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Medicine year 3- EOCP > Abdominal pain- quizlet > Flashcards

Abdominal pain- quizlet Flashcards

1
Q

Mallory Weiss tear

A

A tear in the lower oesophageal mucosa
Often secondary to violent coughing or vomiting
Presents as severe vomiting, blood in vomit, retching, abdominal pain
Therapeutic endoscopy to inject with adrenaline

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2
Q

Peptic ulcer disease

A

A break or ulceration in the protective mucosal lining of the stomach or duodenum
Causes 35-50% of upper GI bleeds
Typically presents as epigastric/chest pain, heartburn, malaena, upper GI bleeding

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3
Q

Risk factors for peptic ulcers

A

> 65
H.pylori infection
High dose NSAIDS
Smoker
Alcohol consumption
Blood group O (duodenal)
Increased gastric emptying (duodenal)
Decreased gastric emptying (gastric)

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4
Q

Gastric ulcers

A

20% of ulcers
Peptic ulcers in the stomach mucosa typically due to medications/ H.pylori

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5
Q

Signs and symptoms of gastric ulcers

A

Epigastric pain
Pain is not relieved by food - it is made worse
Pain occurs 30m-1hr after food
May cause early satiety and weight loss
Not as common
More likely to get vomiting
More likely to be malignant than duodenal ulcers

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6
Q

Signs and symptoms of duodenal ulcers

A

Epigastric pain
Pain is relieved by food
Pain peaks 2-3 hours after a meal
Pain is more likely to wake a patient at night
95% are due to H.pylori
High reoccurrence rate
Vomiting is less common

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7
Q

Investigations into peptic ulcers

A

Lab tests for H.pylori- CLO can be done after endoscopy
Upper GI endoscopy

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8
Q

Management of peptic ulcer

A

No stigmata of haemorrhage:
- start a PPI for 4-8 weeks with repeat endoscopy after 6-8 weeks
- stop any NSAIDs / aspirin
- eradicate H.pylori if confirmed via antibiotics
- antacids (not long-term use)

Stigmata of haemorrhage:
- application of heat
- injection of ulcers
- clips

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9
Q

Perforated peptic ulcer

A

Creates free air
Air under the diaphragm causes pain in the left shoulder
Peritonism
Absent bowel sounds
Do a laparotomy to repair

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10
Q

Gastroesophageal varices

A

Abnormal, enlarged veins within the oesophagus

Develop when blood flow to the liver is blocked causing portal hypertension and pushing blood through smaller vessels which are weaker so become swollen/ leaky/ prone to rupture

Risk factors: Portal hypertensions, large varices, Liver failure/cirrhosis, chronic alcohol use

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11
Q

Symptoms of gastroesophageal varices

A

Lots of blood in the vomit
Malaena
Dizziness
Loss of conscious in severe cases

May also be signs of liver disease i.e. jaundice/itchy/skin.ascites

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12
Q

Treatment of gastroesophageal varices

A

Hypotensive drugs e.g. propranolol for prevention
IV Terlipressin 2mg
Endoscopy to tie elastic bands to stop the bleeding (band ligation)
Transjugular intrahepatic portosytemic shunt to direct blood away from the portal vein
Liver transplant
Prophylactic broad spectrum antibiotics reduce mortality

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13
Q

Indications for a transjugular intrahepatic portosystemic shunt

A

Secondary prophylaxis for gastroesophageal varices
Refractory ascites
Treating portal hypertension in Budd-Chiari syndrome

Can cause or worsen hepatic encephalopathy though
Heart failure is an absolute contraindication

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14
Q

Symptoms of oesophageal cancer

A

Dysphagia - progressive from solids to liquids
Odynophagia
Indigestion
Reflux
Nausea
Vomiting
Hoarse voice - in upper oesophageal cancer due to involvement of the recurrent laryngeal nerve
Weight loss

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15
Q

Risk factors for oesophageal cancer

A

Long term acid refflux
Obesity
Male gender
Age >40
Smoking
Alcohol use
Previous cancer
Diet high in fat and cholesterol
High intake of hot foods

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16
Q

Types of oesophageal cancer

A

Squamous cell carcinoma: most common worldwide, seen in the top two thirds of the oesophagus
Adenocarcinoma- lower third of the oesophagus, associated with obesity and GORD

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17
Q

Haemorrhoids

A

Varicosities in the lower rectum or anus
Associated with constipation / straining / pregnancy / obesity / raised intra-abdominal pressure
These may bleed

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18
Q

Haemorrhoids: symptoms and management

A

Get tenesmus, perianal itch, constipation, pain is very rare, bright red blood in the stool that is not mixed in

Manage with topical corticosteroids - rubber band ligation if prolapsing - haemorrhoidectomy if severe

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19
Q

Anal fissure

A

A small tear in the lining of the anus
Risk factors include IBD / constipation / pregnancy and childbirth

Pain on defecation

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20
Q

Red flag ESR level

A

50- cancer until proven otherwise

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21
Q

Management of acute upper GI bleeding

A

Stabilise the patient with the ABCDE approach
Insert 2 large bore IV cannula
Take FBC, UE, LFT, clotting, cross match
Give fluids if hypotensive
Catheterise
Correct clotting if needed / reverse anticoagulation with prothrombin complex (works quicker than vitamin K)
Risk stratification based on Rockall and Blatchford score
Endoscopic management in due course - within 24 hours

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22
Q

Rockall score

A

Score for upper GI bleeds after endoscopy

Estimates the risk of re-bleeding and mortality based on clinical presentation and endoscopy findings:
- signs of shock
- age
- co-morbidities
- diagnosis e.g. cause of bleeding
- visible stigmata of recent haemorrhage e.g. clots / visible bleeding vessels

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23
Q

Glasgow-Blatchford bleeding score

A

Stratifies high and low risk patients with upper GI bleeds at their initial presentation to help make a management plan
Used prior to endoscopy

0 = low chance of medical intervention requirement
>0 = high risk GI bleed likely to require medical intervention

Intervention may be transfusion / endoscopy / surgery

24
Q

Features of the Glasgow-Blatchford bleeding score

A

Features:
- drop in Hb
- rise in urea (due to blood being broken down by digestive enzymes)
- bp
- hr
- melaena
- syncope

25
Q

H.pylori: tests and antibiotics

A

Urea breath test: accuracy of >95%, preferred non invasive technique
Raid urease test: less accurate

Antibiotics: amoxicillin and either clarithromycin or metronidazole

26
Q

Pathology of jaundice

A

Haemoglobin is broken down in to unconjugated bilirubin
This binds to albumin in the blood and is taken to the liver
In the liver it is taken up by hepatocytes
It is then conjugated with glucuronic acid to make it water soluble
The conjugated bilirubin is then excreted in bile in to the duodenum
Here is it metabolised by bacteria to form urobillinogen
Some urobillogen is excreted in faeces, some undergoes enterohepatic circulation

Jaundice occurs when this pathway is disrupted and the liver cant get rid of the bilirubin

27
Q

Unconjugated hyperbilirubinaemia

A

Classification:
Pre-hepatic - due to increased bilirubin production
Hepatocellular - due to reduced hepatocyte uptake of bilirubin

Causes:
- haemolysis e.g. haemolytic anaemia or malaria
- Gilbert disease (conjugation disorder)
- drugs e.g. chloramphenicol, gentamicin
- physiology e.g. neonatal jaundice

28
Q

Conjugated hyperbilirbunemia

A

Classification:
Hepatocellular - diminished ability to conjugate
Intrahepatic obstruction
Extrahepatic obstruction

Causes:
- hepatitis
- cirrhosis
- drugs e.g. halothane, paracetamol, MAOI
- Dublin-Johnson syndrome
- tumour
- gallstones
- alcohol

29
Q

Post hepatic jaundice

A

Impaired excretion of conjugated bilirubin - leading to cholestasis
This makes the urine dark and the stools pale as less reaches the gut
Get pruritis

Causes:
- primary biliary cirrhosis
- primary sclerosing cholangitis
- bile duct gallstones
- drugs e.g. steroids / some antibiotics
- malignancy

30
Q

Urine urobilinogen

A

Normally 1-4mg/day
Absence= biliary obstruction/hepatic disease
Increased levels: haemolytic disease

31
Q

Hepatitis symptoms

A

Temperature
RUQ pain
Muscle and joint pain
Nausea and vomiting
Fatigue
Loss of appetite
Dark urine
Pale stools
Itchy skin
Jaundice

32
Q

Hepatitis A

A

Faecal-oral route (Ends in a vowel, comes from the bowel)
RNA virus
Causes jaundice, N&V, fever
Resolves within months
Manage with basic analgesia

Most common hepatitis worldwide but rare in the UK - usually due to contaminated water or food
Notifiable disease

33
Q

Hepatitis B

A

Blood borne / vertical transmission
DNA virus
Most common worldwide cause of chronic liver disease - likely to develop to cirrhosis and hepatocellular carcinoma

Vaccination is available in 3 doses - part of the 6 in 1

34
Q

Hepatitis C

A

Blood borne
RNA virus
1 in 4 fight off the infection
3 in 4 becomes chronic - can lead to cirrhosis, liver failure and liver cancer

Screen with anti-HCV antibody
Treat with direct acting antivirals which cure the infection in 90% of patients
No vaccine is available

35
Q

Hepatitis D

A

Blood borne
RNA virus
Can develop in to chronic hepatitis
Only affects people who have hepatitis B as it requires hep B for its replication
Can be prevented by hepatitis B immunisation

36
Q

Hepatitis E

A

Faecal-oral
RNA
Very mild disease which improves within a month
No vaccination

37
Q

Type 1 autoimmune hepatitis

A

In adults
- get anti-nuclear antibodies
- anti-smooth muscle antibodies
- anti-soluble liver antigen
- presents around / after the menopause with fatigue and features of liver disease

38
Q

Type 2 autoimmune hepatitis

A

In children
- anti-liver kidney microsomes 1
- anti-liver cytosol antigen type 1
- presents in teens / early twenties with acute hepatitis with high transaminase and jaundice

Treat with prednisolone

39
Q

Gilberts syndrome

A

Autosomal recessive non-haemolytic jaundice
Causes a deficiency in the bilirubin uridine diphosphate glucuronosyltransferase enzyme - therefore get decreased processing of bilirubin so hyperbilirubinemia

It is harmless
Tends to become apparent due to stressors e.g. illness, fasting, dehydration, mensturation, exercise, lack of sleep
Only complication is increased risk of gallstones
No treatment - fluctuations tend to resolve

40
Q

Non alcoholic fatty liver disease

A

The development of a fatty liver resulting from excessive quantities of fats being deposited from causes that exclude alcohol

Most likely asymptomatic unless it develops to NASH
May get some mild fatigue and discomfort in the upper right abdomen

Causes: Obesity, Insulin resistance and type 2 diabetes, Hypercholesterolaemia, Metabolic syndrome

41
Q

Non alcoholic steatohepatitis

A

The aggressive form of non alcoholic fatty liver disease which can develop in people with non alcoholic fatty liver disease

Symptoms include ascites, jaundice, weight loss, right upper quadrant pain, fatigue

42
Q

Liver fibrosis

A

The excessive accumulation of extracellular matrix proteins e.g. collagen which causes the liver tissue to become scarred
This is the step before liver cirrhosis
Doesnt cause many symptoms but it does cause problems

Causes: NAFLD/NASH, Autoimmune hepatitis, Alcoholic liver disease, Biliary obstruction

43
Q

Cirrhosis

A

Severe scarring of the liver which leads to non-reversible architectural damage

The liver is now severely damaged and cant function normally

This is when symptoms really start to show e.g. decreased appetite, weakness, fatigue, weight loss, nausea and vomiting, RUQ pain

44
Q

Decompensated liver disease

A

An acute deterioration in liver function in a patient with known cirrhosis

The symptoms come on suddenly and are very bad:
- jaundice
- ascites
- hepatic encephalopathy
- hepatorenal syndrome

Occurs due to stressors in the life

45
Q

Hepatic encephalopathy

A

Caused in liver damage due to accumulated toxin i.e. ammonia in the blood

Symptoms include confusion, personality/mood changes, poor concentration, tremor, seizures, slow movement, slurred speech

Can give laxatives to try get rid of ammonia

46
Q

ALT, AST, ALP, GGT

A

ALT, AST: released in hepatocyte damage
ALP: released in liver pathology in response to cholestasis, marker of bile duct pathology
A raised ALP and GGT: indicative of a non-hepatobiliary pathology i.e. bone metastasis/fractures
GGT: raised in bile flow obstruction/bile duct damage

47
Q

Bilirubin, albumin, PT time

A

Bilirubin- raised in liver damage, anaemia, cholestasis
Albumin- low in liver disease
PT- time it takes for blood to clot, raised in liver disease

48
Q

Inhibitors of the p450 system

A

Antibiotics e.g. erythromycin / ciprofloxacin
Isoniazid
Omeprazole
Amiodarone
Allopurinol
SSRIs
Sodium valproate
Acute alcohol intake

Caution with these if a patient takes warfarin - will cause increased risk of bleeding - cause INR levels to be higher

49
Q

Inducers of the p450 system

A

Antiepileptics
Barbiturates
Rifampicin
St joins wort
Chronic alcohol intake
Smoking

Cause INR levels to be lower

50
Q

Cholangitis

A

Inflammation of the biliary tree
Caused by a stone blocking one of the ducts
Therefore bile flow is obstructed
This becomes. a medium for bacteria to grow - most commonly E.coli
Can also be caused by pancreatitis / tumour / clots
Can be autoimmune - anti-mitochondrial antibodies causing interlobular bile duct granulomatous destruction

51
Q

Cholangitis: symptoms, investigations and treatment

A

Get Charcot’s triad:
- RUQ pain
- Fever
- Jaundice

Reynolds pentad- contains Charcot’s triad alongside confusion and signs of septic shock

May also get itchy skin / pale stool / dark urine

On bloods there will be raised ALP, raised GGT and raised bilirubin
USS should be done
MRCP

Treatment:
- fluids
- antibiotics
- biliary drainage
- ERCP
- assessment of the cause (if gallstones consider a cholecystectomy)

52
Q

Coeliac disease

A

A T cell mediated autoimmune disease due to the immune system reacting to gluten (prolamin)

Can cause villus atrophy which is atrophy of the villi in the small intestine due to coeliac disease which can lead to severe malabsorption which includes anaemia

53
Q

Symptoms of coeliac disease

A

Abdominal pain
Constipation
Diarrhoea
Weight loss
Fatigue
Nausea and vomiting
Bloating
Dermatitis herpetiformis
Steatorrhoea

54
Q

Investigations into coeliac disease

A

Patients must be eating gluten before diagnosis for at least 6 weeks as negative results in the above will occur if they have cut it out

BEDSIDE: stool culture to exclude IBD and infection

BLOODS:
- FBC - may see IDA
- CRP
- first line measurement = anti-TTG- IgA i.e. tissue transglutamine antibodies

IMAGING:
- gold standard = endoscopy and biopsy of the duodenum/jejunal (will see villus atrophy, crypt hyperplasia, intra-epithelial lymphocytes)
- DEXA scan
- jejunal biopsies are of better quality

Associated with the HLA-DQ2 allele

55
Q

Complications of coeliac disease

A

Macrocytic anaemia - either iron deficiency or B12 / folate
Osteoporosis
Lactose intolerance
Enteropathy associated T cell lymphoma - the more a patient eats gluten the higher the chance of developing this
Hyposplenism and therefore increased infection risk - seen by Howell-jolly bodies on film - these patients need annual influenza vaccine and pneumococcal booster every 5 years

56
Q

Difference between MRCP and ERCP

A

ERCP- treatment and imaging
MRCP- imaging only

57
Q

Coffee bean sign

A

Shows sigmoid volvulus

Medicine year 3- EOCP (27 decks)

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