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Week 14- GI/Liver > Lectures > Flashcards

Lectures Flashcards

1
Q

Upper GI bleed presentation

A

Haemateesis
Coffee ground vomiting
Malena

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2
Q

Causes of upper GI bleed

A 
Peptic ulcer
Oesophagitis
Gastritis
Duodenum is
Varices
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3
Q

Rockall reissue score components

A 
Age
Shock 
Comorbidities
Diagnosis
Stigmata of haemorrhage
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4
Q

Endoscopic therapy options

A

Adrenaline injection
Heater probe
Endoscopic clip
Hemostatic powder

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5
Q

If bleeding uncontrolled by endoscopic therapy

A

Radiological embolisation

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6
Q

Drugs to restart after UGIB

A

Aspirin after haemostasis achieved, add PPI
Stop NSAIDs
Restart clopidogrel after haemostasis

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7
Q

When to give blood products on UGIB

A

Transfuse= hub <7-8g/dL

Platelets= actively bleeding + plts <50x10^9/L

FFP= INR >1.5

Prothrombin complex concentrate= if on warfarin

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8
Q

Pathogenesis of varices

A

Increased hepatic pressure (cirrhosis)
Increased portal inflow

Increased portal pressure

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9
Q

Acute variceal bleeding treatment

A

Prophylaxis= b-blocker or band ligation

Acute bleed:
resuscitate
Abx + terlipressin 
Banding 1st line
TIPS for uncontrolled 
Balloon tamponade

Prevention= b-blocker + repeated band ligation

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10
Q

Hepatitis A clinical features

A

Incubation 30 days
Children asymptomatic
Mortality 1.5% if >50

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11
Q

Hep A treatment

A

Hydration, avoid alcohol
Usually self limiting
No vaccine

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12
Q

Diagnosis of Hep A

A 
Acute= IgM positive or HAV RNA
Previous= IgG positive
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13
Q

Hep A prevention

A

Vaccine= 95% efficacy after 4 weeks, 2nd dose life protection

Immune globulins= vaccine allergic, <4weeks until travel, 3-6 months immunity

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14
Q

Transmission of Hep E

A

Faecal oral
Pork
Minimal person to person

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15
Q

Clinical features of Hep E

A

Higher fatality in pregnant if genotype 1

Chronic in immunosupressed

Neuro manifestations in GT3 (GBS, encephalitis, ataxia, myopathy)

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16
Q

Hep B epidemiology

A

300million worldwide
2 million deaths per year
Vaccine preventable
0.3% UK population

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17
Q

Transmission of Hep B

A 
Transfusion
Fluids
Transplant
Mother to baby
Contaminated needles
Child to child
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18
Q

How age impacts Hep B

A 
Young= asymptotic but higher risk of chronic
Adult= symptomatic but cleared
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19
Q

Problems with Hep B

A

Weight loss, abdo pain, fever

Ache is
Mass in abdomen
Bloody ascites
sAg positive

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20
Q

Problems with chronic HBV

A 
Chronic liver disease
Cirrhosis
Decompensation
Hepatocellular carcinoma
Death
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21
Q

Hep B lab tests

A 
sAg= surface antigen (marker of infection)
sAb= surface ab (marker of immunity
cAb= core ab (have been infected)
eAg= e antigen (high infectivity)
eAb= e ab (low infectivity)
HBV DNA
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22
Q

Hep B treatments

A

Acute= no treatment

Chronic:

  • only if liver inflammation
  • interferon
  • tenofovir or entecavir
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23
Q

Prevention of mother to child

A

HBV vaccination to new born
HBV Ig if eAg positive or high VL
Tenofovir during last trimester

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24
Q

Hep D transmission and treatment

A

Co-infection with hep B
Requires Hep B to replicate
Treatment= IFN

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25
Q

Hep C diagnosis

A

Anti-HCV IgG positive= chronic or cleared infection

PCR/antigen positive= current infection

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26
Q

Hep C treatment

A

Direct acting anti-viral inhabitants
Cures 95%
Given with methadone in pharmacy

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27
Q

Natural history of Hep C

A

25% symptomatic

70% chronic, 30% cleared

25% cirrhosis, 1-5% HCC

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28
Q

Chromosome instability pathway

A

Mutation in tsg (APC/TP53)

