Brainscape's Knowledge GenomeTM

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


See full index

Danny's Phase 2A Medicine > Gastrointestinal/ Liver > Flashcards

Gastrointestinal/ Liver Flashcards

1
Q

IBD

Epidemiology?

A
  • Presents in 20’s

- 40 in UK per 100,000

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

IBD

What mutation increases the risk of Crohn’s?

A

NOD 2

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

IBD

Describe the macroscopic changes of Ulcerative Colitis

A
  • only in the colon
  • continuous
  • has red mucosa that bleeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

IBD

Describe the macroscopic changes of Crohn’s Disease

A
  • any part of the gut
  • skip lesions
  • deep ulcers/ fissures in mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

IBD

Describe the microscopic changes of Ulcerative Colitis

A
  • no granulomas
  • mucosal inflammation
  • depleted goblet cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IBD

Describe the microscopic changes of Crohn’s Disease

A
  • (50%) granulomas
  • transmural inflammation (across whole width of the wall)
  • more goblet cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IBD

Signs and Symptoms?

A
  • Bloody diarrhoea with URGENCY
  • abdo pain/ tenderness
  • weight loss, fever, nausea, vomit, malaise (general)
  • Perianal abscess/ tag/ fistula- Crohn’s
  • Clubbing of nails
  • Erythema nodosum
  • Conjunctivitis
  • Enteropathic arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IBD

Investigations?

A
  • 2 stool tests (culture and faecal calprotectin)
  • FBC
  • Colonoscopy
  • Video Capsule Endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IBD

Treatment of Ulcerative Colitis

A

Sulfasalazine, add oral
prednisolone if no
response

Severe: Infliximab, PR steroids, surgery, IV hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

IBD

Treatment of Crohn’s Disease

A

Oral corticosteroids

IV hydrocortisone in severe flare ups

Add anti-TNF antibodies e.g. Infliximab if
no improvement

Consider adding Azathioprine or
Methotrexate to remain in remission if
frequent exacerbations/ SURGERY

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

HERNIAS

Name the two types of common Hiatus Hernias

A
  • Sliding Hiatus hernia (80%)

- Rolling Hiatus Hernia (20%)

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

what is a Sliding Hiatus hernia

A

when the gastro- oesophageal junction slides into the chest

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

what is a rolling hiatus hernia

A

when the bulge of stomach rolls into chest alongside oesophagus

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

Epidemiology of Inguinal Hernias

A

M:F 8:1

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

What is an Indirect Inguinal Hernia?

A

When the periotoneal sac goes through deep inguinal ring into the canal (also passing through the superficial ring of the inguinal cancal) - lateral to the inferior epigastric artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a Direct Inguinal Hernia?

A

when abdominal contents pushes into the inguinal canal through a weak spot (Hasselbach triangle) and passes through the superficial inguinal ring, medial to the inferior epigastric artery

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

What is a Femoral Hernia?

A

when the bowel enters femoral canal. Can be felt as a mass in upper thigh

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

What is Dyspepsia?

A

heartburn

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

How long must symptoms last to be diagnosed with GORD

A

Over 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GORD

Causes?

A
  • Sliding Hiatus Hernia (Reflux uncommon in rolling hiatus hernia)
  • Slow gastric emptying
  • alcohol
  • smoking
  • pregnancy
  • obesity
  • over-eating
  • loss of peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GORD

Presentation?

A

1) Heartburn/ retrosternal/ epigastric burning sensation
2) Aggravated by lying down
3) Cough
4 Belching
5) Acid taste
6) Increased saliva

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

GORD

6 RED flags for a Gastroscopy?

A

1) Anaemia/ Age >55
2) Loss of weight
3) Anorexia
4) Recent onset
5) Melaena/ haematemesis
6) Swallowing is difficult (dysphagia)

ALARMS

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

GORD

Complications?

A

1) Barratts Oesophagus
2) Oesophagitis
3) Ulcers
4) Increased risk of cancer

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

GORD

1st line treatment

A

Lifestyle adaptations (food, alcohol, smoking, weight, spicy food)
Antacids
Gaviscon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

GORD

2nd line treatment

A

PPI’s (lansoprazole, omeprazole)

H2 receptor agonists (Ranitidine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GORD

3rd line treatment?

A
  • Surgery (laparoscopic fundoplication)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you get a Mallory- Weiss Tear

A

persistent vomiting causes haematemesis via oesophageal mucosal tear

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

PEPTIC ULCERS

What is the most common peptic ulcer

A

Duodenal - 4x more common

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

PEPTIC ULCERS

Aetiology?

A

1)h.pylori- urease splits urea into NH3
NH3 then damages the epithelium

2) NSAIDs- inhibit COX-1 - reduced prostaglandin production = reduced mucosal protection as this is a prostaglandin fucntion

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

PEPTIC ULCERS

Risk Factors?

A
  • Smoking
  • Alcohol
  • Obesity
  • h.pylori
  • NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

PEPTIC ULCERS

Symptoms?

A
  • Burning epigastric pain (relieved by food&milk)
  • Bloating/ tender
  • ALARMS symptoms
  • Normally acute and GORD is chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

PEPTIC ULCERS

Diagnosis?

A

No red flags? = non invasive H.pylori breath tests ( 13C urea breath test)

Red flags? = gastroscopy + H.pylori tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

PEPTIC ULCERS

Treatment

A
  • Triple therapy (omeprazole, metronidazole, clarithromycin)

6-8 weeks follow up to exclude gastric cancer
Eradication confirmed with stool/ breath tests

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

COELIAC DISEASE

What genes is coeliac disease associated with?

A

HLA class II molecules DQ2 and DQ8

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

COELIAC DISEASE

Pathology?

5 steps

A

1) Alpha- gliadin peptide (toxic bit of gluten) passes through epithelium
2) It is deaminated by tissue transglutamase
3) Interactions with APC’s in lamina propria via HLA-DQ2 & HLA-DQ8
4) This activates gluten- sensitive T-cells and inflammatory cascade
5) Inflammatory cascade and mediator release leads to VILLOUS ATROPHY & CRYPT HYPERPLASIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

COELIAC DISEASE

at what age is it normally the worst

A

it peaks at infancy and 50-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

COELIAC DISEASE

Symptoms

A

1) General - tired - malaise

2) GI symptoms
- Diarrhoea
- steatorrhea (foul smelling stools)
- Bloating
- Pain/discomfort
- Anorexia
- - vomiting
- aphthous ulcers (mouth ulcers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

COELIAC DISEASE

What diseases is it associated to

A
  • type 1 DM
  • hyper/hypothyroidism
  • Addison’s
  • osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

COELIAC DISEASE

tests?

A
  • IgA tissue transglutamase antibodies test (endomysial antibodies)

-Duodenal biopsy
stage 1= increased in intraepithelial lymphocytes
stage 2= crypt hyperplasia
stage 3= flattening and atrophy of villi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

COELIAC DISEASE

treatment

A

lifelong gluten free diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

IRRITABLE BOWEL SYNDROME

What are the three types

A
  • diarrhoea
  • constipation
  • mixed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

IRRITABLE BOWEL SYNDROME

Diagnostic criteria?

A

recent abdo pan for 1x week for 3 months, PLUS 2 of:

1) relief by defecation
2) Change In habit (urgency)
3) Change in stool appearance

AND bloating, food makes worse, lethargy, mucous in stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

IRRITABLE BOWEL SYNDROME

Tests?

A
  • Enquire of red flags to ensure nothing threatening

- Do faecal calprotectin- if +ve do colonoscopy or if theyre over 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

IRRITABLE BOWEL SYNDROME

Lifestyle changes?

A

Change diet avoid alcohol, fizzy drinks, caffeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

IRRITABLE BOWEL SYNDROME

Treatment of Diarrhoea?

A

Loperamide (bulking agent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

IRRITABLE BOWEL SYNDROME

Treatment of constipation?

A

senna

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

IRRITABLE BOWEL SYNDROME

Treatment of pain?

A

1) Hyoscine butyl bromide
2) Amitriptyline
3) CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

ACHALASIA

What is it?

How does it happen?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS)

due to degenerative loss of ganglia from Auerbach’s plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ACHALSIA

Pathology?

A

Decrease in number of ganglionic nerve cells in oesophageal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ACHALASIA

Features?

A
  • dysphagia for BOTH solids/liquids

- regurgitation / heartburn leading to cough / aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

ACHALASIA

Investigations?

A

oesophageal manometry -
excessive LOS tone which doesn’t relax on swallowing
considered the most important diagnostic test

barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance

chest x-ray
wide mediastinum
fluid level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

ACHALASIA

Treatment?

A

CCBs, Long acting nitrates, BBs (relax oesophageal muscle)

1st - pneumatic (balloon) dilation
2nd - Heller Myotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

JAUNDICE

What is pre-hepatic jaundice

A

unconjugated hyperbilirubinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

JAUNDICE

What is post- hepatic jaundice

A

conjugated hyperbilirubinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

JAUNDICE

Causes of pre-hepatic?

A
  • over haemolysis- e.g. Malaria
  • impaired hepatic intake (drugs)
  • decreased conjugation (gilberts syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

JAUNDICE

Causes of hepatic jaundice

A
  • hepatitis
  • drugs
  • alcohol
  • haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Name two causes of post hepatic jaundice?

A
  • gallstones

- PBC (primary biliary cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is cholestasis?

A

Impaired hepatic excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

APPENDICTIS

Causes?

A

Lumen of appendix blocked by faecolith (solid immovable faeces), lymphoid hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

APPENDICTIS

Symptoms?

A
  • Periumbilical pain to RIF (McBurney’s)
  • anorexia
  • vomiting
  • flushes
  • tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

APPENDICTIS

Signs?

A

rebound tenderness in RIF, guarding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

APPENDICTIS

Diagnosis?

A
  • CT scan
  • Rovsing’s sign- pain in RIF increased when LIF pressed
  • Psoas Sign - pain on extending hip
  • Cope sign- pain on flexion and internal rotation of hip
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

APPENDICTIS

Treatment?

