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Regulation of Body Function > GI problem III - Ow > Flashcards

GI problem III - Ow Flashcards

1
Q

Give some signs that are stigmata of chronic liver disease

A

Yellowing of the sclera - Jaundice
Palmar erythema
Spider naevi - often in chest, upper arms and back

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2
Q

what are the two main patterns of liver test abnormality?

A

Cholestaysis: when the GGT and ALP together rise
Hepatitis or hepatocellular pattern: AST and ALT go up.
Mixed picture: both transaminases and GGT are up.

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3
Q

What are some causes of high GGT

A

If obstruction expect to see the ALP go up with it

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4
Q

What tests mark synthetic function of the liver?

A

Albumin and prothrombin

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5
Q

Causes that lead to a fall in albumin

A

Inflammation (dec)

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6
Q

Low albumin in the contest of liver disease suggests?

A

They’ve had liver dysfunction for some time (chronic)

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7
Q

what is a good indicator of acute liver failure?

A

Raised prothrombin ratio in the context of liver disease

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8
Q

GGT up alone

A

Usually indicates steatosis i.e fat deposited into liver cells (either from alcohol or non-alcoholic fatty liver disease)

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9
Q

GGT and ALP

A

Think of cholestasis i.e obstruction to biliary drainage e.g. bile duct obstruction

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10
Q

AST and ALT

A

Think of hepatitis i.e. hepatocellular drainage

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11
Q

Steatosis - causes

A 
Alcohol 
Non-alcoholic fatty liver disease 
- metabolic syndrome 
i.e: diabetes 
Dyslipidaemia 
Hypertension 
Increased BMI
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12
Q

Hepatitis - causes of hepatocellular damage

A
  • viral hepatitis
  • Alcoholic hepatitis (separate to alcoholic steatosis)
  • Non-alcoholic hepatitis (what you get from the inflammation caused by non-alcoholic steatosis)
  • Autoimmune hepaitis
  • Ischaemic hepatitis (e.g. in severe blood loss or dehydration)
  • Haemochormatosis(iron overload)
  • Drugs/ herbal or natural supplements
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13
Q

What do drugs do to the liver?

A

Cholestasis
Hepatitis
Mixed

Not just new drugs, sometimes drugs that people have been on for a long time can cause abnormal liver tests

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14
Q

Liver tumors

  • can present with?
  • Types?
A

Cholestasis
mixed pattern

primary: hepatocellular carcinoma (above) only really develops in people with cirrhosis or chronic liver diseases
Secondary: liver mets (right)

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15
Q

lets talk about alcoholic liver disease

A

spectrum between steatosis and hepatitis
As the normal liver becomes exposed to alcohol you get fatty change e.g. fatty deposits in the liver, this is reversible so if you abstain from alcohol steatosis can improve and may disappear.
If people are binge drinkers they may get episodes of hepatitis with sudden or large volume exposure e.g. binge drinking
If you have chronic progressive steatosis, the liver doesn’t like to have fat in it, so over time will contribute to hepatitis and you will get inflammation from that. similarly if you abstain the hepatitis will go away and you’ll be left with steatosis.
And over time (usually with episodes of binge drinking) get cirrhosis, irreversible scarring of the liver (when fibrosis isn’t given time to repair itself)

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16
Q

Lets talk about Non-alcoholic fatty liver disease

A

instead of alcohol the cause is metabolic syndrome (encompasses a number of conditions including insulin resistance and risk factors for that e.g. diabetes, obesity, high lipids, hypertension)
Normal liver –> steatosis –> fat cells –> fibrosis/cirrhosis

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17
Q

Diagnosis of ALD and NAFLD?

A

Usually clinically

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18
Q

Transmission Hep A, B and C

A

A: fecal oral, contaminated food or water
B: Body fluids and blood - sex, transfusion and IDU
C: Blood: IDU
Problems with blood transfusions in underdeveloped contruies

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19
Q

Hepatitis D can only cause infection of you have?

A

Hep B, co infection. or superinfection. Cant have D alone

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20
Q

Hep E

A

Very much like Hep A also fecal oral

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21
Q

EBV and CMV

A

mostly asymptomatic in healthy adults
EBV –> infectious mono / glandular fever
CMV –> similar mono like syndrome

22
Q

autoimmune hepatitis

A

Chronic autoimmune disease
Unknown aetiology
Autoantibodies attack the liver causing inflammation and damage
Episodic (flares), recurrent
More common in females than males
bimodal age distribution: young groups: 10-20 years, older group 45-70 years
Diagnosis:
- Autoimmune screen for certain liver antibodies
- Liver biopsies

23
Q

Islamic hepatitis

A

results form severe haemodynamic compromise

  • cariogenic
  • severe dehydration
  • severe sepsis
  • blood clot to hepatic artery
24
Q

Haemochromatosis

A 
Hereditary 
- Autosomal recessive 
- Mutation of HFE gene 
- Most common: homozygous for C282Y 
- Europeans at highest risk 
- Low hepcidin levels --> increased iron absorption in GI tract 
Secondary 
- blood disorders 
- repeated blood transfusions 
Diagnosis: ferritin and iron saturation
25
Q

Drugs and what they can do to the liver?

A

Paracetamol overdose

  • antidote is NAC (N-acetylcysteine)
  • narrow window period to give antidote
  • History: at risk of self harm?
  • Paracetamol - need to know time of ingestion
  • Or give empirically if high risk

many drugs can affect liver function tests and present as

  • Cholestasis
  • Mixed
  • predominantly hepatitis
26
Q

Risk factors for liver tumours?

A 
for heptocellular carcinoma 
- underlying liver cirrhosis 
- chronic hepatitis B with or without cirrhosis --> oncogenic virus 
for liver mets 
- known cancer elsewhere
27
Q

If AST and ALP are in the thousands, typically 3 possibilities

A
  • viral
  • Ischemia
  • paracetamol
    … if AST and ALP in the hundreds no so helpful as it can be anything
    AST >2x ALT usually suggests alcoholic hepatitis
28
Q

How to work up a patient with abnormal LFTs

A

Is there jaundice? - indicates severity of disease (bilirubin)
Is synthetic function impaired?
- low albumin suggests possible cirrhosis
- Normal prothrombin ratio suggests no acute liver failure

29
Q

Investigations

A 
US 
- Gallstones, normal looking gall bladder 
- Bile ducts not obstructed 
- check echogenicity of liver, nodules?
Hep A, B and C serology
Iron studies 
Auto antibodies
30
Q

Treatment of portal hypertension

A

Started on diuretics to treat ascites
Protein supplements to improved nutrition and albumin
Advised must stop alcohol

31
Q

How canyon have no alcohol for years but liver failure?

A

brought on by infection

32
Q

How can you treat hepatic encepalopthy?

A

Lactulose and fleet enema

33
Q

What happens after decompensation

A 
cant fix, liver gets worse 
medical emergency 
Code red for large volume haematemesis 
BP low, HR inc 
Peripheries cold 
IV fluid started for ressus 
Urgent full blood count 
Blood transfusion commenced
34
Q

Spontaneous bacterial peritonitis

A

A complication that can occur in patients with cirrhosis and ascites
- Translocation of bacteria and endotoxins from the gastrointestinal tract to peritoneal fluid
Facilitated by: impaired defensive mechanisms in cirrhotic patients.
Spontaneous infection in peritoneal cavity i.e. peritonitis
Diagnosis: ascitic tap - neutrophils 250x10^6/L
Treatment:
- identify organism on culture
- treat with appropriate antibiotic

35
Q

Acute versus chronic hepatitis B, the different types of transmission

A

Acute hep B
- adult transmission
- Parenteral (IV drug use/ contaminated blood transfusion) and sexual
Because your immune system will clear hep B as an adult

Chronic Hep B

  • Neonate or childhood transmission
  • perinatal / vertical and horizontal (child to child) comm
36
Q

The different stages of HBV infections and the antigens / antibodies present

A

HBsAg - when initially infected
Shortly after this you develop symptoms
Start to develop immune response
Core antibodies: IgM is initial immune response to virus, when these rise the surface antigen levels start to fall. This is an acute antibody that doesnt stay in the system forever.
Over time the IgM core antibodies are replaced by the more permanent anti HB surface antibodies

37
Q

Window period

A

if you do a blood test at a particular point in time it may not show you that the person has actually been exposed e.g. time between when the surface antigen disappears and when the surface antigen appears, so you need to request a core IgM antibody

38
Q

if you’ve been successfully vaccinated, but not exposed to HBV what will show up on the antigen / antibody test?

A

Anti-HBs

39
Q

The stages of chronic Hep B from childhood onwards

A

Phase 1: when baby / child infected, because their immune system is underdeveloped they are tolerant to the hep B so they don’t develop an immune response and therefore don’t have inflammation, typically they have very high levels of virus and the ALT is usually normal
Phase 2: as the child matures and enters adulthood in their 20’s and 30’s, the body tries to clear the virus, in this phase you’re most at risk of inflammation and fibrosis caused by the immune system attacking infected hepatocytes. Viral load will start to drop, get fluctuating levels of ALT, from inflam. Chronic Hep B is one of the leading causes of cirrhosis.
Phase 3: The body controls the virus, inflammation gone. this can last for many years
Phase 4: in some people the virus escapes from the immune regulation and reactivates –> ongoing liver damage

So chronic Hep B patients need regular blood tests to check for immune activation and inflammation.

40
Q

briefly describe the progression of symptoms of hepatic encephalopathy

A
  1. mild confusion, limited attention span, irritability, inverted sleep, incoordination, tremor, impaired handwriting
  2. drowsiness, personality changes, intermittent dterioirdation, asterixis, ataxia, dysarthria
  3. somnolent, gross disporietaiton, marked confusion, slurred speech, hyperreflexia, muscle rigidity, babinski sign
  4. coma, no response to pain, decrebarte posture
41
Q

Liver functions summary

A
  • removes toxins
  • metabolises glucose, produces energy
  • removes bacteria from blood, helps body fight infection
  • produces bile so we can absorb fats
  • stores vitamins, minerals and sugar
  • Produces most of the proteins needed by the body
  • Produces most of the substances that regulate blood clotting
42
Q

What is the Child-pugh score?

A

classifies the severity of cirrhosis and predicts mortality without transplantation (uses, billlirubin, albumin, PR ratio, degree of ascites and encephalopathy)

43
Q

Complication of cirrhosis result from?

A 
portal hypertension (variceal haemorrhage, ascites) of liver insufficiency (jaundice)
both give encephalopathy
44
Q

Manifestations of portal hypertension

A

arteriovenous shunting and or mechanical obstruction

hypersplenisim

  • moderate anaemia
  • neutropenia
  • thrombocytopenia

oesophageal varices
caput medusae
Haemorrhoids

45
Q

Pathogenesis of ascites

A 
cirrhosis 
Inc resistance to portal flow 
Portal hypertension 
Two pathways: 
1. Inc hydrostatic pressure + decreased albumin 
2. Splanchnic vasodilation 
systemic arterial underfilling 
Activation of ADH and RAAs 
Renal Na and H20 retention
46
Q

What is hepatic encephalopathy

A

the inability to get rid of the ammonia in the circulation, which we all form through breakdown of proteins in the gut.
It passes through the BBB

47
Q

Mechanism of action of lactulose

A
  • a non-absorbable daiassachride
    produces osmosis of water - Diarrhoea
    Reduces pH of colonic content and thereby prevents absorption of NH3
    Converts NH3-NH4 that can be excreted
48
Q

Some causes of portal hypertension other than cirrhosis

A

Right heart failure
Portal vein thrombosis
Budd chiari syndrome

49
Q

how does portal hypertension lead to ascites?

A 
PH 
splanchnic vasodilation 
Decreased effective circulatory volume 
Activation of RAAs 
1. Renal sodium retention 
--> ascites 
2. Renal vasoconstriction 
--> heptorenal syndrome
50
Q

Definition of hepatorenal syndrome: types 1 and 2

A

Type 1:
doubling of serine creatinine over 24 hours
frequently follows a precipitating event such as infection
Survival without treatment in the order of weeks

Type 2:
less rapid renal functional deterioration than type 1
Mainly presents with refractory ascites
Survival without treatment in order of months

51
Q

HCC treatment

A

if detected early can be cured
all patients with cirrhosis need HCC surveillance
- liver ultrasound and alpha fetoprotein every 6 months

Regulation of Body Function (31 decks)

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