Due to deletion, point mutation, hypermethylation of promoter region

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29
Q

Micro satellite instability pathway

A

Defective DNA repair

MSH2,6 genes

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30
Q

Adenocarcinoma sequence

A

Normal mucosa —> APC mutation —> aberrant crypt focus —>KRAS—> early adenoma —> late adenoma—> TP53, PIK3–> invasive carcinoma

31
Q

Colorectal cancer risk factors

A 
Adenoma
History of IBD (ulcerative colitis)
Increasing age
Obesity
Sedentary life style
High fat/low fibre diet
Smoking, alcohol
Family history
32
Q

TNM8 staging colorectal cancer

A 
T:
1= submocosa
2= into but not through muscularis
3= through muscularis, into serosa 
4= invasion of visceral peritoneum (a) other organs (b)

N:
0= no mets in LN, 1= 1-3, 2= >3

M:
0= no mets, 1= mets

33
Q

Colorectal cancer treatment options

A

Stage 1-2= surgery

Stage 3-4= adjuvant therapy (chemo/immune therapy

34
Q

Infective colitis presentation

A

Short history of diarrhoea
Abrupt onset and resolution
Systemic upset and fevers
Travel, unwell contact

35
Q

Infective colitis investigation

A

Stool culture (need 4 for 90% sensitivity)

36
Q

Ischaemic colitis presentation and investigation

A

More in elderly, CVD, HF
Abrupt onset pain, bloody diarrhoea, SIRS

CT

37
Q

Investigations for colitis

A

Abdominal x-ray:
- megacolon >5.5cm

Flexible sigmoidoscopy

38
Q

Acute changes in CIBD

A

Acute inflammation
Ulceration
Loss if goblet cells
Crypt abscess formation

39
Q

Chronic changes in CIBD

A 
Architectural changes (haphazard glands)
Paneth cells metaplasia
Chronic inflammatory infiltrates (plasma cells) in laminate propria 
Neuronal hyperplasia
Fibrosis
40
Q

Ulcerative colitis clinical features

A

Diffuse involvement of lower GIT

No fibrosis or granulomas

41
Q

Ulcerative colitis treatment

A

Acute:

  • IV methylprednisolone
  • if fails then infliximab

Mesalazine
Azathioprine (for severe relapse)

42
Q

Complications of ulcerative colitis

A

Local:

  • haemorrhage
  • toxic megacolon

Systemic:

  • skin= erythema nodosum, pyoderma gangrenosum
  • liver
  • eyes= uveitis
  • AnkSpon
43
Q

Symptoms of Crohn’s disease

A

Abdominal pain
Diarrhoea (watery)
Weight loss
Fistula, abscesses

Extra-intestinal:

  • eyes
  • sacroilitis
  • erythema nodosum
44
Q

Investigations for Crohn’s

A

Ileocolonoscopy
Faecal calprotectin
MR/CT enterography

45
Q

Pathology of Crohn’s

A 
Small and large bowed inflammation
Proximal large bowel
Patchy inflammation
Skip lesions
Transmural
Granulomas
46
Q

Treatment of Crohn’s

A

Azathiprine
Methotrexate

Biological:

  • infliximab (TNFa)
  • vedolizumab (intergins)
  • ustekinumab (il-12/23)

Surgery

47
Q

Presentation of gallstones

A

Right upper quadrant pain
Usually after meals
Crampy in nature
No jaundice or fever

48
Q

Investigations for suspected gallstones

A

LFT

US

49
Q

Composition of gallstones

A

Pure (cholesterol or bile pigment)

Mixed

50
Q

Causes ofBile stone formation

A

Excessive secretion of cholesterol
Decreased secretion of bile salts
Excess bilirubin

51
Q

Common bile duct obstruction presentation

A

Severe+acute RUQ pain
Darker urine
Paler faeces
Increased ALP, bilirubin

52
Q

Investigations and treatment for blocked CBD

A

US
MRCP

Treatment= ERCP, lap chole

53
Q

Presentation and causes of acute pancreatitis

A 
Severe acute upper abdo pain
Onset in hours
Feverish
light headed
vomiting
Abdo tender all over
Tachycardia, pyrexial, hypotensive
Increased amylase

Causes= gallstones, alcohol, ERCP, mumps, drugs

54
Q

Complications of acute pancreatitis

A

Fat necrosis
Haemorrhaging pancreatitis
Pancreatic abscess

55
Q

Presentation of pancreatic carcinoma

A

Painless obstructive jaundice
New onset diabetes
Abdo pain
Obstruction of pancreatic and bile duct

56
Q

Treatment options in pancreatic carcinoma

A

Whipples resection

Neoadjuvant therapy

57
Q

Definition of cirrhosis

A

End stage liver disease

Diffuse process with fibrosis and nodule formation

58
Q

Abnormal LFTs

A 
Hepatic= AST, ALT, GGT, bilirubin 
Cholestatic= ALP, GGT, bilirubin
59
Q

Investigations for acute liver injury

A

US
Acute viral hepatitis (hep A-E, CMV)
Autoimmune (ANA/SMA/LKM, IgG)
Paracetamol level

60
Q

Drugs cause it liver injury

A

Paracetamol
Co-amoxiclav
Methotrexate

61
Q

Investigations for chronic liver injury

A 
US
Chronic hepatitis (HBV, CMV)
Autoimmune:
- AI hepatitis= ANA, SMA, LKM, IgG
- PBC= ANA, IgM
- PSC= ANCA

Metabolic:

  • haemochromatosis (ferritin, Tf)
  • Wilson’s (caeruloplasmin)
  • a1 anti-trypsin
62
Q

Causes of chronic abnormal LFTs

A 
Alcoholic fatty liver
NAFLD
Chronic hepatitis
Autoimmune 
Haemochromatosis
63
Q

Specific features of hep B

A

Ground glass cytoplasm in hepatocyte

64
Q

Autoimmune hepatitis presentation

A 
Non specific symptoms (fatigue, fever, general ill health)
Acute jaundice arthralgia
Middle RUQ pain
Increased AST, ALT
ANA, SMA, LKM, IgG
65
Q

Autoimmune hepatitis treatment

A

Steroids (prednisolone, budesonide)

Azathioprine, mycophenolate

66
Q

Features and treatment of primary biliary cholangitis

A
  • most common chronic cholestatic disease
  • 9F:1M
  • 90% have AMA against pyruvate dehydrogenase complex
  • increased GGT, ALP (early)
  • symptoms= tiredness, itching, jaundiced
  • treatment= ursodeoxycholic acid
67
Q

Wilson’s disease presentation and treatment

A

CLD
5% fulminant acute liver failure

50% neuro/psychological:
- Parkinsonism, slurred speech, ataxia

Treatment= copper chelation (penicillamine)

68
Q

Hereditary haemochromatosis presentation and treatment

A

Presentation:

  • CLD
  • polyarthropathy
  • adrenal insufficiency
  • HF
  • diabetes
  • skin pigmentation

Treatment= venesection

69
Q

Alcoholic hepatitis features

A

Excess alcohol within 2 months
Bilirubin >80umol/l
Exclusion of other liver disease
AST <500 (AST:ALT >1.5)

Hepatomegaly, fever, leukocytosis, hepatic bruit

70
Q

Ascites treatment

A

Low salt diet

Spironolactone, furosemide

71
Q

Hepatic encephalopathy treatment

A

Non-absorbable disaccharides (lactulose)

Non-absorbable antibiotics (rifaximin)

72
Q

Benign liver neoplasms

A

Hepatocellular adenoma
Bile duct adenoma
Haemangioma

73
Q

Malignant liver neoplasms

A

Hepatocellular carcinoma
Cholangio-carcinoma
Angiosarcoma
Metastases

74
Q

Hepatocellular carcinoma treatment

A 
Kinase inhibitors= sorafanib, lenvatanib
Radio frequency ablation
Transarterial chemoembolisation
Resection
Liver transplant

Week 14- GI/Liver (1 decks)

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