GI Flashcards

1
Q

Pathophysiology of alcoholic liver disease

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

Location of hepatic damage vs autoimmune

A

Alcohol- centrilobar, around the portal vein

autoimmune- peri-portal- around portal tracts

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

Signs of chronic liver disease

A

clubbing- associated with primary biliary sclerosis

palmar erythema

Dupuytren’s

spider naevi

gynacomastia

testicular atrophy

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

What is feminisation?

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

Signs of liver cell failure

A

jaundice

leuconychia

Bruising

ascites

encephalopathy

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

Pathophysiology of ascites

A

dysregulation of RAAS

increased hydrostatic

decreased oncotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Signs of portal hypertension

A

varicies

ascites

splenomegaly

caput medusa- veins flowing down below umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IVC Obstruction vs Caput medusae

A

in IVC Obstruction blood flows up below the umbilicus, to bypass the IVC. In caput medusae, they flow down.

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

Causes of ascites

A

cirrhosisHypoalbuminaemic states

peritoneal secondaries

constrictive pericarditis

severe biventricular failure

hepatic Vein thrombosis

TB

ovarian tumours

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

Features of encephalopathy

A

falpping tremour- asterixis

confusion, irritability

constructional apraxia e.g. difficulty drawing 5 point star

coma

convulsions

fetor hepaticus

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

Severity of encephalopathy grading

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

Signs of shock

A

I SHOCKS

Increased RR- early sign

Sinus tachycardia

Hypotension

Oliguria

Cold

Klammy

Slow cap. Refill

plus confusion, cyanosis, acidosis

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

How does systemic inflammatory response cause hypotension?

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

Signs of peritonitis

A

TRAPPED

Tenderness

Reflex guarding

Absent bowel sounds

Pyrexia

Percussion pain

Extremely unwell

Distant-local sign - e.g. Rovsing’s sign

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

Causes of acute pancreatitis

A

I GET SMASHED

I: idiopathic

G: gallstones

E: ethanol (alcohol)

T: trauma

S: steroids

M: mumps (and other infections) / malignancy

A: autoimmune

S: scorpion stings/spider bites

H: hyperlipidaemia/hypercalcaemia/hyperparathyroidism (metabolic disorders)

E: ERCP

D: drugs

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

Acute Pancreatitis management

A

IV fluids, pain control, NG tube if vomiting

80% improve in 3 days

20% have more severe- nasogastric tube, IV antibiotics, ITU

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

What is ARDS?

A

’shock lung’

pulmonary oedema

due to leaking pulmonary capillaries due to cytokines storm

first organ to fail in multi-organ failure

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

Scoring of Acute Pancreatitis

A

P - PaO2 <8kPa

A - Age >55-years-old

N - Neutrophilia: WCC >15x10(9)/L

C - Calcium <2 mmol/L

R - Renal function: Urea >16 mmol/L

E - Enzymes: LDH >600iu/L; AST >200iu/L

A - Albumin <32g/L (serum)

S - Sugar: blood glucose >10 mmol/L

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

qSOFA score

A

Hypotension <100

techypnoea >22

altered mental state (GCS <15)

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

Sepsis six

A

BUFALO

blood cultures

Urine output

Fluids

antibiotics

lactate

oxygen

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

Symptoms of intestinal obstruction

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

Causes of intestinal obstruction

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

Small bowel vs large bowel on xray

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

Risks in AP resection

A

Parasacral plexus lies between sacrum and rectum

parasympathetic fibres are easily damaged

risk of erectile impotence in men, vaginal lubrication and anorgasmia in women

risk reduced by total mesorectal excision

25
Complications of a stoma
FOUL SHITS fluid loss odour ulceration of skin leakage stenosis herniation Ischaemia terminal ileum loss- failure to absorb bile salts and B12 sexual and psychological problems
26
Causes of haematemesis
peptic Ulcer disease varices oesophagitis gastritis mallory-weiss malignancy AVMs
27
H.pylori eradication
7 days tripple therapy PPI (omeprazole), amoxicillin, carithromycin/ metronidazole
28
Blood tests in haematemesis
FBC- Anaemia/ thrombocytopenia U&E- prerenal failure, risk of rebleed clotting- INR LFTs- Liver disease Group & save/ cross match - 4-6 units if active bleeding
29
Why give Terri-resin in active bleeding varicies
constricts splanchnic bessels, restricting portal inflow
30
Glasgow blatchford score
The Blatchford score is calculated prior to endoscopy and is based on simple clinical and laboratory parameters. Its principal use is to identify low-risk patients’ who do not require any intervention (blood transfusion, endoscopic therapy, surgery). Approximately 20% of patients’ presenting with upper GI haemorrhage have a Blatchford score of zero. Such patients’ can largely be managed safely in the community, as the mortality in this group is ni
31
Rockall score
It is important to identify those patients who are at risk of ongoing bleeding and death. The Rockall scoring system is used for risk categorisation based on simple clinical parameters. Rockall scores can be calculated both before and after endoscopy, but the post endoscopy Rockall score provides a more accurate risk assessment. It provides independent risk factors which have been shown to accurately predict the risk of rebleeding and mortality.³ With increasing age, there is an increased risk of death: ³ Mortality in those aged below 40 is negligible Mortality increases to 30% in those aged over 90 Patients’ who have evidence of active bleeding and signs of shock have an 80% risk of death Those with a non-bleeding visible vessel at endoscopy have a 50% chance of re-bleeding
32
Signs of a variceal rebleed
Tachycardia decreased BP decreased CVP Decreased urine output haematemesis malena
33
Abdominal signs of chronic liver disease
Hepatomegaly/ small liver in late ascites splenomegaly caput medusae
34
Blood tests to assess liver synthetic function
Albumin INR
35
Liver function tests
AST/ALT- hepatocellular damage ALP/gGT intra/extrahepatic
36
How is the severity of liver failure calculated?
37
Complications of liver cirrhosis
38
Grading of hepatic encephalopathy
39
Complications of gallstones
Biliary colic cholecystitis empyema obstructive jaundice cholangitis gallbladder perforation gallstone ileus
40
Complications of cholecystectomy
Death \<1/1000 bile duct injury bile leakage jaundice due to retained ductal stoned general surgical complications
41
Causes of bloody diarrhoea
UC colorectal Ca polyps ischaemic colitis pseudomembranous colitis infective
42
Extraintestinal manifestations of IBD
43
What class of drug is used to maintain remission of UC?
aminosalicylates- active ingredient is 5ASA mesalazine, sulfasalazine
44
Severity of UC attack scoring
45
Complications of UC
perforqrion bleeding malnutrition toxic dilation of the colon PSC colon cancer risk increased
46
Causes of erythema nodosum
sarcoid sterptococcal infection TB IBD drugs- sulphonamides, OCP
47
Features of both UC and Crohns
young age chronic innapropriate activation of mucosal immune system abdo pain and diarrhoea may cause total colitis—\> toxic mega colon associated with extraintestinal manifestations e.g. iritis, arthritis, erythema nodosum, pyoderma gangrenosum
50
Features of Crohn’s disease
peak incidence in 20s (30s in UC) transmural Disease with patchy distribution and non-caseating granulomas mouth to anus more likely to present with weight loss, ill health, Anaemia of chronic disease
51
Site of disease in Crohns
skip lesions terninal ileum involvement —\> malabsorption due to loss of bile salts rectum commonly spared strictures, typically in terminal ileum peri-anal disease is common
52
Types of ulceration in Crohns disease
superficial- mucosal only- apthous deep- mucosa and submucosa- fissures leading to cobblestone mucosa transmural- full thickness, down to muscle layer, rose thorn ulcers
53
Features of Crohns
CAMPERS ## Footnote Clubbing / Cobblestone Apthous ulcers Mass in RIF/ Malabsorption Peri-anal Disease- skin tags, fistula, abscess Erythema nodosum Rosethorn ulcers/ Rectal sparing Skip lesions/ Strictures
54
Features of UC
peak incidence 30s diarrhoea, blood mucus superficial mucosal ulceration inflammatory cells extending into lumen of colonic glands ‘crypt abscesses’ pseudopolyps Confined to colon (backwash ileitis) recutm nearly always involved risk of colonic carcinoma
55
IBD differentials
infection pseudomembranous colitis iscaemic colitis radiation colitis
56
Severity grading of UC
mild- \<4 stools per day, systemically well moderate- \>4 stools per day, systemically unwell severe- \>6 stools per day or systemically unwell systemically unwell- tachycardia, fever, Anaemia, hypoalbuminaemia
57
borders of the inguinal canal
floor- inguinal ligament roof- internal oblique anterior- external oblique posterior- transversalis
58
complications of hernias
incarceration, strangulation, obstruction
59
what is a Richter's hernia?
only part of the bowel herniates --\> strangulation without herniation commoner in femoral hernias
60
mid inguinal point vs mid-point of the inguinal ligament
mid-inguinal point--\> pubic symphysis to ASIS--\> femoral pulse mid point of the inguinal ligament--\> pubic tubercle to ASIS--\> deep inguinal ring
61