Brainscape's Knowledge GenomeTM

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


See full index

PRIYA GI > Zeros to Finals > Flashcards

Zeros to Finals Flashcards

1
Q

what are the 3 progressive steps to alcoholic liver disease?

A
  1. alcohol related fatty liver
  2. alcoholic hepatitis
  3. cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does alcoholic hepatitis actually mean?

A

drinking alcohol over a long period of time causes inflammation in the liver sites (binge drinking is associated with the same effect)

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

what is the basic definition of cirrhosis?

A

when your liver is made up of scar tissue rather than healthy liver tissue

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

what are the alcohol consumption reccomendations?

A
  • no more than 14 units a week
  • spread evenly over 3 days or more
  • not more than 5 units in a single day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which investigation results indicate alcohol misuse/ overuse / use?

A
  • FBC shows raised MCV (as chronic heavy drinking increases the size of RBCs)
  • elevated ALT, AST and GGT
  • reduced PT (due to reduced synthetic function of the liver - reduced production of clotting factors)
  • U+Es may be derranged in hepatorenal syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

general management for alcohol misuse?

A
  • nutritional support with vitamins (esp thiamine) and a high protein diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the symptoms (based on hours) of alcohol withdrawal?

A
  • 6-12 hours = tremor, sweating, headache, craving + anxiety
  • 12-24 hours = hallucinations
  • 24-48 hours = seizures
  • 24-72 hours = delerium tremens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is delerium tremens and is it dangerous?

A
  • mortality of 35% if untreated
  • alcohol stimulates GABA receptors in the brain (GABA receptors have a relaxing effect on the rest of the brain)
  • alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain
  • chronic alcohol use results in the GABA system being up-regulated + the glutamate system being down-regulated to balance the effects of the alcohol
  • when alcohol is removed from the system, GABA under-functions and glutamate over functions = extreme excitability of the brain with excessive adrenergic activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you manage alcohol withdrawal?

A
  • CIWA-Ar used to score patient on their symptoms
  • chlordiazepoxide = a benzodiazepine used to combat effects of alcohol withdrawal
  • IV high dose vitamin B (parabinex) followed by thiamine (used to prevent wernicke-korsakoff syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is wernicke-korsakoff syndrome?

A
  • alcohol excess leads to thiamine (vit B) deficiency
  • thiamine is poorly absorbed in the presence of alcohol
  • wernicke’s encelopathy comes before korsakoffs syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the features of WK syndrome?

A

W - confusion, oculomotor disturbances + ataxia

K - confabulation + behavioural changes

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

what are the 4 most common causes of liver cirrhosis?

A
  • alcoholic liver disease
  • non alcoholic fatty liver disease
  • hepatitis B
  • hepatitis C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which blood test results suggest liver cirrhosis?

A
  • reduced albumin (because of dilution)
  • increased PT (synthetic function worse)
  • hypobatraemia (indicated fluid retention in severe liver disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which scoring system is used for cirrhosis?

A

child-pugh

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

what is the management of cirrhosis?

A
  • regular meals every 2-3 hours
  • low sodium diet to minimise fluid retention
  • high protein and high calorie diet (esp if underweight)
  • avoid alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does portal hypertension / varices come about?

A
  • the portal vein comes from the SMV and the splenic vein + delivers blood to the liver
  • liver cirrhosis increases the resistance of blood flow in the liver
  • there is increased back pressure into the portal system (portal hypertension)
  • this causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and torurous (varices)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where do varices appear? (4)

A
  • gastro-oesophageal junction
  • ileocaecal junction
  • rectum
  • anteiror abdominal wall via the umbilical vein (caput medusae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

basic treatment of stable varices?

A
  • propranolol (reduces portal hypertension)
  • elastic band ligation of varices
  • TIPS (wire inserted under xray guidance into the juguular vein, down the vena cava and into the liver via the hepatic vein) to put in a stent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

basic treatment of bleeding varices?

A
  • vasopressin (terlipressin) causes vasoconstriction and slows bleeding
  • vitamin K + fresh frozen plasma
  • broad spec antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how does ascites come about?

A
  • increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel into the peritoneal cavity –> reduction in blood pressure entering the kidneys –> release renin –> increased aldosterone relesae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how to treat ascites?

A

spironolactone + paracentesis

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

what is hepatic encephalopathy?

A
  • a build up of toxins (ammonia) which affect the brain
  • ammonia is produced by intestinal bacteria when they break down toxins
  • functional impairment of the liver cells prevents then from metabolising ammonia into harmless waste products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how to treat encephalopathy?

A

laxatives (lactulose) + antibiotics (rifampixin)

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

what are the 4 stages of NAFLD

A
  1. nonalcoholic fatty liver disease
  2. NASH
  3. fibrosis
  4. cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

when someone presents with abnormal LFTs you should screen for which conditions?

A
  • Hep B and C
  • autoantibodies
  • immunoglobulins
  • caeruloplamsin (wilsons)
  • alpha 1 anti trypsin deficiency
  • haemachromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

first line investigation for NAFLD

A

US

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

what are the causes of hepatitis (inflammation of the liver) ?

A
  • alcoholic hepatitis
  • NAFLD
  • viral hepatitis
  • autoimmune hepatitis
  • drug induced hepatitis (paracetamol overdose)
28
Q

liver function test results which suggest heptitis?

A
  • high AST + ALT (less of a rise in ALP)

- high bilirubin

29
Q

discuss Hepatitis A

A
  • most common worldwide but rare in UK
  • RNA virus
  • faecal-oral
  • nausea, vomiting, anorexia + jaundice
  • cholestasis, dark urine + pale stools
  • resolves in 1-3 months
30
Q

discuss hep B

A
  • DNA virus
  • bodily fluids eg sexual intercourse / sharing needles + mother to child
  • recover in 2 months
31
Q

surface antigen HBsAG =

A

active infection

32
Q

E antigen HBeAg =

A

marker of viral replication and implies high infectivity

33
Q

core antibodies HBcAb =

A

implies past or current infection

34
Q

surface antibody HBsAB =

A

implies vaccination of current infection

35
Q

hepatitis B virus DNA HBV DNA =

A

direct count of the viral load

36
Q

discuss hepatitis C

A
  • RNA virus
  • spread via blood/body fluids
  • curable with direct acting antiviral medications
37
Q

discuss hepatitis D

A
  • RNA virus

- can only survive in patients who also have hep B infection

38
Q

discuss hepatitis E

A
  • RNA
  • faecal oral route
  • rare in UK
39
Q

what is autoimmune hepatitis?

A
  • unknown cause

- T cells recognise liver as being harmful and alert the rest of the immune system to attack these cells

40
Q

what are the 2 types of autoimmune hepatitis?

A

type 1 - adults

type 2 - children

41
Q

describe type 1 autoimmune hepatitis?

A

women in 40s/50s present around/ after menopause with fatigue and features of liver disease

42
Q

describe type 2 autoimmune hepatitis?

A

patients in their teenage years / early twenties present with acute hepatitis and high transaminases and jaundice

43
Q

type 1 autoimmune hepatitis antibodies

A

ANA
anti-actin
anti-SLA-LP

44
Q

type 2 autoimmune hepatitis antibodies

A

anti-LKM1

- anti-LC1

45
Q

how to treat autoimmune hepatitis

A

prednisolone / azathioprine

46
Q

why is caeruloplasmin investigated for wilson’s disease?

A

it is the protein which carries copper in the blood and will be decreased

47
Q

what does alpha 1 antitrypsin deficiency result in

A

an excess of protease enzymes that attack the liver and lung tissue and cause liver cirrhosis and lung disease

48
Q

what is primary billary cirrhosis?

A
  • immune system attacks the small bile ducts
  • causes obstruction of the outflow of bile = cholestasis
  • build up of bile acids, bilirubin + cholesterol (jaundice, itching + xanthelasma)
  • bile acids are responsible for digesting fats (lack of these = greasy stools)
49
Q

what are the autoantibodies associated with PBC?

A
  • anti-mitochondrial antibodies

- anti-nuclear antibodies

50
Q

what is the treatment for PBC?

A
  • ursodeoxycholic acid (reduces intestinal absorption of cholesterol)
  • cholestyramine (bile acid sequestrate - it binds to bile acids to prevent absorption in the gut and can help with pruritis)
51
Q

what is primary sclerosing cholangitis?

A
  • intrahepatic / extrahepatic ducts become strictures and fibrotic = obstruction to the flow of bile out of the liver and intestines
52
Q

which condition is primary sclerosing cholangitis associated with?

A

UC

53
Q

who gets primary sclerosing cholangitis?

A
  • males
  • 30-40
  • UC
54
Q

GS investigation for primary sclerosing cholangitis?

A

MRCP

55
Q

what are the 2 main types of primary liver cancer?

A 
hepatocellular carcinoma (80%) 
cholangiocarcinoma (20%)
56
Q

which condition is cholangiocarcinoma associated with?

A

primary sclerosing cholangitis

57
Q

what is used as a marker for hepatocellular carcinoma?

A

Alpha-feroprotein

58
Q

what is used as a marker for cholangiocarcinoma?

A

CA19-9

59
Q

which scoring system is used for suspected upper GI bleeding?

A

glasgow-blatchford score

60
Q

is urea high or low in an upper GI bleed?

A

high because blood in the GI tract gets broken down by the acid and digestive enzymes - one of the breakdown products is urea and this urea is then absorbed in the intestines

61
Q

which scoring system is used for patients who have had an endoscopy?

A

rockall score
it provides a risk of rebleeding and mortality
- it takes into account age, features of shock, co-morbidities, cause of bleeding (eg mallory weiss tear) etc

62
Q

mnemonic for chrons NEST

A

no blood or mucus
entire GI tract
skip lesions on endoscopy
terminal ileum most affected and transmural (full thickness) inflammation
smoking is a risk factor (dont set the nest on fire)

63
Q

mnemonic for UC - UCCLOSEUP

A 
continuous inflammation
limited to colon and rectum
only superficial mucosa affected
smoking is protective
excrete blood and mucus
use aminosalicylates
primary sclerosing cholangitis
64
Q

what is the criteria for diagnosing IBS?

A

EXCLUDE OTHER PATHOLOGY

  • normal FBC, ESR and CRP blood tests
  • faecal calprotectin negative to exclude IBD
  • negative anti TTG antibodies
  • cancer excluded
65
Q

what are the symptoms of IBS?

A

abdominal pain / discomfort relived on opening bowels or associated with a change in bowel habbits

66
Q

first line treatment in IBS?

A
  • loperamide

- amitriptyline

PRIYA GI (2 decks)

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