A

Surgery- appendicectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

PERITONITIS

Cause of Primary?

A
  • spontaneous bacterial peritonitis (SBP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

PERITONITIS

Cause of secondary?

A
  • ectopic pregnancy
  • appendicitis
  • ischaemic colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

PERITONITIS

Symptoms?

A

gradual abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

PERITONITIS

Signs?

A
  • guarding
  • tenderness
  • tachycardia
  • silent abdomen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

PERITONITIS

Investigations?

A
  • CXR
  • AXR (rule out obstruction)
  • CT

bloods- amylase, increased WCC, B-HGC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

PERITONITIS

Treat?

A
  • resuscitate (ABCDE)
  • treat underlying cause (Abx)
  • surgery- repair perforated viscus (tear of Abdo organ)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Overdose treatment of Opioid?

A
  • IV naloxone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Overdose treatment of Paracetamol

A
  • Activated charcoal

- N- acetylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do you give to all people who have overdosed and why

A

Activated charcoal as it stops absorption in the bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Treatment of Anaphylaxis? (degranulation of mast cells)

A

antihistamines, adrenaline, steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

GASTRO-OESOPHAGEAL VARICES?

what ARE THEY?

A

LOCAL DILATION OF VEINS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

GASTRO-OESOPHAGEAL VARICES?

How do they occur?

A

1) Hepatic blood flow impaired (cirrhosis)
2) Pressure in portal vein increased and blood forced into smaller veins
3) Enlarged oesophageal veins elevate the mucosa and protrude into lumen
4) Here, easily traumatised by passing food= acute haemorrhage ( frequent and life- threatening)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

GASTRO-OESOPHAGEAL VARICES?

Tests?

A

urgent gastroscopy to find location of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

GASTRO-OESOPHAGEAL VARICES?

Treatment?

A

clotting- vit K and platelets

Terlipressin (vasopressin analogue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

GASTRITIS

What is it?

A

inflammation of gastric mucosa (red)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

GASTRITIS

Cause? Acute/ chronic

A

H.pylori
Acute= neutrophil infiltration
Chronic= lymphocytes/ macrophages/ mononuclear/ plasma infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

GASTRITIS

Symptoms?

A
  • Asymptomatic OR

- epigastric pain/ vomit/ haematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

GASTRITIS

Treat?

A

PPIs

H2 blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is Haemochromatosis

A

excess iron deposits in parenchymal organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Cause of Haemochromatosis

A

The HFE gene is located on chromosome 6. …

When a mutant or nonfunctional variant of the HFE gene is present, increased uptake of transferrin occurs and leads to accumulation of iron in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Diagnosis of Haemochromatosis

A

1) Increased iron/ferritin

liver= hepatomegaly
pancreas= diabetes
skin= bronze discolouration
pituitary= reduced libido
myocardium= cardiomegaly and HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How is Haemochromatosis treated

A

Venesection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is WIlson’s Disease

A

Decreased intake of copper = accumulation in organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Diagnosis of Wilson’s

A
  • Increased Copper and increased 24hr urinary copper
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Organ complications for someone with Wilson’s?

A

liver- cirrhosis
basal ganglia- dementia + Parkinson’s
cornea- Fleischer rings (dark rings of bronze colour- copper around iris)
renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Treatment of Wilson’s?

A

Lifelong penicillamine (chelating agent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is Volvulus?

A

Twisting of digestive organs which causes constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How can you tell on an AXR if someone has volvulus?

A

inverted U bowel looks like ‘coffee bean’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

treatment of Volvulus?

A

Resuscitation/ laparotomy/ sigmoidoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is Cirrhosis?

A

a chronic disease of the liver marked by degeneration of cells, inflammation, and fibrous thickening of tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Cause of Cirrhosis?

A

alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

treatment of Cirrhosis?

A

need liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

PRIMARY BILIARY CIRRHOSIS

What is it?

A
  • Autoimmune destruction of intrahepatic bile ducts- Cholestasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

PRIMARY BILIARY CIRRHOSIS

What is the Epidemiology?

A

F:M 9:1 and onset average is around 50yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

PRIMARY BILIARY CIRRHOSIS

What is it due to?

A
  • Environmental trigger in genetically susceptible people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

PRIMARY BILIARY CIRRHOSIS

Main distinguisher?

A

Antimitochondrial antibodies are PRESENT (AMA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

PRIMARY BILIARY CIRRHOSIS

Signs?

A

1) Pruritis +- jaundice
2) Xanthelasma (yellow lesions of cholesterol)
3) hepatosplenomegaly
4) Xanthomata ( fatty lesions on skin)
5) Fatigue
6) Steatorrhoea - decreased bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

PRIMARY BILIARY CIRRHOSIS

Tests?

A
  • AMA test (positive result for PBC)
  • IgM
  • alkaline phosphate (high)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

PRIMARY BILIARY CIRRHOSIS

Pathology?

A

T cells attack on bile duct epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

PRIMARY BILIARY CIRRHOSIS

Treatment?

A
  • Pruritis (itching)- cholestyramine
  • Specific

1) Ursodeoxycholic Acid (UDCA)
2) Vitamin Supplements (a, d, k)
3) Eventually liver transplant ( Prognosis is <2 years once jaundice develops without transplant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

PRIMARY BILIARY CIRRHOSIS

What is found on biopsy?

A
  • Hepatic granuloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

PRIMARY BILIARY CIRRHOSIS

What does it increase the risk of?

A
  • Increased risk of hepatocellular carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

VIRAL HEPATITIS

What is it?

A

Inflammation of the liver

107
Q

VIRAL HEPATITIS

Symptoms of Acute?

A

<6 months:

  • Malaise
    -Myalgia
  • Upset GI
    May have jaundice
  • Tender hepatomegaly
  • Raised AST, ALT, GGT, ALP
  • May have raised bilirubin
  • Nausea
108
Q

VIRAL HEPATITIS

Symptoms of Chronic

A

Acute +- Palmar erythema and clubbing

109
Q

VIRAL HEPATITIS

Investigations?

A
  • Serology and viral PCR
110
Q

VIRAL HEPATITIS

Which type of Viral Hepatitis is DNA?

111
Q

VIRAL HEPATITIS

Which types of Viral Hepatitis are RNA?

A

A, C, D, E

112
Q

VIRAL HEPATITIS

How are Hepatitis A and E spread?

A
  • Foecal-oral
113
Q

VIRAL HEPATITIS

How are Hepatitis B, C and D spread?

A

bloodbourne

114
Q

VIRAL HEPATITIS

Risk factors of Hepatitis B, C and D?

A
  • IV drug users
  • Healthcare workers
  • Sex workers
115
Q

VIRAL HEPATITIS

Risk factors of Hepatitis A?

A
  • travel
  • shellfish
  • food-handlers
116
Q

VIRAL HEPATITIS

Risk factors of Hepatitis e?

A
  • Contaminated water
  • poor sanitation
  • farm animals
117
Q

VIRAL HEPATITIS`

What is the incubation time of Hep A and E?

118
Q

VIRAL HEPATITIS

Incubation time of Hep B,C and D?

A 
B&amp;D= 1-6 month
C= shorter than HBV
119
Q

VIRAL HEPATITIS

Are Hep A/B/C/D/E Acute or Chronic?

A 
A= acute
B= acute but can be chronic
C= chronic
D= chronic
E acute but chronic in immunosuppressed
120
Q

VIRAL HEPATITIS

Describe the vaccination process of the 5 types

A 
A= 100% immunity after vaccination
B = inactivated HBsAg 
C= N/A
D= Vaccination against HepB
E= Vaccine available in China
121
Q

VIRAL HEPATITIS

Complications of B/C/D?

A
  • Cirrhosis
  • HCC
  • B&C= cholangiocarcinoma
122
Q

VIRAL HEPATITIS

Complications of hep A and E?

A

Fulminant hepatitis

123
Q

VIRAL HEPATITIS

Test and treatment of A?

A
  • Anti HAV, IgM and IgG tests

- self- limiting supportive care and avoid alcohol

124
Q

VIRAL HEPATITIS

tests and treatment of B?

A

Anti - HB core, IgM, IgG tests

  • supportive care and antivirals
  • (PEG-IFN, Tenoflavir, Entecavir)
125
Q

VIRAL HEPATITIS

What Antiviral can be used for Hep B/C/D?

126
Q

VIRAL HEPATITIS

What antiviral can be used for chronic C and E?

127
Q

In all the types of hepatitis what is the main test?

A
  • If there is Antibodies for that type (e.g. HDV antibody if someone has Hep D)
128
Q

What is bile made up of?

A
  • Cholesterol
  • Phospholipids
  • Bile acids
  • Bile pigments
  • Electrolytes
  • water
129
Q

GALLSTONES

Risk factors of of cholesterol gallstones?

A

1) Age (8% over 40)
2) Female
3) Obesity
4) Cirrhosis

130
Q

GALLSTONES

Risk factors of pigment gallstones? (<10% of all cases)

A

haemolytic anaemia

131
Q

what is biliary colic?

A

pain from cystic duct obstruction

132
Q

GALLSTONES

Symptoms?

A

1) RUQ/ Epigastric pain (radiating to back/shoulder and subsides after hours)
2) maybe jaundice

133
Q

GALLSTONES

Tests?

A

1) Ultrasound of abdo

2) Bloods have increased alkaline phosphate and bilirubin

134
Q

GALLSTONES

Treatment?

A
  • Analgesia
  • Rehydration
  • Elective Cholecystectomy
135
Q

ACUTE CHOLECYSTITIS

What is it?

A
  • Impaction of stone into wall of neck of gallbladder
136
Q

ACUTE CHOLECYSTITIS

Difference to biliary colic?

A

1) Pain doesn’t subside
2) Fever, guarding and tenderness
3) Inflammatory (increased WCC)
4) Murphy’s Sign- pain on inspiration

137
Q

ACUTE CHOLECYSTITIS

tests?

A
  • FBC (increased WCC)

- Ultrasound (distended gallbladder)

138
Q

ACUTE CHOLECYSTITIS

Treatment?

A
  • Analgesia
  • IV Fluids
  • Laparoscopic Cholecystectomy (48 hrs)
139
Q

CHOLANGITIS

What is it?

A
  • infection of the biliary tree, secondary to CBD stones & cholecystitis
140
Q

CHOLANGITIS

Features?

A
  • Charcots Triad

1) RUQ pain 2) Fever 3) Obstructive Jaundice (cholestatic)

141
Q

CHOLANGITIS

tests?

A

1st line= ultrasound

2nd (gold standard)= ERCP (imaging and removal of stones)

142
Q

Treatment of CHOLANGITIS?

A
  • Abx ( Cefuroxime & Metronidazole)
143
Q

For Biliary Colic, Acute Cholecystitis and Cholangitis:

do they have RUQ pain, increased WCC and jaundice?

A 
BC= RUQ pain
AC= RUQ pain and Increased WCC
Cholangitis= All three (RUQ pain, WCC and jaundice)
144
Q

What is Acute Hepatic Failure?

A

sudden Liver failure in a previously healthy liver

145
Q

What is acute-on-chronic liver failure?

A

decompensated chronic liver disease

146
Q

What is Fulminant Hepatic Failure?

A

Huge necrosis of liver cells and severe impairment of function

147
Q

HEPATIC ENCEPHALOPATHY

Pathology?

A

1) Failing liver leaks out ammonia
2) Ammonia builds up in brain where astrocytes clear it (glutamate into glutamine)

3) Excess glutamine= fluid imbalance= fluid into cells = oedema

148
Q

HEPATIC ENCEPHALOPATHY

What are the 3 grades?

A

Grade 1= altered moods/ sleep disturbance

Grade 2= Confusion, drowsy, slurred speech

Grade 3= Liver flap, restless = COMA

149
Q

HEPATIC ENCEPHALOPATHY

Causes?

A
  • Hepatitis
  • Paracetamol OD
  • Alcohol
  • Primary Biliary Cirrhosis
  • Hemochromatosis/ Wilson’s
150
Q

HEPATIC ENCEPHALOPATHY

Signs?

A
  • jaundice
  • encephalopathy
  • Asterixis/ Flap (tremor hand/ wrist= bird flap)
151
Q

HEPATIC ENCEPHALOPATHY

Tests?

A
  • Bloods (FBC, Hepatitis antibodies, U&E, LFT, clotting, glucose)
  • Ultrasound of Abdo
152
Q

HEPATIC ENCEPHALOPATHY

Treatment?

A
  • Monitor bloods and fluid output

- treat cause and complications

153
Q

COLO-RECTAL CANCER

what is a Polyps?

A

A polyp is an abnormal growth of tissue projecting from a mucous membrane

154
Q

COLO-RECTAL CANCER

What is HNPCC?

A

Hereditary Non-polyposis Colorectal Cancer

155
Q

COLO-RECTAL CANCER

How is HNPCC caused?

A

Mutations in DNA repair genes = increased formation of adenocarcinoma sequence

156
Q

COLO-RECTAL CANCER

What is FAP?

A

Familial Adenomatous Polyposis

157
Q

COLO-RECTAL CANCER

How is FAP caused?

A

Mutated APC gene

158
Q

COLO-RECTAL CANCER

Sign of FAP?

A

hundreds of colorectal polyps in teenage years = 100% chance of colorectal cancer so colectomy is required

159
Q

COLO-RECTAL CANCER

Risk factors?

A
  • AGE
  • Smoking
  • red meat
  • low fibre
  • alcohol
  • IBD
  • HMPCC and APC gene
160
Q

COLO-RECTAL CANCER

What is Dukes staging?

A

A- Not invaded through muscle wall (93%)
B- Invaded through muscle wall (77%)
C- Local lymph node involvement (48%)
D- Distant Metastases (6.6%)

percentages are the treated survival rates, 2nd biggest cancer killer in the U.K

161
Q

COLO-RECTAL CANCER

Where is it most commonly found?

A
  • rectal and Left colon
162
Q

COLO-RECTAL CANCER

Signs?

A

1) Blood and mucous in stool
2) Obstruction (colicky pain, vomit, abdo distension)
3) rectal Mass
4) Weight Loss
5) Thin stool and tenesmus (feeling of needing a bowel movement

163
Q

COLO-RECTAL CANCER

What shows up on blood tests?

A
  • iron deficiency anaemia

- abnormal LFT’s if Liver metastases

164
Q

COLO-RECTAL CANCER

Gold standard investigation?

A
  • Colonoscopy with biopsy
    2nd- barium enema
  • Check for metastases with CT, if yes, do PET scan
165
Q

COLO-RECTAL CANCER

Treatment?

A

Dukes A+B= Surgery (part of bowel removed)
Dukes C= pre- op chemo adjunct
Rectal Cancer= pre- op radiotherapy offered
Liver Mets= liver resection

166
Q

OESOPHAGEAL CANCER

Cause?

A

Barratt’s Oesophagus

167
Q

OESOPHAGEAL CANCER

Risks?

A

smoking, obesity, alcohol, hot drinks

168
Q

OESOPHAGEAL CANCER

Pathology

A

Adenocarcinoma in distal 1/3

169
Q

OESOPHAGEAL CANCER

Symptoms? (RED FLAG)

A
  • Progressive Dysphagia
  • Haematemesis (blood vomit)
  • Weight loss
  • Melaena (black stool)
170
Q

OESOPHAGEAL CANCER

Diagnosis?

A
  • gastroscopy and biopsy
171
Q

OESOPHAGEAL CANCER

How is the cancer staged?

A

CT chest/ abdomen +- PET scan

172
Q

OESOPHAGEAL CANCER

Treatment?

A

oesophagectomy with pre&post op chemo

173
Q

OESOPHAGEAL CANCER

What do palliative patients receive?

A

stent to help swallowing

174
Q

OESOPHAGEAL CANCER

List the different stages? (order of least to most)

A 
T1- Invading Lamina propria
T2- " muscularis propria
T3- " adventitia
T4- " adjacent structures
N0- no nodal spreads
N1- regional node metastases
M0- no distant spreads
M1- distal metastases
175
Q

GASTRIC CANCER

Epidemiology?

A
  • 2nd in worldwide cancer deaths
  • common in japan
  • decreased incidence in U.K
176
Q

GASTRIC CANCER

Pathology?

A

1) Insult to gastric mucosa= intestinal metaplasia

2) genetic changes lead to adenocarcinoma formation

177
Q

GASTRIC CANCER

Symptoms?

A
  • similar to peptic ulcer pain
  • weight loss
  • nausea
  • anorexia
178
Q

GASTRIC CANCER

Risk?

A
  • salty food
  • smoking
  • pernicious anaemia
    H.pylori
179
Q

GASTRIC CANCER

Tests?

A

Diagnosis? = Gastroscopy and Biopsy

Staging? CT- (epigastric mass&lymph node in jugular notch on exam)

180
Q

GASTRIC CANCER

Treat?

A
  • surgery with pre/post op chemo

- laparoscopy before to see any spread not seen in scans

181
Q

GASTRIC CANCER

What is a GIST?

A

Gastrointestinal stromal tumours (most common stromal tumour)

182
Q

GASTRIC CANCER

How do you treat later staged tumours?

A
  • Treated palliatively

- removal to relieve symptoms

183
Q

INFECTIVE DIARRHOEA

What is it?

A
  • decreased stool consistency from water&fat (steatorrhoea), or inflammatory discharge

OSMOTIC, SECRETORY OR FUNCTIONAL

184
Q

INFECTIVE DIARRHOEA

Risks?

A
  • elderly
  • infants
  • travellers
  • food workers
  • immunocompromised
185
Q

INFECTIVE DIARRHOEA

Cause

A

virus e.g. Norovirus

Bacteria:

Vomiting= S.aureus, B.cereus

Watery Diarrhoea= Enterotoxigenic E.coli, Rotavirus, V.choloerae

186
Q

INFECTIVE DIARRHOEA

What is A common cause in the U.K

A
  • Campylobacter jejuni (cattle & poultry meats)
187
Q

What bacteria may cause meningitis?

A

Listeria monocytogenes causes meningitis in the immunocompromised

188
Q

INFECTIVE DIARRHOEA

Treatment?

A

acute- fluids, electrolytes, loperamide if diarrhoea

189
Q

What Antibiotics are commonly used for treating E.coli infections?

A

Cefuroxime

190
Q

What Antibiotics are commonly used for treating gram negative infections?

A

Metronidazole

191
Q

What Antibiotics are commonly used for treating Cholera infections?

A

tetracycline

192
Q

What Antibiotics are commonly used for treating

Salmonella/shigella/campylobacter
infections?

A

Ciproflaxin

193
Q

ALCOHOLIC LIVER DISEASE

What are the 3 types and describe each one?

A
  • fatty Liver (triglycerides in Hepatocytes- reversible)
  • Alcoholic Hepatitis (triglycerides and Mallory bodies in Hepatocytes)
  • Alcoholic Cirrhosis (destruction of Liver/ fibrosis)
194
Q

ALCOHOLIC LIVER DISEASE

Sign?

A
  • rapid jaundice
  • increased AST/ALT, bilirubin and prothrombin time
  • decreased Albumin
195
Q

ALCOHOLIC LIVER DISEASE

Treatment?

A
  • stop drinking alcohol

- treat complications

196
Q

Parenchymal causes of Hepatomegaly?

A

alcoholic, viral Hepatitis, PBC

197
Q

Malignant causes of Hepatomegaly?

A

tumour and metastases

198
Q

Haematological causes of Hepatosplenomegaly?

A

lymphoma and leukaemia

199
Q

rare causes of Hepatosplenomegaly?

A

Amyloidosis

200
Q

infective causes of Splenomegaly?

A

Glandular fever and Endocarditis

201
Q

ASCITES

What is it?

A

fluid in peritoneal cavity

202
Q

ASCITES

causes?

A

Transudate- 1) Portal HTN- cirrhosis 2) HF

Exudate- 1) Malignancy 2) Pancreatitis 3) Peritonitis

203
Q

ASCITES

How does Cirrhosis lead to Ascites?

A

1) Increased pressure in vessels leads to peripheral vasodilation
2) causes release of AG-II = vasoconstriction and salt/water retention
3) Along with hypalbuminaemia from liver disease = transudate in peritoneal cavity

204
Q

ASCITES

signs?

A
  • distended abdomen
  • fluid thrill
  • shifting dullness
  • fullness in flanks
205
Q

ASCITES

Investigations?

A
  • Aspiration
  • Albumin (find if exudate or transudate)
  • Neutrophil count (bacterial peritonitis?)
  • Gram stain and culture for bacteria
  • Cytology for malignant cells
  • amylase (check no pancreatitis/ exclude pancreatic exudate)
206
Q

ASCITES

Treatment?

A

1st line- restrict salt- furosemide- aim to lose 1kg/day

2nd line- paracentesis (hollow needle to remove fluid or gas)

207
Q

ASCITES

complications?

A

bacterial peritonitis - suspect in ascites patient with fever
- check with WCC on ascetic tap
if so treat with IV Cefotaxime

208
Q

HEPATOCELLULAR CARCINOMA

how many cancers of the liver are secondary tumours and what are the causes?

A

90%

hepB and hepC virus

209
Q

HEPATOCELLULAR CARCINOMA

Features?

A

Most have Cirrhosis

+ weight loss, fever, anorexia, ascites, RUQ pain

210
Q

Investigation of HEPATOCELLULAR CARCINOMA

A
  • Alpha- fetoprotein increase

- Ultrasound

211
Q

HEPATOCELLULAR CARCINOMA

treatment?

A
  • percutaneous ablation

- surgical resection

212
Q

PANCREATIC CARCINOMA

Risk factors and common onset?

A

Smoking, DM, Chronic Pancreatitis, Alcohol, Obesity

> 60 years

213
Q

PANCREATIC CARCINOMA

Features of Cancer Of the head?

A

Painless Jaundice,
weight loss,
Scratch marks,
Distended bladder

214
Q

PANCREATIC CARCINOMA

Features of cancer of the body/tail?

A

Epigastric pain radiating and back- relieved by sitting forwards

anorexia and weight loss

215
Q

PANCREATIC CARCINOMA

Investigations?

A

Ultrasound and CT

216
Q

PANCREATIC CARCINOMA

Treatment?

A

poor prognosis, most care is palliative

  • chemo and radiotherapy
  • 5yr survival= 3%
217
Q

PANCREATIC CARCINOMA

Treatment of palliative patient?

A

ERCP

(Endoscopic retrograde cholangiopancreatography (ERCP) is a technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems.)

218
Q

ACUTE PANCREATITIS

Aetiology?

A 
Gallstones
Ethanol (alcohol)
Trauma
Steroids
M
Autoimmune
Scorpion venom 
Hyperlipidaemia
ERCP
Drugs
219
Q

ACUTE PANCREATITIS

Pathology?

A

1) Increased calcium
2) Increased proteases and pancreatic enzymes
3) Migration of inflammatory cells, mediators ands cytokines

220
Q

ACUTE PANCREATITIS

Symptoms

A
  • vomiting

- severe epigastric pain radiating to back

221
Q

ACUTE PANCREATITIS

Signs?

A

SEVERE= grey- turners Sign (flank bruising) and Cullen’s Sign (umbilical bleeding)

  • tenderness and guarding
  • Tachycardia
  • Fever
  • increased amylase
222
Q

ACUTE PANCREATITIS

Investigations?

A
  • FBC, LFT U&E, CRP
  • CXR- exclude peptic ulcer
  • Abdo US/CT/MRI to confirm
223
Q

ACUTE PANCREATITIS

Treatment?

A

Analgesia, O2, IV fluids, NG nutrition

224
Q

CHRONIC PANCREATITIS

What is it?

A

Irreversible, inappropriate activation of enzymes

225
Q

CHRONIC PANCREATITIS

Cause?

A

-Alcohol ,CF, Autoimmune

226
Q

CHRONIC PANCREATITIS

Signs?

A
  • epigastric pain radiating to back
  • weight loss
  • diabetes
  • steatorrhoea
  • jaundice!

pancreatic calcification

227
Q

Tests of CHRONIC PANCREATITIS?

A

ABDO US/CT

228
Q

CHRONIC PANCREATITIS

Treatment?

A
  • analgesia
  • no alcohol
  • surgery
229
Q

GASTRIC CANCER

What is Bowman’s staging?

A

Type 1= tumour polyp
Type 2= ulcerated tumour
Type 3= ulcerating and infiltrating
Type 4= diffusely infiltrative carcinoma

230
Q

DIVERTICULAR DISEASE

What is Diverticulum?

A

An outpouching of gut wall, sites of entry of perforating arteries

231
Q

DIVERTICULAR DISEASE

What is Diverticulosis?

A

presence of diverticula

232
Q

DIVERTICULAR DISEASE

What is Diverticulitis?

A

Inflammation of diverticula (when faeces obstructs the diverticula)

233
Q

DIVERTICULAR DISEASE

Aetiology?

A

1) low fibre = intracolic pressure increase

2) = herniation of mucosa @ BV’s

234
Q

DIVERTICULAR DISEASE

It is commonly asymptomatic but found on barium enema/ colonoscopy, what are other possible signs?

A
  • LIF pain
  • fever
  • nausea
  • perforation causes an abscess (bad)
    OR
  • intestinal obstruction (bad)
235
Q

DIVERTICULAR DISEASE

Diagnosis?

236
Q

DIVERTICULAR DISEASE

Treatment of:

Diverticulosis?
Diverticulitis?

A

Diverticulosis- high fibre diet and paracetamol

Diverticulitis- Abx & surgery if complications

237
Q

OBSTRUCTION

Causes? (small and large bowel)

A

Small bowel- hernias and adhesions

large- colon cancer, constipation,, diverticula, volvulus

238
Q

OBSTRUCTION

Features?

A

1) Colicky pain
2) Vomiting
3) Constipation
4) Distension

239
Q

OBSTRUCTION

Features of small bowel obstruction?

A
  • early vomit
  • late constipation
  • less distension
  • pain higher on abdomen
240
Q

OBSTRUCTION

Features of large bowel obstruction?

A
  • more constant pain
  • vomiting late
  • early constipation
241
Q

OBSTRUCTION

Describe the AXR?

A

small bowel obstruction X-ray:

  • central gas shadow
  • plicae circularis across whole bowel

Large bowel obstruction X-ray:

  • peripheral gas shadows
  • haustra not completely across width
242
Q

Describe simple Obstruction?

A

1 obstruction , no vascular compromise

243
Q

Describe closed-loop obstruction?

A

2 obstructions, distended bowel/ high risk of perforation

244
Q

Describe strangulated obstruction?

A

blood supply compromised, very ill and painful

245
Q

What is Ileus Obstruction?

A

functional obstruction from reduced motility - no pain and no bowel sounds

246
Q

Treatment of Ileus and Small bowel Obstruction?

A

TREATED conservatively

247
Q

Treatment of strangulated and large bowel Obstruction?

A

surgery

+

1) Nasogastric tube for nutritional support
2) Pain relief

248
Q

Tests for obstruction?

A
  • AXR/CXR

- Bloods

249
Q

MESENTERIC ISCHAEMIA

Signs? (classic traid)

A
  • possible AF
    1) abdo pain
    2) not really any signs
    3) Hypovolaemic shock
  • increased WCC
250
Q

MESENTERIC ISCHAEMIA

Test and sign of Ischaemic Colitis?

A
  • bloody diarrhoea

confirmed by colonoscopy and biopsy

251
Q

MESENTERIC ISCHAEMIA

Treatment?

A
  • surgery
  • fluids
  • Abx
252
Q

What are haemorrhoids?

A

DISRUPTED AND DILATED ANAL CUSHIONS

253
Q

Describe how piles form and what turns these into haemorrhoids?

A

1) Straining while passing stool and stress can cause anal cushions to become loose and bulky, causing them to protrude (piles)
2) They are then vulnerable to trauma and bleed = haemorrhoids

254
Q

How are haemorrhoids classified?

A

1st degree- remain in rectum
2nd degree- prolapse on defecation but reduce
3rd degree- prolapse and placing back manually
4th degree- remain prolapsed

255
Q

How do haemorrhoids present and how would you investigate?

A
  • Bright red, painless rectal bleeding, coats stool and on tissue/ drips after
  • abdo and PR exam
256
Q

What is the 1st and 2nd line treatments of haemorrhoids?

A

1st - stool softener, increased fluid/fibre

2nd- non- operative but invasive- rubber band ligation

257
Q

What can cause an anorectal abscess? what would you do to investigate and treat?

A
  • Crohn’s
  • diverticular disease
  • give MRI
  • treat with fistulotomy
258
Q

What can an anorectal abscess lead to?

A

anal fistula

259
Q

GIve 3 causes and the treatment of Pruritis ani

A
  • threadworm, poor hygiene, tight underwear

- treated with better hygiene and anaesthetic cream

260
Q

Name the ALARMS symptoms?

A
  • Bleeding
  • Vomiting
  • Fever
  • Weight Loss
  • Dysphagia
    Chest Pain

BCDFVW

261
Q

What is the AST/ALT ratio

A

The AST/ALT ratio is the ratio between the concentrations of the enzymes aspartate transaminase (AST) and alanine transaminase, aka alanine aminotransferase (ALT).

It can show possible liver damage e.g.

AST:ALT ratio of more than 2:0 is suggestive of alcoholic liver disease

262
Q

What is ERCP

A

Endoscopic retrograde cholangiopancreatography

263
Q

What is Cholestasis

A

decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts

Danny's Phase 2A Medicine (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions