Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 NnD > Liver Pathologies > Flashcards

Liver Pathologies Flashcards

1
Q

Main signs of liver failure

A

Jaundice, coagulopathy and encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is acute liver failure

A

loss of liver function that occurs quickly in days or weeks in a person with NO pre-existing liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How to identify ALI, and how to diff. with ALF and severe ALI

A
  • High ALT ⇒ Acute Liver Injury
  • High ALT + Jaundice/coagulopathy ⇒ Severe acute Liver injury
  • High ALT + Jaundice/coagulopathy + encephalopathy ⇒ Acute Liver Failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signs and LFTs of paracetamol overdose

A

Nausea and abdominal paim
ALT significantly elevated, in the 1000s
PT prolonged, albumin may be normal since acute problem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What should be given as treatment for paracetamol overdose

A

VItamin K, NAC infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Unlikely to recover spontaneously from paracetamol overdose if:

A
  • Significant coagulopathy ⇒ PT > 100 AND
  • Renal dysfunction (Anuric/ creatinine > 300) AND
  • Encephalopathy ⇒ Grade 3-4 ( stupor/coma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What drugs may cause liver failure

A
  • Antibiotics esp. anti-TB meds
  • Antiepileptics
  • Herbal remedies
  • Ecstasy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most common acute viral infection to cause liver failure

A

Hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is seronegative hepatitis

A
  • Unrecognised viral infection or environmental trigger
  • Rapid onset within weeks, unusual to get spontaneous recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Symptoms of seronegative Hepatitis

A

Painless jaundice, malaise, nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

LFTs of Hepatitis

A

Bilirubin very high, significantly jaundice, ALT high, but not as high as paracetamol, coagulopathy present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Wilson’s disease

A

Accumulation of copper in the liver, can present as very rapid onset liver failure in teens or twenties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can ALF present early on

A

non-specific; malaise, nausea, vomiting, abdominal pains, dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can ALF present later on

A

fully developed syndrome manifests with acidosis, profound hypoglycaemia, coagulopathy and encephalopathy leading to coma. renal failure, multi-organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to prognosticate Non-paracetamol ALF

A
  • 3 out of 5 ⇒ unlikely to recover spontaneously
    • Age (worse for under 10 or over 40s )
    • Drug/ seronegative worse than viral
      (Acute viral hepatitis more likely to spontaneously recover)
    • PT > 50 or INR > 3.5
    • Bilirubin > 300
    • Time from jaundice to encephalopathy < 7d
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pt for parcet vc non-paracet ALF

A

PT for Paracet ALF can be more than 100, rapid progression of coagulopathy over hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

progression to encephalopathy for parcet vc non-paracet ALF

A

Usually encephalopathy in less than 1 week (progressing to failure) for Paracet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of autoimmune hep

A

Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Should excess of Vitamin K be given to treat coagulopathy

A
  • If dietary deficiency, clotting will look worse than liver function really is, so should give excess
    • Replacement will not “mask” liver dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Should excess of FFP be given to treat coagulopathy

A

Replacement will prevent use of clotting times as a
marker of liver function, so try to avoid giving except in highly significant bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is chronic liver failure

A

Injury over the years has caused the cirrhosis ⇒ complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Two main complications of liver failure

A

Hepatic encephalopathy and ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the signs of hepatic encephalopathy

A

Flapping tremor, confusion, foetor hepaticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the other possible causes of encephalopathy apart from NH3 clearance and portosystemic shunting

A
  • Constipation ⇒ More opportunity for bacteria to proliferate and stay in bowel and get observed, one of the most common causes of encephalopathy
  • Drugs (opiates and sedatives) ⇒ make patients confused
  • Dehydration (diuretics)
  • Infections
  • GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Causes of ascites

A
  • Low albumin ⇒ synthetic liver failure, oncotic intravascular pressure is lower so fluid more likely to leave blood vessels and leak into cavities
  • Portal hypertension ⇒ Increased pressure in portal vein that causes vasodilation of splanchnic vessels ⇒ blood around intestine starts to pool → Renal hypoperfusion ⇒ salt and water retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Most common cause of CLF in the UK

A

Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Signs of Alcoholic CLF

A

Jaundice, distended abdoment, spider naevi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Possible ALT , PT, albumin in Alcoholic CLF

A

Normal ALT, PT high, albumin LOW ( suggests chronic problem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How to treat alcoholic CLF patient

A

observe closely for alcohol withdrawal with diazepam and give Vitamin B supplements like IV pabrinex to protect against Wernicke’s or brain inury from withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How to treat oesophagal varices

A

Treat with B blocker to reduce pressure/ risk of bleeding, treated with band ligation at later stages .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Causes of CLF/ Cirrhosis

A
  • Alcohol
  • Non-alcoholic fatty liver disease ⇒ obesity related
  • Hepatitis B or C
  • Haemochromatosis
  • Wilson’s disease
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does early fibrosis occur

A
  • Response to repeated injury to liver
    • Causes hepatocyte cell death which leads to release of inflammatory mediators ⇒ collagen matrix deposition ⇒ early fibrosis
      Cell death and angiogenesis also present
    • Resolution is mediated by macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does fibrosis progress to cirrhosis

A

Cirrhosis developed when there is disruption of architecture of liver and failure of hepatocytes to regenerate, and loss of metabolic function ⇒ resolution now no longer possible

development of regenerative nodules of hepatocytes surrounded by fibrous bands in response to chronic liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What chronic viral heps can cause Cirrhosis. Which one is rarer and when does it occur.

A

Typically B and C, but E in those immunosuppressed and those who received solid organ transplantation and pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What leads to collagen deposition in cirrhosis

A

Kupffer cells activate stellate cells, Transformation of stellate cells into myofibroblast like cells ⇒ Collagen deposition leading to fibrosis

36
Q

Gold standard of diagnosis of cirrhosis and cons

A

Liver biopsy - Quantitative, can confirm aetiology of disease
- Prone to sampling error
- Morbidity due to invasiveness ⇒ can cause damage to the surroundings

37
Q

How to diagnose cirrhosis without serum markers or biopsy

A
  • Fibroscan- transient elastography
    • Ultrasound based shockwaves sent through liver to measure how stiff it is ⇒ surrogate marker for fibrosis
    • May also be able to quantify steatosis
    • Machine costs, user experience, patient factors
    • Severe inflammation- liver is stiffer and causes falsely elevated reading, also affected by high BMI above 40
38
Q

How does portal hypertension affect other blood vessels

A

Vasodilators released when portal blood shunts directly into systemic circulation, causes splanchnic vasodilation and increases RAAS and ANP

39
Q

whan vein can form gastric varices in stomach

A

splenic vein

40
Q

Difference between compensated and decompensated cirrhosis

A

Compensated ⇒ Asymptomatic, liver function maintained biochemically

Decompensated ⇒ Symptomatic, jaundice, ascites, variceal bleeding, encephalopathy
multi-organ/system dysfunction

Acute on chronic liver failure ⇒ Cirrhosis characterized by multi-organ failure and high mortality

41
Q

Treatment for encephalopathy

A

Laxatives and antibiotics

42
Q

Treatment for ascites

A

Low salt diet and diuretics

43
Q

Which Hep Viruses are parenteral and which are faecal-oral

A

BCD, A and E

44
Q

Which Hep viruses are heat and acid stable

A

A and E

45
Q

Which hep viruses cause chronic disease

A

BCD(?), E in transplant patients

46
Q

Which hep viruses have drugs

A

B and C and E

47
Q

Which hep viruses are enveloped

A

BCD, - those that are parenteral

48
Q

How does HAV resolve and is there any carrier state

A

Resolves spontaneously, does not cause chronic infection or carrier state, will have life-long immunity

49
Q

ALTs in Hep A and any symptoms
in which group is jaundice more common

A

Dramatic increase in ALT, several thousands and pyrexia may be present
adults

50
Q

How is Hep A transmitted

A

faeco oral. via shellfish in particular

51
Q

Treatment for Hep A

A

Supportive, but inactivated virus vaccine and Ig available

52
Q

What are the two anribodies present in HAV patients and what do they mean

A

IgM - recent infection, persists 4-6 months post infection
IgG - indicates infection or vaccine response, detectable by onset of symptoms/signs, persist for life

53
Q

How is HBV commonly transmitted

A

Parenteral, vertical, sexual most common

54
Q

What pop group is HBV most common in

A

babies and young adults

55
Q

How long does HBV last

A

Virus remains in hepatocytes for life and may re activate under immunosuprpression

56
Q

What does chronic infection of HBV mean

A

Surface antigen positve for more than 6 months

57
Q

Vaccine or treatment for HBV

A

Recombinant HBV surface antigen vaccine available, INF a or antiviral for chronic infection

58
Q

What are the main antigens found on HBV and what do they mean

A

Surface - found on envelope, indicates active infection, found in serum during acute and chronic infection
ANtibodies indicate past HBV infection or immune response to vaccine, or passice antibody following administration of HBV Ig

Core- nucleocapsid, IgM indicates recent infection, persists 406 monhts, IgG indicates recent or past infection, detectable by onset of acute symptoms, persists for life

59
Q

What are the main antigens found on HBV and what do they mean

A

Surface - found on envelope, indicates active infection, found in serum during acute and chronic infection
Antibodies indicate past HBV infection or immune response to vaccine, or passive antibody following administration of HBV Ig

Core- nucleocapsid, IgM indicates recent infection, persists 4-6 months, IgG indicates recent or past infection, detectable by onset of acute symptoms, persists for life

E antigen, also nucleocapsid, indicates active HBV infection( high virus load), antibody indicates seroconversion

60
Q

When are HBV surface antigens eliminated

A

When surface antibodies are produced

61
Q

symptoms in HCV

A

often completely asymptomatic

62
Q

how common is chronic infection in HCV

A

70-90% of cases

63
Q

treatment for HCV

A

INF a togerther with ribavirin or direct acting antivirals such as protease inhibitors or polymerase inhibitors

64
Q

HCV antibodies, antigen, PCR meaning

A

ANtibodies- recentor past infection, takes up to 3 months to develop. Antigen- active infection. PCR - determines active infection

65
Q

HDV - what antigen does it contain

A

Envelope has HBsAG

66
Q

co-infection ve superinfection

A

co- severe acute disease, low risk of chronicity. Super- chronic, high risk of severe chronic liver disease

67
Q

vacciination for HDV??

A

HBV vacc

68
Q

HEV transmission

A

faeco-oral

69
Q

HEV treatmet

A

supportive, ribavarin for chronic

70
Q

Primary cause of fatty liver

A

NAFLD associated with diabetes and obesity

71
Q

Secondary causes of fatty liver

A

Alcohol, Malnutrition and a low-protein diet or rapid weight loss. Hep C and HIV, Wilson’s disease

72
Q

HCV Tansmission

A

parenteral, may be sexual

73
Q

Pathophysiology of ALF

A
  • Alcohol is associated with increased ROS which lead to mitochondrial dysfunction
  • Alcohol increases hepatic glycerol 3-phosphate (3-GP) due to NADH/NAD
    • Increased 3-GP enhances lipogenesis and esterification of fatty acids which stay in liver
  • Large amount of alcohol enhances lipolysis and release of free fatty acids ⇒ Liver regulates amount of fat in the circulation and will mop it up
  • Oxidation of fatty acids is inhibited by alcohol ⇒ Triglyceride production is increased in the liver and VLDL are released in the blood and causes damage in other organs in the body
  • The end result is steatosis (macrovesicular with large droplets of fat accumulating within the hepatocyte)
  • Also activates kupffer cells which activate stellate cells
74
Q

Staining of what is indicative of ALF

A

Mallory’s haline bodies

75
Q

What is the criteria for Metabolic syndrome

A

> 3 of the following
Abdominal obesity
High serum triglycerides
HDL low
High BP
High fasting blood glucose

76
Q

What stge of fibrosis is present in cirrhosis

A

Stage IV

77
Q

Clinical features of NAFLD
- Symptoms??

A
  • May be asymptomatic, but may be tired, unable to conentrate, may have mental fog
  • Abnormal liver biochemistry on routine check up
  • RUQ abdominal pain ⇒ Liver may expand, resulting in fullness in RUQ
  • Hepatomegaly
  • Acanthosis nigricans in morbidly obese children ⇒ pigmentation at back of neck
78
Q

Pathophysiology of NAFLD

A
  • Insulin resistance leads to dysregulation of fatty acid metabolism
    • FFA metabolism in liver leads to ROS production (oxidative stress) ⇒ Mitochondrial dysfunction ( in glucose and lipid metabolism) ⇒ Activation of fibrosis pathway eventually
      • FFA-b oxidation within the mitochondria also generates ROS ( due to mitochondrial dysfunction) which cause:
        • Stellate cells activated ( collagen production and deposition) ⇒ Directly by ROS and cytokines and lipid peroxidation products
        • Cell death ⇒ By lipid peroxidation and Cytokines like FasL being induced leading to apoptosis.
        • Neutrophil infiltration and inflammation ⇒ By LPP and cytokines
79
Q

Is visceral or subcu fat responsible for secreting pro-inflammatory cytokines

A

Visceral

80
Q

How to diagnose NAFLD

A
  • Chronic elevation of serum aminotransferases
    • What is upper normal value?
  • Exclusion of other liver diseases eg. Alcohol
    • Autoantibodies are present up to 30% of NAFL (ANF -ASMA) ⇒ Autoimmune hepatitis can imitate NAFLD
  • Imaging studies (USSA/CT/MRI) : cannot easily distinguish steatosis from NASH or other liver diseases
  • Fatty changes only detected if > 1/3 of liver involved ⇒ A bit hard to detect fat
  • Liver biopsy is diagnostic and should be performed if diagnostic doubt exists mainly to exclude Autoimmune CAH.
  • Need to be insulin resistan (High HOMA-IR)
  • Increased ALT and AST (only slightly high, usually < 3x upper limit)
  • Increased GGT ( usually <x5 upper limit)
  • Alk phosp (moderately increased in 1/3)
  • Increased glucose and HOMA-IR (Homeostasis model assessment technique⇒ to determine insulin resistance)
  • Increased total cholesterol, increase in triglycerides
81
Q

HBV symptoms

A

May be apyrexic, insidious

82
Q

Can HEV be chronic

A

yes, for immunocompromised, eg. transplant patients

83
Q

Clinical features of NAFLD

A
  • obese (50–90%)
  • hepatomegaly (50%)
  • stigmata of CLD (rare)
84
Q

ferritin and transferrin levels in NAFLD patients

A

Increased ferritin (in 50%), increased transferrin

85
Q

Pro vs anti inflammatory adipocytokines

A
  • Leptin, TNFa, IL-6 etc
    • Leptin is raised in NAFL and correlated with degree of steatosis
  • Visceral fat rather
  • Anti-inflammatory (adiponectin)
    • Brown fat reduces inflammation
    • Adiponectin is an insulin sensitizer and the adipoR2 is in NAFL.
86
Q

How to treat nafld

A
  • Weight reduction ⇒ max 1.5 kg /week
    • 5% reduction has visible effects on ALT
    • Increased insulin sensitivity and improvement of diabetes
    • Can return back to normal as long as no cirrhosis and fibrosis
  • Diet
    • Low in carbohydrates and saturated fat ⇒ As combination of fat and carbs is lethal
    • Rich in polyunsaturated fat, fibre, vit E and C
    • 2-3 cups of Coffee / day (possibly die to benefits of Caffeine?)
      • Antioxidants present
  • Exercise
    • Improves insulin sensitivity
  • Anti-obesity agents
    • Orlistat (malabsorption), sibutramine(appetite reduction and metabolic rate)
  • Cannabinoid receptor antagonists to improve lipid metabolism-research
  • Bariatric surgery to remove fat
  • Insulin sensitizers
    • Metformin( Used in TIID, also beneficial in liver disease)
    • PPARgamma agonists? eg. TZDs
    • ibrates (cholesterol reducing drugs) ⇒ PPARa agonists)
  • Antioxidants eg.Vit E
87
Q

Splenomegaly cause

A

Portal hypertension

Y2 NnD (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions