancreatic cancer epidemiology

A

99% of the pancreases cancer are form the exocrine component
More comm in men and useually occus after 60
adenocarcinoma (formed from glandular tissue) and are of ductal origin

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78
Q

Pancreatic cancer risk factors

A
  • Smoking
  • Excessive alcohol or coffee
  • Aspirin
  • Diabetes
  • Genetic mutation
    Family history
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79
Q

Pancreatic cancer pathophysiology

A

Pre malignant lesions to full invasive cancer
60% arise in pacreatic head, 25% in the body and 15% in the tail

If it is in the head it can compress the bile duct and lead to obstructive jaundice

They tend to metastasis early, particularaly to the liver
Very bad prognosis of 5 year <25%

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80
Q

Pancreatic cancer courvoisiers sign

A

Coursosicirs law states that a palpable gallbladder and jaundice is unlikely to be gllastonesm its more like to be cholangiocarcinoma ot pancreatic cancer

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81
Q

Pancreatic cancer trousseaus sign of malignancy

A

Trousseaus sign of malignacy is that migratory thrombophlebitis is a sign of malignancy, particularly in pancreatic cancer. Thrombophlebitis is where blood vessels become inflamed wih a blood blot form the area, migratory refert to the blood clot moving over time.

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82
Q

Pancreatic cancer key presintations

A
  • Anorexia
  • Weight loss
  • Pancreatitis
  • Change in bowel habits
  • Nausea and vomiting

Body and tail:
* Epigastric pain in the back the is relieved by sitting fore awards

Head:
* Painless jaundice - yellow skin, pale stools, dark urine, itching
Weight loss

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83
Q

pancreatic cancer test

A
  • Abdominal ultrasound
  • If over 40 with jaundice refer for 2 weeks
  • If >60 with weight loss and an additional symptom of (diahorrhea, back pain, abdominal pain, nausea, vomiting, constipation, new onset diabeties) refer for a DIRECT CT SCARN
  • Imaging o a CT sca
  • Histology biopsy
  • CA 19-9 (carbohydrate antigen) is a tumour marker that may be raised in pancreatic cancer. It is also raised in cholangiocarcinoma and a number of other malignant and non-malignant conditions.
  • Magnetic resnance cholangio pacreatography - MRCP my be used t asses the billary system in detail
    ERCP - to put in a stent and relieve obstruction, also to obtian a biopsy
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84
Q

pancreatic cancer tx

A
  • Surgery to recover tumour
  • Total pancreatectomy
  • Distal pancreatectomy
  • Pylorus preserving pancreaticoduodenectomy (modified Whipple)
    Radical pancreaticoduodenectomy (Whipple procedure)

In most cases it is palliate care that is needed, stents to relieve biliary obrution surgery to improve symptoms, chemotherapy nd radiotherapy, symptom control.

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85
Q

what would you do if a patient has worsening diabeties despite good medication and lifesytle?

A

If someone has rapidly worsening diabetes T2 despite good lifestyle and measures it can be pancreatic CANCER!!!

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86
Q

hepatocellular cancer defornition

A

Primary is when it develops in the liver and secondary is when it has metastasised to the liver, there is a poor prognosis for when there are liver metastasis.

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87
Q

hepatocellular cancer risk factors

A

The main risk factor is liver cirrhosis due to:
* Viral hep Banc C
* Alcohol
* Non alcoholic fatty lover disease
Chronic liver disease

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88
Q

hepatocellular cancer key presintations

A

Asymptomatic for a long time with a lat presentation which often means a poor prognosis.
Non-specific symptoms:
* Weight loss
* Abdominal pain
* Anorexia
* N&V
* Jaundice
Priutus

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89
Q

hepatocellular cancer first line tests

A
  • Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma.
  • Liver ultrasound to find tumours
  • CT and MRI for diagnosis and staging of tumours
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90
Q

hepatocellular cancer treatment

A
  • Resection of early disease
  • Kinase inhibitors - sorafenib, regorafenib, Lenvatinib
  • Chemo (TACE) and radiotherapy for palliative treatment
    Liver transplant if it is contained
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91
Q

what is heamangioma

A

Heamangioma - benign tumours of the liver that have no symptoms and arent cancerous

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92
Q

what is focal nodular hyperplasia

A

Focla nodular hyperplasia - benign liver tumour made of fibrotic tissue - often foun incidentallu it asyptomatic and has no malignant potential

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93
Q

Cholangiocarcinoma defornition

A

Cancer of the cells of the bile ducts

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94
Q

Cholangiocarcinoma key presintations

A

Painless jaundice

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95
Q

Cholangiocarcinoma risk factors

A

It is heavily associaed woth primary sclerosing cholanigitis but only 10% of patiens with cholangiocarcinoma had primary sclerosing cholangitis

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96
Q

Cholangiocarcinoma tests

A

CA19-9 is a tumour marker for cholangiocarcinoma.
ERCP can be used to take biopsies to diagnose cholangiocarcinoma

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97
Q

Cholangiocarcinoma treatment

A
  • Surgical resection, but overall poor prognosis
  • ERCP can be used to stent the bile duct to allow for the drainage of bile
    Resistant to chemo and radio
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98
Q

what are teh classifications of herinas

A

Classifications:
* Reduicable -can be pushed bac in with manula mavouvering
* Irriducable - cannor be pushed back in
- obstructed, the opening is too small for it to go back in
- incarcerated - the hernia is stuck by adhesions so can’t go back in

* Strangulated - blood supply is cut off resulting in ischiamia, gangree and perforation of contetns
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99
Q

what are the causes of hernias forming

A

Causes - heavy lifting, pregnancy, trauma, age, constipation/straining

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100
Q

surgery tp fix hernias

A
  • Surgery to fix hernias - the bowel is pushed back in and then it is stitched up and there is a mecsh pt over ot sto it from coming though again.
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101
Q

what is a hernia

A
  • Hernia - Protrusion of an organ or tissue out the cavity it normally lies in.
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102
Q

what are is a direct and an indierct hernia

A

Direct - protrudes through the back wall of the inguinal canal die to heavy lifting and straining, this is less common and rarely strangulates
Indirect - protrudes through the inguinal ring, congenital, 80% of inguinal hernias and can causes strangulation

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103
Q

inguinal hernia risk factors

A
  • Most common form of hernia
  • More common in males
  • 70% of all abdominal hernias
  • Men over 40!!!!
  • Chronic cough
  • Ascites
    Heavy lifting
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104
Q

inguinal hernia pathophysiology

A
  • The inguinal canal allows structures to pass from the abdomen into the external genetalia
    Hesslecachs traingle is the albdominal wall weakness for a direct hernia - RIP - rectus abdominas, inferior epigastic, pouparts ligament (inguinal ligamnet)
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105
Q

ingunal hernias key presintations

A

Ususally asympotmatic but if there is pain it indicates straungulation

Bulging, especailly with coughing or strainnig
Appearance of a lump

106
Q

inguinal hernias test

A

Look for a lump!

For an direct hernia, pressure over the lump will not sio the herniation

107
Q

inguinal hernias differential diagnosis

A

Femorla hernai
Testicular torsion
Groin abcess
Undescended teste’s
Hydrocele

108
Q

femoral hernia what is it

A

Herniation through the femoral canal, it s a very small ring which mean the hernias are at high risk of incarceration, obstruction and strangulation.

109
Q

femoral canal boundreis

A

The bounderies of the femoral cnal are FLIP
* Femoral vein
* Lacunar ligamnt
* Inguinal ligamnet
Pectinal ligamnet

110
Q

who is most likely to get a femoral hernia

A

more common in womne
more common in older age

111
Q

what are teh contents of the femmoral canal

A

N – Femoral Nerve
A – Femoral Artery
V – Femoral Vein
Y – Y-fronts
C – Femoral Canal (containing lymphatic vessels and nodes)

112
Q

how do you differentiate between a femoral and inguinal hernia

A
  • Bowel enters the femoral canal where it points down the leg, in inguinal hernais it points towards the groin
    • The neck of eh hernia is felt infterior and lateroal to the punic tubercle.
113
Q

differential diagnosis for femoral hernia

A

Inguinal hernia
Lipoma
Femoral anyerism
Saphenous variz dilation of saphenous bein at junction of femoral vein in groin

114
Q

treatent for femoral hernias

A

Surgical repair to put it back in and put a mesh over the top.

115
Q

what is an umbilical hernia

A

Occur around the umbilicus due to a defect in the muscle, they are common in neonates and can reslovel spontaneously, they can also occur in older adults.

116
Q

inscisional heria

A

Occur at the site of a previous surgery due to weakness form the closing of the muscles and tissues. The bigger the incision the larger the risk of herniation. Comorbidities put patients at risk of poor healing. They can be hard to fix with surgery due to a high rate of reoccurrence, they are often left alone if they have a wide neck and low risk of complications.

117
Q

epigastic hernia

A

A hernia is the upper abdomne

118
Q

what is a hiatal hernia

A

Part of the stomach herniated though the oesophageal hiatus of the diaphragm

119
Q

what are the tow types of hiatal hernia

A
  • Sliding - oseohpogeaoul gastirci junction slides through the heaitus and lies above the diaphragm, this cauuses acid reflux
    Rolling - uncommen, the fundus rolls up alongisde the oesophogus and the oesopgoguel gastro juncion remains beow the diaphragm
120
Q

what are teh risk factors for hiatus hernia

A

over 50
obesity

121
Q

what are teh symptoms of a hiatus hernia

A

GORD

122
Q

what are the tests for a hiatus hernia

A

Barium swallow
Upper GI edndoscopy

123
Q

what is the treatment for a haitus hernia

A

Weight loss
Treat reflux symptoms
Surgery to prevent strangulation

124
Q

define cholestasis

A

Cholestasis: blockage to the flow of bile

125
Q

define * Cholelithiasis

A
  • Cholelithiasis: gallstone(s) are present
126
Q

define choledocholithias

A
  • Choledocholithiasis: gallstone(s) in the bile duct
127
Q

define billary cholic

A
  • Biliary colic: intermittent right upper quadrant pain caused by gallstones irritating bile ducts
128
Q

define cholecystitis

A

Cholecystitis: inflammation of the gallbladder

129
Q

define cholangites

A
  • Cholangitis: inflammation of the bile ducts
130
Q

define gallbladder empyema

A
  • Gallbladder empyema: pus in the gallbladder
131
Q

define cholecystectomy

A
  • Cholecystectomy: surgical removal of the gallbladder
132
Q

define cholecystomy

A
  • Cholecystectomy: surgical removal of the gallbladder
133
Q

what is teh difference between billary cholic, acute cholecystitis and cholangitis

A

bilary colic - RUQ pain

Acute cholecystitis - RUQ pain and fever

cholangitis - RUQ pain, jaundice and cholangitis

134
Q

what are teh 5 Fs of gallstones

A

The 5 Fs:
* Fat
* Fair
* Female
* Forty
Fertile

135
Q

what are the two different types of gallstones

A

There are two different types:
* Cholesterol gallstones (80%) these form in bile which has excess cholesterol and is caused by cholesterol crystals forming
Pigment gallstones - consist of billirubin and calcium billirubinate seen in patiens with chronic heamolysis in which the billirubin is increased anc causes cirrhosis

136
Q

why do people with gallstones have to avoid eating fatty meals

A

Eating high amount of fat causes eh release of CCK (an enterogastrone released from the I cells of the duodenum) which causes te contractoiu of the gallbladder. Therefore fatty meals should be acoided

137
Q

what are teh tests for gall stones

A

A history of bilary cholic befre
Abdominal ultrasouds
LFT

138
Q

what is teh treatment for gall stones

A
  • Ursodeoxycholic acid – decreases cholesterol
  • Gallbladder stones: Laparoscopic cholecystectomy, Bile acid dissolution therapy (<1/3 success)
  • Bile duct stones:
    ERCP with sphincterotomy and:
    removal (basket or balloon)
    crushing (mechanical, laser)
    stent placement

Surgery (large stones)

139
Q

what is billary cholic

A

Billary cholic - the pain associated wth tempoay obstruction of the cystic or common l=bile duct by a stone migrating from the gall bladder
The pain is sudden, severe, constant and has crechendo patterns
The pain stops when the gall stone dislodges

It is oftern triggerd by melas and lasts between 30 mins and 8 hours.

May cause N&V

140
Q

what causes cholecystitis

A
  • Fatty mals stimulate CCK which signals bile release fomr the gallbladder, this also causes gall sotne ti be squeezed out which cuases them to get logded I the cystic duct
    Bile stasis in the gallbladder causes chemical irritation leading to inflammation distention and pressure build up.
141
Q

what are the symptoms of cholecystitis

A
  • Pain in RUQ
  • Palpable mass
  • Posisitve murhys sign
  • Fever/chills
  • Rigth shoulder pain
  • Anorexia
  • N&V
  • Muslce gaurding on examination
142
Q

what is murphys sign

A

firmly palpating the RUQ subcostal regionpushing under the ribs, get the patient to breathe in and normally this will elecit significant pain, this is a positive sign. this is for cholecystitis

143
Q

what are teh tests for cholecystitis

A
  • Abdominal ultrasound - it will show a thicked gallbladder waol, tones/sludge in the gallbladder and fluid aroug it
144
Q

what is teh treatment for cholecystitis

A
  • Nil by mouth
  • IV fluids
  • Antibiotics
  • Endoscopic retrograde cholangio-pancreatography (ERCP) can be used to remove stones trapped in the common bile duct.
  • Cholecystectomy (removal of the gallbladder) is usually be performed during the acute admission, within 72 hours of symptoms. In some cases, it may be delayed for 6-8 weeks after the acute episode to allow the inflammation to settle.
145
Q

what are teh complication of cholecysitits

A
  • Sepsis
  • Gangrenous gallbladder
  • Perforation
    Gallbladder empeyma - infected tissue and ps collecting in the gallbladder
146
Q

what is ascending cholangitis

A
  • Infection of the gallbladder
    Choledocholithiasis - caused by gall stone obstruction
147
Q

what are teh three main bacterial cuases of ascending cholangitis

A

E Coli
Kelbsiella species
Enterococcus species

148
Q

what is the pathophysiology of ascending cholangitis

A
  • Normally bacteria cant travel up the bile duct the the release of bile washes it away but when there is an obstruction it causes invasion of bacteria form the duodenum
  • High pressure on eh cyctic bile duct cuases spcae between eth cells to widen wihc also lets in bacteria form eth blood stream
    It can be obstucted by a gallstone, cancer or parasite it can also be introduced by medical intervention such as ERCP
149
Q

what is charcots triad for cholangitis

A

Charcots triad - jaundice rUQ pain, fever

150
Q

what is reynolds pentad for cholangitis

A

Signs:
* Reynols pentad - Jaundice, RUQ pain, fever, shock, confusion

151
Q

what are teh tests for cholangitis

A

Ultrasound of the abdomen
* Abdominal ultrasound scan
* CT scan
* Magnetic resonance cholangio-pancreatography (MRCP)
* Endoscopic ultrasound
* endoscopic retrograde cholangio-pancreatography (ERCP)
Blood cultures

152
Q

what are the treatments for ascening cholangitis

A
  • Nil by mouth
  • IV fluids
  • Blood cultures
  • IV antibiotics (as per local guidelines)
  • endoscopic retrograde cholangio-pancreatography (ERCP) to remove the stone s a few different procedures can be perfored in an ERCP -
  • Cholangio-pancreatography: retrograde injection of contrast into the duct through the sphincter of Oddi and x-ray images to visualise biliary system
  • Sphincterotomy: making a cut in the sphincter to dilate it and allow stone removal
  • Stone removal: a basket can be inserted and pulled through the common bile duct to remove stones
  • Balloon dilatation: a balloon can be inserted and inflated to treat strictures
  • Biliary stenting: a stent can be inserted to maintain a patent bile duct (for strictures or tumours)
    Biopsy: a small biopsy can be taken to diagnose obstructing lesions
153
Q

what are teh complications of ascending cholangitis

A
  • Nil by mouth
  • IV fluids
  • Blood cultures
  • IV antibiotics (as per local guidelines)
  • endoscopic retrograde cholangio-pancreatography (ERCP) to remove the stone s a few different procedures can be perfored in an ERCP -
  • Cholangio-pancreatography: retrograde injection of contrast into the duct through the sphincter of Oddi and x-ray images to visualise biliary system
  • Sphincterotomy: making a cut in the sphincter to dilate it and allow stone removal
  • Stone removal: a basket can be inserted and pulled through the common bile duct to remove stones
  • Balloon dilatation: a balloon can be inserted and inflated to treat strictures
  • Biliary stenting: a stent can be inserted to maintain a patent bile duct (for strictures or tumours)
    Biopsy: a small biopsy can be taken to diagnose obstructing lesions
154
Q

what is Primary biliary cholangitis

A

An autoimmune condition caused by the destrucion of the small bile ducts in the liver. The first ones to be affected are the interlobar ducts, which causes the obstruction of bile flow which is called cholestasis. The back pressure of bile causes fibrosis and then cirrhosis.

155
Q

Primary biliary cholangitis epidemiology

A

Women agen 40-50 mainly

156
Q

Primary biliary cholangitis risk factors

A

Family history
UTIs
Smpking
Automimmine diseases

157
Q

Primary biliary cholangitis pathophysiology

A

Te bile dics are damaged by autoimmune disease which results in bile leaking into the blood and other lover cell which cuses jaunduce and bile stasis

158
Q

Primary biliary cholangitis key presintations

A

Asymptomatic
Legarthy nd fatigue
Hepatomegally
Leakage of bile- priutis, jaundice
Leakeage fo cholesterol - xanthelasma, corneal arcus

Joint pain
Variceal bleeding

Fatigue
GI distrubace and abdominal pain
Jaundice
Pale stools
Signs of cirrhsis and liver faliure

159
Q

Primary biliary cholangitis test

A
  • Antibody tests - presence of antimitochondrial antibodies and raised serum IgM
  • LFT - railsed ALP and GGT, raised cholesterole
  • Ultrasoud
  • Liver biopsy - for diagnosing and stagin the diseases
  • ESR raised
160
Q

Primary biliary cholangitis differential diagnosis

A

Autoimmune cholangitis
Extrahepatic biliary obstruction

161
Q

primary billary cholangitis treatments

A
  • Ursodeoxycholic acid – reduces cholesterol absorption and improves bilirubin and aminotransferase levels
  • Cholestyramine – reduces cholesterol absorption
  • Bisphosphonates – for osteoporosis
  • Vitamin ADEK supplementation
  • Liver transplant
    Immunosuppression with steroids
162
Q

primary bilary chloangitis complications

A

It may lead to advanced liver cirrhosis and portal hypertension

163
Q

Primary sclerosing cholangitis defornition

A

Intrahepatic ducts becie stictured and fibrotic. This causes obstruction of bile and hardening of the bile ducts.

Sclerosis refers to the stiffening and hardening of the bile ducts, and cholangitis is inflammation of the bile ducts. This leads to bile obstruction which will lead to fibrosis and cirhosis

164
Q

Primary sclerosing cholangitis risk factors

A

70% of cases are associated with ulcerative colitus
Male ages 30-40
Family history

165
Q

Primary sclerosing cholangitis key presintations

A
  • Jaundice
  • Ruq pain
  • Priutus
  • Fatigue
    Hepatomegally
166
Q

Primary sclerosing cholangitis first line test

A

LFT - raised alkaline phoshatase (ALP)
Raised billirubin as the diseases progresses
More LFT as the disease progresses shows ALT and AST deranged as well
Antibody tests - Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%

167
Q

Primary sclerosing cholangitis gold standard test

A

MRCP, which is short for magnetic resonance cholangiopancreatography is the diagnostic test. This involves an MRI scan of the liver, bile ducts and pancreas. In primary sclerosis cholangitis it may show bile duct lesions or strictures.

168
Q

Primary sclerosing cholangitis treatment

A
  • ERCP ( endoscopic retrograde cholangio pancreatography. It is a test to help diagnose conditions of the liver, bile ducts, pancreas or gallbladder) can be used to dilate and stent any strictures
  • Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
  • Monitoring for complications (such as cholangiocarcinoma, cirrhosis and oesophageal varices)
169
Q

Primary sclerosing cholangitis complications

A

Acite bacteria cholangitis
Chlangiocarcinoma
Colerectal cnaer
Cirrhosis and lover faliure
Fat soluble vitamin deficancies

170
Q

acute pancreatitus defornition

A

Rapid onset of inflammation and symptoms, after an episode of time normal function occurs, useulaly due to its own digestive enzymes

171
Q

acute pancreatitis causes

A
  • GALLSTONES
  • ALCOHOL
  • POST-ERCP

I GET SMASHED

Idiopathic
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpain sting
Hyperlipidemia
Ercp prodecured
Drugs - azathioprine, metronidazole, tetracycline, furosemide

172
Q

acute pancreatitis pathophysiology (alcohol and gallstones)

A

Alcohol induced - women and older
* increased zymogen production from acinar cells and decreased bicarbonate leads to thick pancreatic juice which can obstruct the ducts
* This leads to a pressure build u and also causes autodigestion of the pancreas

Gallstones -
Blockade causes stasis of bile and pancreasetic juices which leads to the autodegestino and inflammation

173
Q

acute pancreatitis glasgow score

A

The glasgow score is the severity f the pancreatitis, it is caluculated by one point for each:

0-1 is mild, 2 is moderate and 3 or more is seen as severe.

  • P – Pa02 < 8 KPa
  • A – Age > 55
  • N – Neutrophils (WBC > 15)
  • C – Calcium < 2
  • R – uRea >16
  • E – Enzymes (LDH > 600 or AST/ALT >200)
  • A – Albumin < 32
    S – Sugar (Glucose >10)
174
Q

acute pancreatitis signs

A

Cullen’s sign – bruising around periumbilical region
Grey Turner’s sign – bruising on flanks
Tachycardia
Abdominal guarding and tenderness
Distension

175
Q

acute pancreatitis symptoms

A
  • Epigastric pain radiating to the back, relieved by sitting forwards
    N&V
176
Q

acute pancreatitis first line test

A

LFT - raised lipase, raised amylase, raised ALT and AST (ALT > 150 suggest gallstones)
CT Abdomen - inflammation, necrosis present
U&E - urea
FBC
Calcium levels
ABG - PaO2 and blood glucose
C reactive protein - increased due to inflammation
CT of the abdomen - if complication are suspected

177
Q

acute pancreatitis goldstandard tests

A

Amylase level is raised more than 3x the upper limit
Lipase is also raised

Ultrasound to look or gallstones

178
Q

acute pancreatitus treatment

A
  • NG tube
  • IV fluid and maintain electrolyte balance
  • Pain relief
  • Treat complications
  • Treatment of gallstonesby ERCP ot choestectomy
    Antibiotics is there is a clear infection (abcess or necrotic tissue)
179
Q

acute pancreatitus complications

A

ARDS
Sepsis
Hypovolemic shock orm ruptured vssles
Pancreatic pseudocyst

180
Q

chronic pancreatitis defornition

A

Longer term inflammation and symptoms, with permeant deteriation of pancreas function. Often due to fibrosis and reduced function of tissues.

181
Q

chronic pancreatitis causes

A

Alcohol s the most common causes.

Repeaed bouts of aute pancreatitis
Alcohol abuse
Cystic fibrosis
Tumours
Pancratic trauma

182
Q

chronic pancreatitis pathophysiology

A

t can lead to chronic epigastric pain, loss of exocrine function, loss of endocrine function (leading to diabeties) damage and strictures of the duct leadign to obstruciton of bile, formation of pseudocysts and accesses.

Every time there is acute pancreatis it leads to ductal dilatino and damage to panceatic tissue which can csues fibrosis and narrowing of ducts
In conditions like alcoholic acute pancreatitis there a recalcium depsosotis tehat plug the ducts

The fibrosis and calcium depostis causes misshapen ducts

183
Q

chronic pancreatitis signs

A

Malabsorbtion - weight loss, stearrhea, vitamin deficency

Exocrine dysfunction, diabeties mellitus

184
Q

chronic pancreatitis tests

A

CT abdomen
Abdo ultrasoud
Abdominal XR to show any calcification
ERCP/MRCP
Bloods - low lipase and amylase maybe
Feacal elastase

185
Q

chronic pancreatitis treatment

A

Abstinence form alcohol ad smoking
Analgesia for the pain
Replacement enzymes (creon) or it may lead to fat malabsorption ad ADEK deficency.

Insulin for diabeties
ERCP with stenting
https://www.cincinnatichildrens.org/health/e/ercp

Surgery - to drain ducts and removed inflated pancreatic tissues, obstruction of the biliary system, pseudocyst, abscess.

186
Q

Ascities defornition

A

Abnormal acumulation of fluid in the abdominal cavity

187
Q

Ascities causes

A

Impaired blood flow:
Raised serum pressure
Cirrhosis
Budd-chairi syndorem
Cardiac faliure
Constirctive pericaridtis

Decreased oncotic pressure:
* Less albumin ot [ul the fluid back ino the intravascular space
* Hypoalbuminaemia, nephrotic syndrome (hight levels of protiens in the urine), malnutrition
Peritonitis and oteh rlocal inflamations

188
Q

Ascities risk factors

A

Low sodium diet
Hepatocellular carcinoma
Splachnic vein thrombosis

189
Q

Ascities types

A

Two types:
* Exudate - high protein fluid, is this EXTREMLY bad
* This is s cloudy fluid, with low serum to ascities albumin gradiesn
* Cause are cancer, sepsis, TB, nephrotci syndomre

* Transudate - low protein fluid 
* Clean fluid, high serum to ascites albumin grades, outflow problem like portal hypertension 
* Decreased oncotic pressure
* No issue with cell membranes 
* Causes - cirrhosis 
* Treat the underlying causes (diet, drugs, drainage, diuretics)

You can use SAAG (serum ascites albumin gradient) as a calculation to work out the causes of it.

190
Q

Ascities signs

A
  • Shifting dullness - percuss left flank when patient is lying on their back and it will sound dull, percuss again when they’re on their side and it won’t as the fluid will have shifted
  • Protruding ascites
  • Flank dullness
    Fluid thrill movement ]bulging flanks
191
Q

Ascities symptoms

A

Abdominal swelling
Severe pain

192
Q

Ascities tests

A

Ascitic tap (culture and protein investigations )
Ultrasound
Prescence of fluid confirmed by demonstrating shifting dullness

193
Q

ascities treatment

A

Treat underlying causes
Reduce na and fluid
Diuretic - oral spirolactone and furosimide
Pancreatitis

194
Q

ascities complications

A

Spntaneous baclerial perionitis, this is when there is an infection into the fluid caused by e.coli, klebsiella, enterococcus that is not caused by an obvious place in the abdomen such as a hole in the intestines or a collection of pus.

Invesitgation for this are an ascitic tap and run test to see raised neutrophlls
Give antibiotics!!!!!!

195
Q

Portal hypertension three types

A

here are three types:
* Preheloatic - blockade of the portal vein
* Helaptic - distortion of liver architecture such as cirrhosis, sarcoidosis, congenital hepatic fibrosis
* Post hepatic - right HF, constrictive pericarditis, IVC obstruction
Budd-chari syndrom is whern tehere is a hepatic vein obstruction via a tumour or thrombosis

196
Q

Portal hypertension pathophysiology

A

Following cirrhosis the contraction of activated myofibrils lead to increased blood flow

This leads to portal hypertension and splanchnic vasodilation such as a drop in BP, slat and water retention in increased the blood volume and increased portal flow

There is a formation of collateral between portal and systemic systems - lower oesophagus and gastric cardia

Simple:
* Endothelin-1 production increased in cirrhosis - more vasoconstriction
* NO production reduces in cirrhosis - less vasodilation
* Reduced radius - increases resistance - higher pressure in portal system
* This causes blood to build up in the portal system

197
Q

Portal hypertension key presintations

A

ABCDE
Ascites
Bleeding
Caput medusa
Diminished liver function
Enlarged spleen

198
Q

Portal hypertension signs nd symptoms

A

Ascities
Hepatic encephalopathy
Splenomegaly
Oesophago gastic varacies

GI bleeding from oesophageal varices

199
Q

Portal hypertension test

A

Duplex dopler ultrasound
Pressure measurement using cataters in the portal vein and IVC

200
Q

Portal hypertension treatment

A

Liver transplant is the only treatment
Treat the cause - heart faliure, preicarditis, obstruction

201
Q

Oesophageal varices defornition

A

Dilated vein at risk of rupture leading to haemorrhage which can cases bleeding in the GI system

202
Q

Oesophageal varices epidemiology

A

90% of patiens with cirrhsis develop ot
Develop in the lower oesohpags and gastic cardia

203
Q

Oesophageal varices pathophysiology

A

They are causes by the backing up of bloood form the liver which asues portal hypertensino to causs a back up of blood into the veins

As these vessles are this and not meant ot hold the extra blood they can ruptre, this causes heamatemiss and if its difested it can causes melaena

204
Q

Oesophageal varices kery presintations

A

Hypotension, tachycardia, pallow, chronic liver damage
Splenomegaly
Asciteis

205
Q

Oesophageal varices test

A

Endoscooy

206
Q

Oesophageal varices treatment

A
  • Blood transfusion if anaemic
  • Beta blocker to reduce portal pressure
  • Nitrate as a vasodialtot
  • Adh analouge t reduce portal pressure
  • Correct clotting abnormalaties
    Varicial banding - put a band aroun it tp stop it form bleeding
207
Q

Spontaneous Bacterial Peritonitis defornition

A

Infection of the ascites in patient with cirrhosis, when there is no clear causes on infection i.e. abscess or intestinal damage.

Defined by an ascitic fluid absolute neutrophil count >250 cells/mm³, whether or not there is culture growth.

208
Q

Spontaneous Bacterial Peritonitis main bacterila causes

A

E. Coli
Klebsiella
Enterococcus

209
Q

Spontaneous Bacterial Peritonitis first line test

A
  • Ascitties cell count
  • Ascities culture

leukocyte esterase reagent strip testing of ascitic fluid has a role in the rapid diagnosis of spontaneous bacterial peritonitis (SBP); highly-sensitive leukocyte esterase reagent strip testing of ascitic fluid may be used to rule out SBP.

210
Q

Spontaneous Bacterial Peritonitis treatment

A
  • Piperacillin/Tazobactam (Tazocin) is often first line
  • Cephalosporins such as cefotaxime are also often used
    Levofloxacin plus metronidazole is an common alternative in penicillin allergy
211
Q

paracetamol overdose defonition

A

A toxic overdoes is defined as over 7mg/kg of paracetamol

212
Q

paracetamol overdose risk factors

A

Depression
Self-harm
Chronic alcoholism
Malnutrition and anorexia

P450 inducers - increases hepatotoxicity due to facilitation of paracetamol metabolism and NAPQI production examples are rifampicin, carbamaze, st johns wort, chonic alcohol use)

213
Q

paracetamol overdose pathophysiology

A

Pathophysiology

Paracetamol is primarily metabolised via a phase II pathway, conjugated with glucuronic acid and sulphate. A small proportion of it is metabolised by the P450 system into the toxic metabolite N-acetyl -p-benzoquinone imine which is a mitochondrial poison

It is detoxified by being conjugated with glutathione. As the overdose goes on, the stores of glutathione are depleted and NAPQI causes hepatocellular damage

Acute liver failure - feared complication of paracetamol overdose

214
Q

paracetamol overdose signs and symptoms

A

Jaundice
Encephalopathy
Tachycardia/hypotension
Evidence of self-harm

Abdominal pain
RUQ pain
N&V
Confusion

215
Q

paracetamol overdose risk assesment questions

A

There should be a risk assessment f the following questions:
- Date of ingestion: is there a delay in presentation?
- Timing of ingestion: single overdose or staggered
- Time since last ingestion (even staggered)
- Weight: if >110 kg, used 110 kg as the maximum weight for calculations.
- Pregnancy: use pre-pregnancy weight to determine toxicity and current weight for treatment
- Total amount ingested (mg/kg)
- Current suicidal risk: consider a registered mental health nurse (RMN) to stay with the patient

216
Q

paracetamol overdose tests

A
  • Serum paracetamol - levels measured 4 hours after ingestion
  • LFT - deranged liver function and rising INR
  • Clotting screen - PT ad APTT raised in hepatocellular damage
  • U&E severe toxicity results in renal failure
  • Arterial blood gas - sever toxicity causes lactic acidosis
217
Q

paracetamol overdoes treatment

A
  • Activated charcoal - reduced intestinal absorption if administered within 1 hour of ingestion
  • N-acetylcystein - NAC replenishes glutathione stores which bind to the NAPQI. This is given if there is doubt over the time the paracetamol was taken, if there was a staggered overdose and they weren’t all taken in 1 hour, if the plasma paracetamol level is on or above the treatment lien on the graph. It is infused over 1 hour to reduce side effects, the second dose is infused over 4 hours. If the INR continues to rise, contrinue NAC.
  • Liver transplant shoud be done if the atreila pH is <7.3 after 24 of ingestion, or
  • Prothrombin time > 100 seconds
  • Creatinine > 300 µmol/l
  • Grade III or IV encephalopathy

Psychiatic input for deliberate overdose

218
Q

paracetamol overdose complications

A
  • Acute liver failure
  • Acute kidney injury
    Anaphalactoid reaction
219
Q

paracetamol overdose pronosis

A

Stagers overdose or delayed presentation has a worse prognosis

220
Q

what does NAPQI and NAC stand for

A

N-acetyl -p-benzoquinone imine

N-acetylcysteine

221
Q

gilbers syndrome defornition

A

Genetic syndrome of mild unconjugated hyperbilliruin

222
Q

gilbers syndrome epidemiology and causes

A

Affects 6% of the general population

Genetic!

223
Q

gilbers syndrome pathophysiology

A

Decreased uridine-diphosphogluconatetransferase (enzyme) leading to decreased conjugation of billirubin, this means that billirubin clearance is reduced by 60%.

224
Q

gilbers syndrome key presintations

A

Asymptomatic
Mild jaundice seen during times of stress ot fasting
post-pubertal age
positive family history of GS
icterus (jaundice)
absence of hepatosplenomegaly

Risk factor of type 1 diabetes

225
Q

gilbers syndrome tests

A

bilirubin levels of <102 micromol/L (<6 mg/dL).
Unconjugated bilirubin
Lactate dehydrogenase
Liver aminotransferases - should be normal
FBC - normal

226
Q

gilbers syndrome differential diagnosis

A

Haemolysis
Cirrhosis
Billary tract disease
Thyrotoxicosis

227
Q

gilbers syndrome tx

A

No treatment, the jaundice meay come on when the body is under stress such as psycholoigal stress, fasting, dehydration, exertion, trauma, surgery, menstration.

228
Q

Haemochromatosis defornition

A

Haemochromatosis is a multisystem disorder of dysregulated dietary iron absorption and increased iron release from macrophages.

229
Q

Haemochromatosis epidemiology

A

Type 1 - hereditary hemochromatosis most commonly occurs in northern European descent (1/10 people carry the mutation)
Effects 1/200 European people
Middle age
Men present earlier than women as menstruation is a protective mechanism

230
Q

Haemochromatosis causes

A
  • HEH (hereditary haemachromatosis) is a mutation on chromosome 6, it is an autosomal recessive gene
  • High intake of iron and chelating agents #
    Alcoholics may have iron overload
231
Q

Haemochromatosis risk factors

A

Family history
Alcoholism
Chorionic transfusions in people with acquires hemochromatosis for example people with thalassaemia

232
Q

Haemochromatosis pathophysiology

A

There are two types:

* Hereditary - an autosomal recessive mutation meaning that there is an iron overload, it interacts with the transferrin receptor 1 which leads to excessive 
* Acquired - frequent transfusion of red blood cells or excessive intake of iron 
* Hepcidin  is a protien made by the liver that helps controll iron absorbtion, In HEH too much is produced leading to iron overload  Iron depositis into multiple tissues leadsing to distrucpiton and falire most commenly affectign eh liver pancreas and heart
233
Q

Haemochromatosis signs and symptoms

A

Bronze skin
Arthiritic joints
Testricular atrophy
Chronic liver diseases
Congestive heart falire
Osteoporesis

Legarthy
Arthralgia I hands
Erectile dysfunction
Loss of libido
Polyuria and polydipsia due to type 1 diabetes

234
Q

Haemochromatosis tests

A
  • Serum ferratin - high
  • Serum transferrin saturation - if this is also high its probably hemochromatosis
  • Serum iron - elevated
  • HBA1C elevated due to damage to the pancreas cells
  • LFTs - may be deranged due to liver dysfunction
  • Genetic testing for HFE gene
  • Liver biopsy for iron accumulation and fibrosis
  • MRI to show iron deposition on liver and heart
  • Ecg and echocardiogram t look for heart disruption
  • Family screening
    X-rays of joints to look for
235
Q

Haemochromatosis treatment

A
  • Venesection - draining a small amout of blood weekly unitll serum ferritin levels are 20–30 lg/l and transferrin saturations <50%
  • After this it is maintinance phlembotomywhihc aims for normal FBC, serum ferritin <50 lg/l and transferrin saturations < 50%
  • Patiens should avoid alcohol and have a low iron diet
    Patiens may need iron chelation such as deferrioxamine if they have contraindications for phlembotomy such as severe aneamia
236
Q

Haemochromatosis monitering

A

Serum ferratin
Treat complications

237
Q

Haemochromatosis complications

A
  • Liver cirrhosis and hepatocellular carcinoma
  • Diabeites due to pancrease damage
  • Hypogonadaism due to pituitry dysfunction
  • Cardaic - dialated cardiomyopathy and congestive heart failure
    Osteopoosis
238
Q

wilsons disease defornition

A

Autosomal recessive diseases of copper accumulation and copper toxicity cause by a mutation in the ATP7B gene which is part of the biliary excretion of copper pathway

239
Q

wilsons disease epidemiology

A

Incidence of 30/million
Onset is 17, diagnosis is 20

240
Q

wilsons disease pathophysiology

A
  • There is dysfunction in the ATP mediated hepatocyte copper transport
  • It is characterised by increased copper absorption from the small intestine, and decreased hepatic copper excretion
  • It causes a lack of copper in the bile which causes reduced biliary secretion of bile
    This means that copper accumulates I the hepatocytes as well as leaking into the serum and causing raised free serum copper levels, the excess copper can accumulate in the ganglia, kidney and cornea which causes oxidative damage
241
Q

wilsons disease key presintations

A

Three main ones:
* Hepatic issues
* Neurological issues
* Psychiatric issues

Neuro:
* Depression
* Loss of libido
* Bad memory
* Delusions
* Parkinsonism (tremor)
* Asterixis (liver flap
* Chorea - sudden uncontrollable jerking of arms, legs and facial muscles
* dysarthria - unclear speech
* Dystonia - muscle spasms
* Dementia

Hepatic
* Hepatosplenomegaly
* Hepatitis and cirrhosis
* Ascites
* Jaundice
* Encephalopathy

Renal
* Reanl tubular acidosis
* Fanconi syndrome
Heamolytic aneamia
Blue nails
Grey skin

242
Q

wilsons disease test

A
  • Reduced cerulopasmin and increased urinary copper excretion
  • Increased free serum copper but reduced total serum copper (copper normally travels bound to ceruloplamin and when this is reduced there will be less overall copper in the blood)
  • LFTs - dereanged due to copper accumulatin and hepatitis especiallt AST and ALT
  • Genetic testing
    The gold standard is a liver biopsy to look for copper content!
243
Q

wilsons disease tx

A
  • Copper chelation - causes the copper to bind and - D-penicallimine, or trientine hydrochloride
  • Avoid high copper foods like shellfish
    Liver transplant
244
Q

wilsons disease monitering

A

FBC
Urinary copper
Protine excretion

245
Q

wilsons disease complications

A

Liver falire
Renal stones
Reanl faliure due to the D-peniccillamine therapy

246
Q

Alpha 1 antitrypsin deficiency defornition

A

Rare autosomal recessive disorder that causes liver and pulmonary disease. A1AT is a erine protease inhibitor.

247
Q

Alpha 1 antitrypsin deficiency pathophysiology

A

In neonates, AATD may cause hepatitis and in children it can cause decompensated cirrhosis. In adults, it is most commonly seen in the fifth decade of life with features of liver and/or lung disease.
* Alpha 1 antitrypsin (A1AT) is a protease inhibitor made in the liver that protects the lings form neutrophil elastase
* Defecency of it causes protease mediated damage
* It is a recessive/co dominant inheritance
* Liver cirrhosis is also a risk with hepotocyets proties getting misfoleded causing cell death, this ciase jaundice, hepaitis, cirrhosis and hepatocellular carcinoma

Neutrophil elastase destroys elasticn in the alviolia dn can lead to parenchymal destruction and parnacinar emphysema

248
Q

Alpha 1 antitrypsin deficiency key presintations

A

Early onset COPD
Dyspone and productive cough
Weight loss
Barrel chest die to hyperexpanded lungs

Liver:
* Jaundice
* Ascities
* Inability to coagulate factors
Hepatic encephalopathy

249
Q

Alpha 1 antitrypsin deficiency tests

A

Serum A1AT levels <20 micromole
LFT - monitored due to risk of hepatocellular
Genetic testing
Ct chest scan

250
Q

Alpha 1 antitrypsin deficiency differentials

A

Asthma
COPD
Bronchiectasis
Viral hepatitis
Aloholic liver disease

251
Q

Alpha 1 antitrypsin deficiency tx

A

Resp:
* Stop smoking
* COPD treatment
* A1AT augmentation
* Surgery such as lung transplant

Liver
* Avoid alcohol
* Hep a nd b vaccine
Liver transplant

252
Q

Alpha 1 antitrypsin deficiency complications

A

Respiratory faliure
Cirrhosis and hpatocellular carcinoa

253
Q

what is the treatment path for oesophogel varacie bleeding

A

In ermergancy:
* fLuid rescusitaion
* Vasporessin analuges (terlipressin) to cauese vasoconstriction and slow bleeding
* Correct coagulopathy with vitamin K and fresh frozen plasma
* Gve prophylatic broad specturm antibiotics
* Urgent endoscopy
* Transjugular intra-hepatic portosystemic shunt (TIPS) is formed between the portal vein and hepatic vein (relieving the pressure on the varices) using xray guided wire.
*

  • Sengstaken-Blakemore tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.
254
Q

what is coursevirs sign

A

for pancreatic cancer and cholangiocarcinoma

  • jaundice and a painless enlarged call ladder probably mean cancer
255
Q

what does ELSA test stand for

A

enzyme linked immunosorbent assay

256
Q

what is the most common bacteria in ascenng cholangitis `

A

E Coli

257
Q

what are teh antibiotics you give for ascending cholanigtis

A

Cefuroxime and metronidazole

258
Q

what is teh gene and chromosome aht is changed on wilsome diseases

A

ATP7B gene on chromasoem 13

this causes dysfuction of the transpant mechanims of the liver so it cuases accumulation

259
Q

what is a chelation for wilsons

A

D-penicallamine

260
Q

what is murphus test

A

for acute cholecystitis - the patine breaths in and the examiner oushed tehri hand under the ribs and there should be lots of pain

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