gastro Flashcards

1
Q

The two main types of inflammatory bowel disease are

A

The two main types of inflammatory bowel disease are Crohn’s disease and Ulcerative colitis. They have many similarities in terms of presenting symptoms, investigation findings and management options.

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2
Q

principle difference in presenting features of crohn’s and ulcerative colitis

A

Crohn’s disease (CD)

Diarrhoea usually non-bloody
Weight loss more prominent
Upper gastrointestinal symptoms, mouth ulcers, perianal disease
Abdominal mass palpable in the right iliac fossa

Ulcerative colitis (UC)

Bloody diarrhoea more common
Abdominal pain in the left lower quadrant
Tenesmus

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3
Q

principle difference in extra-intestinal features of crohn’s and ulcerative colitis

A

Crohn’s disease (CD)

Gallstones are more common secondary to reduced bile acid reabsorption
Oxalate renal stones* (*impaired bile acid rebsorption increases the loss calcium in the bile. Calcium normally binds oxalate.)

Ulcerative colitis (UC)
Primary sclerosing cholangitis more common
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4
Q

principle difference in complications of crohn’s and ulcerative colitis

A

crohn’s :
Obstruction, fistula, colorectal cancer

UC:
Risk of colorectal cancer high in UC than CD

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5
Q

principle difference in pathology of crohn’s and ulcerative colitis

A

CD
Lesions may be seen anywhere from the mouth to anus
Skip lesions may be present

UC
Inflammation always starts at rectum and never spreads beyond ileocaecal valve
Continuous disease

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6
Q

principle difference in histology of crohn’s and ulcerative colitis

A

cd

Inflammation in all layers from mucosa to serosa
increased goblet cells
granulomas

uc

No inflammation beyond submucosa (unless fulminant disease) - inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

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7
Q

principle difference in endoscopy of crohn’s and ulcerative colitis

A

cd

Deep ulcers, skip lesions - ‘cobble-stone’ appearance

uc

Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)

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8
Q

principle difference in radiology of crohn’s and ulcerative colitis

A

CD

Small bowel enema
high sensitivity and specificity for examination of the terminal ileum
strictures: 'Kantor's string sign'
proximal bowel dilation
'rose thorn' ulcers
fistulae

UC

Barium enema
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

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9
Q

what is coeliac disease

A

Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-B8 (80%) as well as HLA-DR3 and HLA-DR7

features:
Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia

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10
Q

what is haemochromatosis

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*. It is often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia

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11
Q

what is Primary sclerosing cholangitis

A

Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

Features
cholestasis: jaundice and pruritus
right upper quadrant pain
fatigue

Investigation
ERCP is the standard diagnostic tool, showing multiple biliary strictures giving a ‘beaded’ appearance
ANCA may be positive
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

Complications
cholangiocarcinoma (in 10%)
increased risk of colorectal cancer

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12
Q

some causes of dysphagia

A

Oesophageal cancer Dysphagia may be associated with weight loss, anorexia or vomiting during eating
Past history may include Barrett’s oesophagus, GORD, excessive smoking or alcohol use

Oesophagitis May be history of heartburn
Odynophagia but no weight loss and systemically well

Oesophageal candidiasis There may be a history of HIV or other risk factors such as steroid inhaler use

Achalasia Dysphagia of both liquids and solids from the start
Heartburn
Regurgitation of food - may lead to cough, aspiration pneumonia etc

Pharyngeal pouch More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen

Systemic sclerosis Other features of CREST syndrome may be present, namely Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is decreased. This contrasts to achalasia where the LES pressure is increased

Myasthenia gravis Other symptoms may include extraocular muscle weakness or ptosis
Dysphagia with liquids as well as solids

Globus hystericus May be history of anxiety
Symptoms are often intermittent and relieved by swallowing
Usually painless - the presence of pain should warrant further investigation for organic causes

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13
Q

what is Telangiectasia

A

Telangiectasias are small, widened blood vessels on the skin. They are usually harmless, but may be associated with several diseases.

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14
Q

what is Ascending cholangitis and how is it managed?

A

Ascending cholangitis is a bacterial infection of the biliary tree. The most common predisposing factor is gallstones.

Charcot’s triad of right upper quadrant (RUQ) pain, fever and jaundice occurs in about 20-50% of patients
fever is the most common feature, seen in 90% of patients
RUQ pain 70%
jaundice 60%
hypotension and confusion are also common

Management
intravenous antibiotics
endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

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15
Q

IBS features, diagnosis and investigation.

A

NICE published clinical guidelines on the diagnosis and management of irritable bowel syndrome (IBS) in 2008

The diagnosis of IBS should be considered if the patient has had the following for at least 6 months:

ABC =
abdominal pain, and/or
bloating, and/or
change in bowel habit

so long as there are no red flags. e.g. weight loss, rectal bleeding, family history of bowel or ovarian cancer.

A positive diagnosis of IBS should be made if the patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:
altered stool passage (straining, urgency, incomplete evacuation)
abdominal bloating (more common in women than men), distension, tension or hardness
symptoms made worse by eating
passage of mucus

Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis

Red flag features should be enquired about:
rectal bleeding
unexplained/unintentional weight loss
family history of bowel or ovarian cancer
onset after 60 years of age

Suggested primary care investigations are:
full blood count
ESR/CRP
coeliac disease screen (tissue transglutaminase antibodies)

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16
Q

what is Primary sclerosing cholangitis - features, associations, investigation, complications

A

Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

Associations
ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
Crohn’s (much less common association than UC)
HIV

Features
cholestasis: jaundice and pruritus
right upper quadrant pain
fatigue

Investigation
ERCP is the standard diagnostic tool, showing multiple biliary strictures giving a ‘beaded’ appearance
ANCA may be positive
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

Complications
cholangiocarcinoma (in 10%)
increased risk of colorectal cancer

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17
Q

how do PPIs work?

A

Proton pump inhibitors (PPI) are a group of drugs which profoundly reduce acid secretion in the stomach. They irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase) of the gastric parietal cell

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18
Q

Helicobacter pylori: tests

A

Urea breath test
patients consume a drink containing carbon isotope 13 (13C) enriched urea
urea is broken down by H. pylori urease
after 30 mins patient exhale into a glass tube
mass spectrometry analysis calculates the amount of 13C CO2
should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
sensitivity 95-98%, specificity 97-98%

Rapid urease test (e.g. CLO test)
biopsy sample is mixed with urea and pH indicator
colour change if H pylori urease activity
sensitivity 90-95%, specificity 95-98%

Serum antibody
remains positive after eradication
sensitivity 85%, specificity 80%

Culture of gastric biopsy
provide information on antibiotic sensitivity
sensitivity 70%, specificity 100%

Gastric biopsy
histological evaluation alone, no culture
sensitivity 95-99%, specificity 95-99%

Stool antigen test
sensitivity 90%, specificity 95%

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19
Q

4 causes of (usually) acute diarrhoea

A

Gastroenteritis May be accompanied by abdominal pain or nausea/vomiting

Diverticulitis Classically causes left lower quadrant pain, diarrhoea and fever

Antibiotic therapy More common with broad spectrum antibiotics. Clostridium difficile is also seen with antibiotic use

Constipation causing overflow A history of alternating diarrhoea and constipation may be given. May lead to faecal incontinence in the elderly

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20
Q

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)

A

King’s College Hospital criteria for liver transplantation (in paracetamol liver failure)

Arterial pH 100 seconds
grade III or IV encephalopathy

Arterial pH 6.5 (PT >100 seconds)
creatinine > 300 µmol/l
encephalopathy (of grade III or IV).

These three are markers of coagulopathy, kidney function and mental status.

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21
Q

Paracetamol overdose: management

A

The following is based on 2012 Commission on Human Medicines (CHM) review of paracetamol overdose management. The big change in these guidelines was the removal of the ‘high-risk’ treatment line on the normogram. All patients are therefore treated the same regardless of risk factors for hepatotoxicity. The National Poisons Information Service/TOXBASE should always be consulted for situations outside of the normal parameters.

Acetylcysteine should be given if:
there is a staggered overdose* or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or
the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity

Acetylcysteine is now infused over 1 hour (rather than the previous 15 minutes) to reduce the number of adverse effects.

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22
Q

complications of coeliac disease

A

Complications
anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies

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23
Q

coeliac disesase vs Crohn’s incidence

A

Coeliac disease is more common than Crohn’s by a factor of around 100.

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24
Q

what happens in Primary biliary cirrhosis

A

Primary biliary cirrhosis is a chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

Associations
Sjogren's syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

Diagnosis
anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
smooth muscle antibodies in 30% of patients
raised serum IgM

NB - don’t get tricked “presence of auto-antibodies against components of the pyruvate dehydrogenase complex”

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25
Interpreting hepatitis B serology:
Interpreting hepatitis B serology: surface antigen (HBsAg) is the first marker to appear and causes the production of anti-HBs HBsAg normally implies acute disease (present for 1-6 months) if HBsAg is present for > 6 months then this implies chronic disease (i.e. Infective) Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months HbeAg results from breakdown of core antigen from infected liver cells as is therefore a marker of infectivity Example results previous immunisation: anti-HBs positive, all others negative previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive
26
C. diff features and management
Clostridium difficile is a Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis. Clostridium difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics. Clindamycin is historically associated with causing Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation cephalosporins are now the leading cause of Clostridium difficile. ``` Features diarrhoea abdominal pain a raised white blood cell count is characteristic if severe toxic megacolon may develop ``` Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool Management first-line therapy is oral metronidazole for 10-14 days if severe or not responding to metronidazole then oral vancomycin may be used for life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used
27
how is the severity of liver cirrhosis assessed
The Child-Pugh classification is a scoring system to assess the severity of liver cirrhosis Score 1 2 3 Bilirubin (µmol/l) 50 Albumin (g/l) >35 28-35 6 Encephalopathy none mild marked Ascites none mild marked Summation of the scores allows the severity to be graded either A, B or C: < 7 = A 7-9 = B > 9 = C
28
Acute treatment of variceal haemorrhage
Acute treatment of variceal haemorrhage ABC: patients should ideally be resuscitated prior to endoscopy correct clotting: FFP, vitamin K vasoactive agents: terlipressin is currently the only licensed vasoactive agent and is supported by NICE guidelines. It has been shown to be of benefit in initial haemostasis and preventing rebleeding. Octreotide may also be used although there is some evidence that terlipressin has a greater effect on reducing mortality prophylactic antibiotics have been shown in multiple meta-analyses to reduce mortality in patients with liver cirrhosis endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation Sengstaken-Blakemore tube if uncontrolled haemorrhage Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
29
Prophylaxis of variceal haemorrhage
propranolol: reduced rebleeding and mortality compared to placebo endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. It should be performed at two-weekly intervals until all varices have been eradicated. Proton pump inhibitor cover is given to prevent EVL-induced ulceration
30
Management of hepatitis B
Management of hepatitis B pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of chronic carriers. A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy whilst NICE still advocate the use of pegylated interferon firstl-line other antiviral medications are increasingly used with an aim to suppress viral replication (not in a dissimilar way to treating HIV patients) examples include tenofovir and entecavir
31
features of Hep B infection
The features of hepatitis B include fever, jaundice and elevated liver transaminases.
32
Alcohol: units The government currently recommend the following:
The government currently recommend the following: men: should drink no more than 21 units of alcohol per week (and no more than 4 units in any one day) women: should drink no more than 14 units of alcohol per week (and no more than 3 units in any one day) One unit of alcohol is equal to 10 ml of alcohol. The 'strength' of an alcoholic drink is determined by the 'alcohol by volume' (ABV). Examples of one unit of alcohol: 25ml single measure of spirits (ABV 40%) a third of a pint of beer (ABV 5 to 6%) half a 175ml 'standard' glass of red wine (ABV 12%) To calculate the number of units in a drink multiply the number of millilitres by the ABV and divide by 1,000. For example: half a 175ml 'standard' glass of red wine = 87.5 * 12 / 1000 = 1.05 units one bottle of wine = 750 * 12 / 1000 = 9 units one pint of 5% beer or lager = 568 * 5 / 1000 = 2.8 units
33
complications and management of hepatitis C infection
Complications chronic infection (80-85%) - only 15-20% of patients will clear the virus after an acute infection and hence the majority will develop chronic hepatitis C cirrhosis (20-30% of those with chronic disease) hepatocellular cancer cryoglobulinaemia porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse Management of chronic infection currently a combination of pegylated interferon-alpha and ribavirin are used up to 55% of patients successfully clear the virus, with success rates of around 80% for some strains the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
34
transmission of hepatitis C
Transmission the risk of transmission during a needle stick injury is about 2% the vertical transmission rate from mother to child is about 6% breast feeding is not contraindicated in mothers with hepatitis C the risk of transmitting the virus during sexual intercourse is probably less than 5%
35
what is Murphy's sign.
(arrest of inspiration on palpation of the RUQ)
36
Acute cholecystitis features
Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder. The patient may be pyrexial and Murphy's sign positive (arrest of inspiration on palpation of the RUQ)
37
features of Viral hepatitis
``` Common symptoms include: nausea and vomiting, anorexia myalgia lethargy right upper quadrant (RUQ) pain ``` Questions may point to risk factors such as foreign travel or intravenous drug use.
38
features of Congestive hepatomegaly
The liver only usually causes pain if stretched. One common way this can occur is as a consequence of congestive heart failure. In severe cases cirrhosis may occur.
39
features of Biliary colic
RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common. It is sometimes taught that patients are female, forties, fat and fair although this is obviously a generalisation.
40
features of Acute cholecystitis
Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder. The patient may be pyrexial and Murphy's sign positive (arrest of inspiration on palpation of the RUQ)
41
features of Ascending cholangitis
An infection of the bile ducts commonly secondary to gallstones. Classically presents with a triad of: fever (rigors are common) RUQ pain jaundice
42
features of Gallstone ileus
This describes small bowel obstruction secondary to an impacted gallstone. It may develop if a fistula forms between a gangrenous gallbladder and the duodenum. Abdominal pain, distension and vomiting are seen.
43
features of Cholangiocarcinoma
Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
44
features of Acute pancreatitis
Usually due to alcohol or gallstones Severe epigastric pain Vomiting is common Examination may reveal tenderness, ileus and low-grade fever Periumbilical discolouration (Cullen's sign) and flank discolouration (Grey-Turner's sign) is described but rare
45
features of Pancreatic cancer
Painless jaundice is the classical presentation of pancreatic cancer. However pain is actually a relatively common presenting symptom of pancreatic cancer. Anorexia and weight loss are common
46
features of Amoebic liver abscess
Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
47
Alcohol - problem drinking: detection and assessment
AUDIT FAST CAGE ICD-10 definitions
48
AUDIT questionnaire
AUDIT 10 item questionnaire, please see the link takes about 2-3 minutes to complete has been shown to be superior to CAGE and biochemical markers for predicting alcohol problems minimum score = 0, maximum score = 40 a score of 8 or more in men, and 7 or more in women, indicates a strong likelihood of hazardous or harmful alcohol consumption a score of 15 or more in men, and 13 or more in women, is likely to indicate alcohol dependence AUDIT-C is an abbreviated form consisting of 3 questions
49
FAST questionnaire
FAST 4 item questionnaire minimum score = 0, maximum score = 16 the score for hazardous drinking is 3 or more with relation to the first question 1 drink = 1/2 pint of beer or 1 glass of wine or 1 single spirits if the answer to the first question is 'never' then the patient is not misusing alcohol if the response to the first question is 'Weekly' or 'Daily or almost daily' then the patient is a hazardous, harmful or dependent drinker. Over 50% of people will be classified using just this one question 1 MEN: How often do you have EIGHT or more drinks on one occasion? WOMEN: How often do you have SIX or more drinks on one occasion? 2 How often during the last year have you been unable to remember what happened the night before because you had been drinking? 3 How often during the last year have you failed to do what was normally expected of you because of drinking? 4 In the last year has a relative or friend, or a doctor or other health worker been concerned about your drinking or suggested you cut down?
50
CAGE questionnaire
CAGE well known but recent research has questioned it's value as a screening test two or more positive answers is generally considered a 'positive' result C Have you ever felt you should Cut down on your drinking? A Have people Annoyed you by criticising your drinking? G Have you ever felt bad or Guilty about your drinking? E Have you ever had a drink in the morning to get rid of a hangover (Eye opener)?
51
Ulcerative colitis: management
The severity of UC is usually classified as being mild, moderate or severe: 1 - mild: 6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) Inducing remission treatment depends on the extent and severity of disease 1 - rectal (topical) aminosalicylates or steroids: for distal colitis 2 - oral aminosalicylates 3 - oral prednisolone is usually used second-line for patients who fail to respond to aminosalicylates. NICE recommend waiting around 4 weeks before deciding if first-line treatment has failed severe colitis should be treated in hospital. Intravenous steroids are usually given first-line Maintaining remission 1 - oral aminosalicylates e.g. mesalazine 2 - azathioprine and mercaptopurine - methotrexate is not recommended for the management of UC (in contrast to Crohn's disease). there is some evidence that probiotics may prevent relapse in patients with mild to moderate disease
52
what is secondary amenorrhoea
Secondary amenorrhea is when a woman who has been having normal menstrual cycles stops getting her periods for 6 months or longer. Women who are pregnant, breastfeeding, or in menopause are not considered to have secondary amenorrhea.
53
what is autoimmune hepatitis
Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present Features may present with signs of chronic liver disease acute hepatitis: fever, jaundice etc (only 25% present in this way) amenorrhoea (common) ANA/SMA/LKM1 antibodies, raised IgG levels liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis Management steroids, other immunosuppressants e.g. azathioprine liver transplantation
54
what is coryza
(pathology) Inflammation of the mucous membranes lining the nasal cavity, usually causing a running nose, nasal congestion and loss of smell. so coryzal symptoms are seen in the common cold
55
what is Gilbert's syndrome
Gilbert's syndrome is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronyl transferase. The prevalence is approximately 1-2% in the general population ``` Features unconjugated hyperbilinaemia (i.e. not in urine) jaundice may only be seen during an intercurrent illness ``` Investigation and management investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid no treatment required *the exact mode of inheritance is still a matter of debate
56
Crohn's disease: management
General points 1 - stop smoking 2 - patchy evidence to stop NSAIDS and COC Inducing remission 1 - glucocorticoids (oral, topical or intravenous) ( Budesonide is an alternative in a subgroup) 2 - enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children) 3 - 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective 4 - azathioprine or mercaptopurine* (not used as mono therapy.) Methotrexate is an alternative to azathioprine 5 - infliximab is useful in refractory disease and fistulating Crohn's. 6 - metronidazole is often used for isolated peri-anal disease Maintaining remission 1 - stopping smoking (smoking makes Crohn's worse, but may help ulcerative colitis) 2 - azathioprine or mercaptopurine is used first-line to maintain remission 3 - methotrexate is used second-line 4 --5-ASA drugs (e.g. mesalazine) should be considered if a patient has had previous surgery Surgery around 80% of patients with Crohn's disease will eventually have surgery *assess thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine
57
Hepatocellular carcinoma risk factors
``` The main risk factor for developing HCC is liver cirrhosis, for example secondary* to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis. Other risk factors include: alpha-1 antitrypsin deficiency hereditary tyrosinosis glycogen storage disease aflatoxin drugs: oral contraceptive pill, anabolic steroids porphyria cutanea tarda male sex diabetes mellitus, metabolic syndrome ``` Features tends to present late features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly possible presentation is decompensation in a patient with chronic liver disease
58
Hepatocellular carcinoma screening
Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as: patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis men with liver cirrhosis secondary to alcohol
59
what is the waterlow score
The Waterlow score is used to estimate the risk of a patient developing a pressure sore. Whilst this includes an assessment of malnutrition as one of it's components the Waterlow score is not designed to screen for malnutrition.
60
screening and management of malnutrition
Screening for malnutrition if mostly done using MUST (Malnutrition Universal Screen Tool). A link is provided to a copy of the MUST score algorithm. it should be done on admission to care/nursing homes and hospital, or if there is concern. For example an elderly, thin patient with pressure sores it takes into account BMI, recent weight change and the presence of acute disease categorises patients into low, medium and high risk Management of malnutrition is difficult. NICE recommend the following points: dietician support if the patient is high-risk a 'food-first' approach with clear instructions (e.g. 'add full-fat cream to mashed potato'), rather than just prescribing oral nutritional supplements (ONS) such as Ensure if ONS are used they should be taken between meals, rather than instead of meals
61
cut off point for toxic megacolon in UC
Toxic megacolon - transverse colon diameter > 6 cm
62
H pylori tests other than urea breath test
Rapid urease test (e.g. CLO test) biopsy sample is mixed with urea and pH indicator colour change if H pylori urease activity sensitivity 90-95%, specificity 95-98% Serum antibody remains positive after eradication sensitivity 85%, specificity 80% Culture of gastric biopsy provide information on antibiotic sensitivity sensitivity 70%, specificity 100% Gastric biopsy histological evaluation alone, no culture sensitivity 95-99%, specificity 95-99% Stool antigen test sensitivity 90%, specificity 95%
63
government recommendations on alcohol consumption
The government currently recommend the following: men: should drink no more than 21 units of alcohol per week (and no more than 4 units in any one day) women: should drink no more than 14 units of alcohol per week (and no more than 3 units in any one day)
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Acute pancreatitis: causes
The vast majority of cases in the UK are caused by gallstones and alcohol Popular mnemonic is GET SMASHED Gallstones Ethanol Trauma Steroids Mumps (other viruses include Coxsackie B) Autoimmune (e.g. polyarteritis nodosa), Ascaris infection Scorpion venom Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia ERCP Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate) *pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
65
oesophageal cancer risk factors
``` Risk factors smoking alcohol GORD Barrett's oesophagus achalasia Plummer-Vinson syndrome rare: coeliac disease, scleroderma ``` Helicobacter pylori may actually be protective against oesophageal cancer (reduce gastric acid secretion)
66
Acute treatment of variceal haemorrhage
Acute treatment of variceal haemorrhage ABC: patients should ideally be resuscitated prior to endoscopy correct clotting: FFP, vitamin K vasoactive agents: terlipressin is currently the only licensed vasoactive agent and is supported by NICE guidelines. It has been shown to be of benefit in initial haemostasis and preventing rebleeding. Octreotide may also be used although there is some evidence that terlipressin has a greater effect on reducing mortality prophylactic antibiotics have been shown in multiple meta-analyses to reduce mortality in patients with liver cirrhosis endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation Sengstaken-Blakemore tube if uncontrolled haemorrhage Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail Tranexamic acid is used to reduce bleeding in a number of situations such as menorrhagia and is being trialled for traumatic head injuries but at the current time it is not recommend for use in patients with upper gastrointestinal bleeds.
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Prophylaxis of variceal haemorrhage
Prophylaxis of variceal haemorrhage propranolol: reduced rebleeding and mortality compared to placebo endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. It should be performed at two-weekly intervals until all varices have been eradicated. Proton pump inhibitor cover is given to prevent EVL-induced ulceration
68
The diagnosis of IBS should be considered if
The diagnosis of IBS should be considered if the patient has had the following for at least 6 months: abdominal pain, and/or bloating, and/or change in bowel habit
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what is hepatorenal syndrome
This is the development of acute kidney injury in a patient who usually has advanced liver disease, either cirrhosis or alcoholic hepatitis. Marked periph- eral vasodilatation leads to a fall in systemic vascular resistance and effective hypovolaemia. This in turn results in vasoconstriction of the renal circulation with markedly reduced renal perfusion. The diagnosis is made on the basis of oliguria, a rising serum creatinine (over days to weeks), a low urine sodium (<10 mmol/L), absence of other causes of acute kidney injury, and lack of improvement after volume expansion (if necessary) and withdrawal of diu- retics. The prognosis is poor, and renal failure will often only respond to an improvement in liver function. Albumin infusion and terlipressin have been used with some success.
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management of hepatorenal syndrome
Management options vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation volume expansion with 20% albumin transjugular intrahepatic portosystemic shunt
71
diagnosis of coeliac disease
Diagnosis is made by a combination of immunology and jejunal biopsy. Villous atrophy and immunology normally reverses on a gluten-free diet. NICE issued guidelines on the investigation of coeliac disease in 2009. If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing. Immunology tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE endomyseal antibody (IgA) anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE anti-casein antibodies are also found in some patients ``` Jejunal biopsy villous atrophy crypt hyperplasia increase in intraepithelial lymphocytes lamina propria infiltration with lymphocytes ```
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what is Waterhouse-Friderichsen syndrome
Waterhouse-Friderichsen syndrome describes adrenal gland failure secondary to previous adrenal haemorrhage that was caused by severe bacterial infection. This patient has bilateral adrenal calcifications most likely secondary to Waterhouse-Friderichsen syndrome. Adrenal insufficiency is an important if uncommon cause of abdominal pain.
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Alcohol - problem drinking: management
Nutritional support SIGN recommends alcoholic patients should receive oral thiamine if their 'diet may be deficient' Drugs used benzodiazepines for acute withdrawal disulfram: promotes abstinence - alcohol intake causes severe reaction due to inhibition of acetaldehyde dehydrogenase. Patients should be aware that even small amounts of alcohol (e.g. In perfumes, foods, mouthwashes) can produce severe symptoms. Contraindications include ischaemic heart disease and psychosis acamprosate: reduces craving, known to be a weak antagonist of NMDA receptors, improves abstinence in placebo controlled trials
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Bile-acid malabsorption - what is it, how do you investigate it and how do you manage it
Bile-acid malabsorption is a cause of chronic diarrhoea. This may be primary, due to an excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. Secondary causes are often seen in patients with ileal disease, such as with Crohn's. Other secondary causes include: cholecystectomy coeliac disease small intestinal bacterial overgrowth Investigation the test of choice is SeHCAT nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT) scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT Management bile acid sequestrants e.g. cholestyramine
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what is Non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is now the most common cause of liver disease in the developed world. It is largely caused by obesity and describes a spectrum of disease ranging from: steatosis - fat in the liver steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below progressive disease may cause fibrosis and liver cirrhosis NAFLD is thought to represent the hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis
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what is Non-alcoholic steatohepatitis (NASH)
Non-alcoholic steatohepatitis (NASH) is a term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse. It is relatively common and though to affect around 3-4% of the general population. The progression of disease in patients with NASH may be responsible for a proportion of patients previously labelled as cryptogenic cirrhosis ``` Associated factors obesity hyperlipidaemia type 2 diabetes mellitus jejunoileal bypass sudden weight loss/starvation ``` ``` Features usually asymptomatic hepatomegaly ALT is typically greater than AST increased echogenicity on ultrasound ``` Management the mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring there is ongoing research into the role of gastric banding and insulin-sensitising drugs (e.g. Metformin)
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what is angiodysplasia
Angiodysplasia is a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis, although this is debated. Angiodysplasia is generally seen in elderly patients
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complications of coeliac disease
Complications anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease) hyposplenism osteoporosis, osteomalacia lactose intolerance enteropathy-associated T-cell lymphoma of small intestine subfertility, unfavourable pregnancy outcomes rare: oesophageal cancer, other malignancies
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management of IBS
The management of irritable bowel syndrome (IBS) is often difficult and varies considerably between patients. NICE issued guidelines in 2008 First-line pharmacological treatment - according to predominant symptom pain: antispasmodic agents constipation: laxatives but avoid lactulose diarrhoea: loperamide is first-line Second-line pharmacological treatment low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors Other management options psychological interventions - if symptoms do not respond to pharmacological treatments after 12 months and who develop a continuing symptom profile (refractory IBS), consider referring for cognitive behavioural therapy, hypnotherapy or psychological therapy complementary and alternative medicines: 'do not encourage use of acupuncture or reflexology for the treatment of IBS'
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IBS dietary advice
General dietary advice have regular meals and take time to eat avoid missing meals or leaving long gaps between eating drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas restrict tea and coffee to 3 cups per day reduce intake of alcohol and fizzy drinks consider limiting intake of high-fibre food (for example, wholemeal or high-fibre flour and breads, cereals high in bran, and whole grains such as brown rice) reduce intake of 'resistant starch' often found in processed foods limit fresh fruit to 3 portions per day for diarrhoea, avoid sorbitol for wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).
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what is Zollinger-Ellison syndrome
Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome Features multiple gastroduodenal ulcers diarrhoea malabsorption Diagnosis fasting gastrin levels: the single best screen test secretin stimulation test Zollinger-Ellison syndrome typically presents with multiple gastroduodenal ulcers causing abdominal pain and diarrhoea. High-dose proton pump inhibitors are needed to control the symptoms. Around a third of patients may have multiple endocrine neoplasia type I (MEN-I), explaining the hyperparathyroidism in this patient.
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what happens in wilson's disease
Wilson's disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13. The onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea: liver: hepatitis, cirrhosis neurological: basal ganglia degeneration, speech and behavioural problems are often the first manifestations. Also: asterixis, chorea, dementia Kayser-Fleischer rings renal tubular acidosis (esp. Fanconi syndrome) haemolysis blue nails
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diagnosis and management of wilsons disease
Diagnosis reduced serum caeruloplasmin increased 24hr urinary copper excretion Management penicillamine (chelates copper) has been the traditional first-line treatment trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future tetrathiomolybdate is a newer agent that is currently under investigation
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management of dyspepsia
``` In 2014 NICE updated their guidelines for the management of dyspepsia. These take into account the age of the patient (whether younger or older than 55 years) and the presence or absence of 'alarm signs': chronic gastrointestinal bleeding progressive unintentional weight loss progressive difficulty swallowing persistent vomiting iron deficiency anaemia epigastric mass suspicious barium meal ``` Deciding whether urgent referral for endoscopy is needed Urgent referral (within 2 weeks) is indicated for patients with any alarm signs irrespective of age Routine endoscopic investigation of patients of any age, presenting with dyspepsia and without alarm signs is not necessary, however Patients aged 55 years and over should be referred urgently for endoscopy if dyspepsia symptoms are: recent in onset rather than recurrent and unexplained (e.g. New symptoms which cannot be explained by precipitants such as NSAIDs) and persistent: continuing beyond a period that would normally be associated with self-limiting problems (e.g. Up to four to six weeks, depending on the severity of signs and symptoms) Managing patients who do not meet referral criteria ('undiagnosed dyspepsia') This can be summarised at a step-wise approach 1. Review medications for possible causes of dyspepsia 2. Lifestyle advice 3. Trial of full-dose PPI for one month* 4. 'Test and treat' using carbon-13 urea breath test *it is unclear from studies whether a trial of a PPI or a 'test and treat' should be used first
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management of an acute upper GI bleed
NICE published guidelines in 2012 on the management of acute upper gastrointestinal bleeding which is most commonly due to either peptic ulcer disease or oesophageal varices. Some of the key points are detailed below. Risk assessment use the Blatchford score at first assessment, and the full Rockall score after endoscopy Patients with a Blatchford score of 0 may be considered for early discharge Resuscitation ABC, wide-bore intravenous access * 2 platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal prothrombin complex concentrate to patients who are taking warfarin and actively bleeding Endoscopy should be offered immediately after resuscitation in patients with a severe bleed all patients should have endoscopy within 24 hours Management of non-variceal bleeding NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy if further bleeding then options include repeat endoscopy, interventional radiology and surgery Management of variceal bleeding terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy) band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
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UC management
Inducing remission treatment depends on the extent and severity of disease rectal (topical) aminosalicylates or steroids: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates oral aminosalicylates oral prednisolone is usually used second-line for patients who fail to respond to aminosalicylates. NICE recommend waiting around 4 weeks before deciding if first-line treatment has failed severe colitis should be treated in hospital. Intravenous steroids are usually given first-line Maintaining remission oral aminosalicylates e.g. mesalazine azathioprine and mercaptopurine methotrexate is not recommended for the management of UC (in contrast to Crohn's disease) there is some evidence that probiotics may prevent relapse in patients with mild to moderate disease
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Examples of one unit of alcohol:
Examples of one unit of alcohol: 25ml single measure of spirits (ABV 40%) a third of a pint of beer (ABV 5 to 6%) half a 175ml 'standard' glass of red wine (ABV 12%)
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diagnosis of coeliac disease
Diagnosis is made by a combination of immunology and jejunal biopsy. Villous atrophy and immunology normally reverses on a gluten-free diet. NICE issued guidelines on the investigation of coeliac disease in 2009. If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing. Immunology tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE endomyseal antibody (IgA) anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE anti-casein antibodies are also found in some patients ``` Jejunal biopsy villous atrophy crypt hyperplasia increase in intraepithelial lymphocytes lamina propria infiltration with lymphocytes ``` Rectal gluten challenge has been described but is not widely used
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what is grave's disease
Graves' disease (or Flajani-Basedow-Graves disease) is an autoimmune disease. It most commonly affects the thyroid, frequently causing it to enlarge to twice its size or more (goitre), become overactive, with related hyperthyroid symptoms such as increased heartbeat, muscle weakness, disturbed sleep, and irritability. It can also affect the eyes, causing bulging eyes (exophthalmos). It affects other systems of the body, including the skin, heart, circulation and nervous system. Thyroid stimulating immunoglobulins recognize and bind to the thyrotropin receptor (TSH receptor). It mimics the TSH to that receptor and activates the secretion of thyroxine (T4) and triiodothyronine (T3), and the actual TSH level will decrease in the blood plasma. The TSH levels fall because the hypothalamus-pituitary-thyroid negative feedback loop is working. The result is very high levels of circulating thyroid hormones and the negative feedback regulation will not work for the thyroid gland.[citation needed] The trigger for autoantibody production is not known. There appears to be a genetic predisposition for Graves' disease, suggesting some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.[6] To date, no clear genetic defect has been found to point to a monogenic cause.
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Primary biliary cirrhosis is most characteristically associated with:
Anti-mitochondrial antibodies Primary biliary cirrhosis - the M rule IgM anti-Mitochondrial antibodies, M2 subtype Middle aged females
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what is PBC
Primary biliary cirrhosis (PBC) is characterized by a T-lymphocyte-mediated attack on small intralobular bile ducts (picture 1A-B). A continuous assault on the bile duct epithelial cells leads to their gradual destruction and eventual disappearance (picture 2). The sustained loss of intralobular bile ducts causes the signs and symptoms of cholestasis, and eventually results in cirrhosis and liver failure The precise cause of PBC is unknown but, as with other autoimmune diseases, is related to genetic susceptibility and environmental factors
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management of PBC
primary biliary cirrhosis ``` Management pruritus: cholestyramine fat-soluble vitamin supplementation ursodeoxycholic acid liver transplantation e.g. if bilirubin > 100 (PBC is a major indication) - recurrence in graft can occur but is not usually a problem ```
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how do the Aminosalicylate drugs work?
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis Sulphasalazine a combination of sulphapyridine (a sulphonamide) and 5-ASA many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia other side-effects are common to 5-ASA drugs (see mesalazine) Mesalazine a delayed release form of 5-ASA sulphapyridine side-effects seen in patients taking sulphasalazine are avoided mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis Olsalazine two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria *pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
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most common cause of HCC
Hepatocellular carcinoma (HCC) is the third most common cause of cancer worldwide. Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe. The main risk factor for developing HCC is liver cirrhosis, for example secondary* to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis
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THE rule in PBC diagnosis
Primary biliary cirrhosis - the M rule IgM anti-Mitochondrial antibodies, M2 subtype Middle aged females it commonly coexists with other autoimmune diseases such as thyroid.
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what is autoimmune hepatitis?
Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present Features may present with signs of chronic liver disease acute hepatitis: fever, jaundice etc (only 25% present in this way) amenorrhoea (common) ANA/SMA/LKM1 antibodies, raised IgG levels liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis Management steroids, other immunosuppressants e.g. azathioprine liver transplantation
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what is Gilbert's syndrome
Gilbert's syndrome Gilbert's syndrome is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronyl transferase. The prevalence is approximately 1-2% in the general population ``` Features unconjugated hyperbilinaemia (i.e. not in urine) jaundice may only be seen during an intercurrent illness ``` Investigation and management investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid no treatment required *the exact mode of inheritance is still a matter of debate An isolated hyperbilirubinaemia in a 22-year-old male is likely to be secondary to Gilbert's syndrome. The normal dipstix urinalysis excludes Dubin-Johnson and Rotor syndrome as these both produce a conjugated bilirubinaemia. Viral infections are common triggers for a rise in the bilirubin in patients with Gilbert's
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assessment and management of malnutrition
NICE define malnutrition as the following: a Body Mass Index (BMI) of less than 18.5; or unintentional weight loss greater than 10% within the last 3-6 months; or a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months Around 10% of patients aged over 65 years are malnourished, the vast majority of those living independently, i.e. not in hospital or care/nursing homes. Screening for malnutrition if mostly done using MUST (Malnutrition Universal Screen Tool). A link is provided to a copy of the MUST score algorithm. it should be done on admission to care/nursing homes and hospital, or if there is concern. For example an elderly, thin patient with pressure sores it takes into account BMI, recent weight change and the presence of acute disease categorises patients into low, medium and high risk Management of malnutrition is difficult. NICE recommend the following points: dietician support if the patient is high-risk a 'food-first' approach with clear instructions (e.g. 'add full-fat cream to mashed potato'), rather than just prescribing oral nutritional supplements (ONS) such as Ensure if ONS are used they should be taken between meals, rather than instead of meals
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what is barrett's oesophagus
Barrett's refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold. Histological features the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
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management of barrett's
Management endoscopic surveillance with biopsies high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett's the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
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risk assessment for acute upper gi bleed
use the Blatchford score at first assessment, and | the full Rockall score after endoscopy
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blatchford score components
``` urea haemoglobin systolic blood pressure pulse malaena syncope hepatic disease cardiac failure ```
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Child-Pugh classification of liver cirrhosis
``` Bilirubin (µmol/l) Albumin (g/l) Prothrombin time, prolonged by (s) Encephalopathy Ascites ```
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define adenoma
a benign tumour formed from glandular structures in epithelial tissue.
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lead time bias is best described as
A longer survival time because the disease is identified by screening and treated at an earlier stage If a screening test leads to a diagnosis before a patient has any symptoms, the patient’s survival time is increased because the date of diagnosis is earlier. This increase in survival time makes it seem as though screened patients are living longer when that may not be happening. This is called lead-time bias. It could be that the only reason the survival time appears to be longer is that the date of diagnosis is earlier for the screened patients. But the screened patients may die at the same time they would have without the screening test.
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what is LENGTH time bias
screening will inherently preferentially pick up cases that persist for a long period of time. these cases that persist for a long period of time tend to be less aggressive and have a longer survival period. thus it may look like screening increases survival time, but this may just be due to this LENGTH time bias.
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At what age does Cervical screening start in England?
25
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Cervical cancer has been linked to infection with which viruses?
Evidence strongly supports the link between Cervical cancer and the HPV virus types 16 and 18. HPV vaccination of girls aged 13-18 years old is now part of the UK screening schedule.
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``` In the UK, the National Screening Committee has set out criteria for screening and considers four elements: –Condition –Test –Treatment –Programme what is meant by these elements? ```
``` Condition: Important health problem Natural history understood Recognisable early stage Cost-effective primary prevention implemented ``` Test: Simple, safe, precise and validated screening test Distribution of test values in target population known, and cut-off value agreed Acceptable to population Agreed policy on further investigation Treatment: Effective intervention and evidence of early treatment producing better outcomes Facilities available Policies covering treatment Programme: Programme is acceptable to public and professionals Evidence-base to eligibility and inter-screening interval Benefits should outweigh harms Value for money Structures for quality assurance Evidence from RCTs that screening programme is effective
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what is PPV?
positive predictive value - the percentage of people with a positive screening test that actually turn out to have the disease. true positive/ all positive tests if I've tested positive, how likely is it that i have the disease
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what is NPV?
negative predictive value - if i test negative, how likely am i not to have the disease? true negative result/total negative tests.
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what is sensitivity of a test
those with a positive test result/ all of those who actually have the disease
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what is the specificity of a test
those with a correct negative result (true negative)/ all those tested who do not have the disease
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how does the prevalence of a disease affect a screening test's NPV and PPV
as prevalence decreases the PPV decreases and the NPV increases, the sensitivity and specificity do not change however. thus if a disease has a low prevalence the NPV might be 99% but the PPV only 8% and thus there would be no point screening. thus you should screen the high risk groups not to the low risk groups.
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what is the point of a screening test
screening is not about diagnosing people with a disease, but is about identifying those people who are more likely to have the disease so that they can go on to have the gold standard diagnostic tests.
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what is the healthy screenee effect ?
those people who turn up to screening tests are statistically more likely to be more healthy anyway. this is because they tend to be from more affluent socioeconomic groups that have less disease.
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what type of organ is the spleen
the largest lymphoid organ of the body. it has 2 anatomical components, the red and white pulp. the red pulp consists of sinuses lined by endothelial macrophages and the white pulp has a structure similar to lymphoid follicles.
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4 functions of the spleen
1 - sequestration and phagocytosis - old and damaged RBCs along with circulating foreign matter are removed. 2 - extramedullary haemopoiesis - can make RBCs in haematological stress such as haemolytic anaemia 3 - immune function - contains about 20% of the body's T and B cells. 4 - blood pooling - sequesters up to a third of platelets and RBCs that can be rapidly mobilised.
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causes of splenomegaly
1 - infection 2 - inflammation - RA, sarcoidosis, SLE 3 - haematological - haemolytic anaemia, haemoglobinopathies, leukaemias 4 - portal hypertension 5 - other - storage diseases, neoplasia massive = myelofibrosis, chronic myeloid leukaemia, chronic malaria.
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effect of hypersplenism
can be caused by any form of splenomegaly. most often due to - RA, portal hypertension, lymphoma, haem disorders. causes: 1 - pancytopenia 2 - haemolysis 3 - increased plasma volume treat underlying cause, sometimes require splenectomy.
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problems after splenectomy
- immediate increased platelet count for a few weeks which can cause thromboembolic problems. long term increase risk of massive infections esp pneumococcal.
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prophylaxis against infection after splenectomy
1 - eduction about risk and need for vigilance and early treatment. 2 - carry a card or bracelet to warn medics 3 - pneumococcal vaccine every 5 years 4 - annual influenza vaccine 5 - HiB vaccine 6 - long term antibiotics = penicillin 500 mg 12hrly or erythromycin if sensitive.
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when is splenic atrophy seen
in sickle cell disease due to infarction. in coeliac disease, sometimes in UC and a couple of other conditions. post-splenectomy haematological features seen.
124
what is a hernia
A hernia is the protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position. Abdominal hernias may be external (i.e. they emerge to the subcutaneous tissues as with inguinal hernias — so there is a lump to feel) or internal (such as with hiatus hernias, where there is no lump to feel).
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what is the hernia sac
• Sac. The sac is the peritoneal lining of the hernia. Within it are the contents of the hernia (usually intestine or omentum). The sac may be complete or incomplete (i.e. not surrounding all the contents), as is found in a sliding hernia.
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what is the Neck of the hernia
Neck. The neck of a hernia is the margin of the defect through which the hernia has emerged.
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what does it mean if a hernia is reducible
Reducible. A hernia is reducible when its contents can return to the abdominal cavity either spontaneously or with manipulation.
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what does it mean if a hernia is irreducible
Irreducible. The hernia cannot be reduced despite pressure or manipulation.
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what does it mean if a hernia is incarcerated
incarcerated. This term is usually used to describe an irreducible hernia where the irreducibility is due to adhesions within the sac in the absence of obstruction or strangulation. Some textbooks, however, define it as meaning a hernia which is irreducible because of faeces within the large bowel. Perhaps because of this confusion about the true definition of this term, it is best simply to refer to a hernia as being irreducible but not obstructed or strangulated
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what does it mean if a hernia is obstructed
Obstructed. The bowel within the hernia is obstructed. The patient may have the four cardinal signs of obstruction (pain, vomiting, distention and constipation).
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what does it mean if a hernia is strangulated
Strangulated. The blood supply to the contents of the hernia is occluded by pressure at the neck of the hernia. If the bowel is within the sac, the viability of the bowel is impaired. Usually, the veins are occluded first and then further swelling leads to arterial occlusion, which precedes gangrene developing. If the hernia contains only omentum, then this too can strangulate, but in this case bowel obstruction does not occur.
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what is a sliding hernia
Sliding hernia. A sliding hernia is one which contains a partially extraperitoneal structure, such as the caecum on the right or the sigmoid colon on the left. Therefore, the sac does not completely surround all the contents of the hernia. The importance of this is that particular care must be taken when excising the sac, to avoid damaging the bowel.
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what is Richter's hernia
Richter’s hernia (see Figure 12.1). This is where just part of the bowel wall is caught in the sac, and may become strangulated. Because only part of the bowel wall is in the sac, the patient is not usually obstructed.
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what is a herniotomy
• Herniotomy. This term is used to describe ligation and excision of the hernia sac.
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what does Herniorrhaphy mean?
Herniorrhaphy. This term is used for actual repair of the hernial defect.
136
what are the common congenital hernias and how do they occur
The commonest types of congenital hernias are inguinal and umbilical hernias appearing in childhood. Infantile inguinal hernias are usually seen in males. In males, when the testes develop and descend in utero they pass down and through the abdominal wall into the scrotum, forming what will subsequently develop into the inguinal canal. As this happens a finger-like projection of peritoneum, called the processus vaginalis, is carried down with the testicle. This usually obliterates, but if it remains patent fluid or abdominal contents may enter down it, forming either a hydrocoele (fluid around the testicle) or a hernia (containing bowel or omentum). The treatment is simple operative ligation of the processus vaginalis, i.e. a herniotomy. Umbilical hernias are com- monly seen in infants and represent failure of complete obliteration of the umbilical opening. They often disappear spontaneously and rarely strangu- late. Surgical repair should therefore be reserved for those which persist after the age of five and those with a defect greater than 1cm in size.
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give 7 factors that may predispose to acquiring a hernia
To acquire a hernia, a weakness of the abdominal wall has to be produced. The following may be predisposing factors: * Chronic cough * Chronic constipation (and straining to pass faeces) * Straining to void urine (prostatism) * Severe muscular effort (heavy lifting) * Obesity * Weakening with age * Surgery
138
how are groin hernias usually subdivided and how do they tend to present.
Groin hernias are the commonest type of hernia encountered in the finals, and indeed they account for about 75% of all hernias. They may be either femoral or inguinal. Inguinal hernias are further divided into direct and indirect. Inguinal hernias are proportionally more common in males than in females, and femoral hernias are proportionally more common in females than in males (possibly because of a wider pelvis and, hence, femoral canal). In both sexes, however, inguinal hernias are more common than femoral hernias in absolute numbers. Hernias may present in three ways: 1. As a lump (which may come and go; classically, the lump would appear on straining or lifting and disappear on lying down or when pressed on by the patient). 2. With pain in the groin. 3. Because of a complication (obstruction or strangulation). To understand groin hernias properly, some basic anatomical knowledge is required.
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how do femoral hernias occur
Femoral hernias emerge through the femoral canal, which normally con- tains only fat and lymph nodes. The medial border of the femoral ring (the upper and widest part of the femoral canal) is the sharp-edged lacu- nar ligament, which makes these hernias more prone to strangulation than inguinal hernias. Anteriorly is the inguinal ligament, posteriorly is the pectineal ligament and laterally is the femoral vein. Consideration of the position of the femoral canal will show why these hernias emerge below and lateral to the pubic tubercle. If identified, all femoral hernias should be repaired because of the risk of strangulation. Elective repair involves excision of the sac (herniotomy) and repair (herniorrhaphy), usually by suturing the inguinal ligament to the pectineal ligament with interrupted nonabsorbable sutures. Emergency repair is similar but usu- ally utilises an incision through the inguinal canal or abdominal wall so that the bowel can be carefully assessed for strangulation and a bowel resection performed if necessary.
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how do inguinal hernias occur
Inguinal hernias emerge into the subcutaneous tissues through the superfi- cial inguinal ring and thus emerge above and medial to the pubic tubercle (see Figure 12.2). They have, however, left the abdominal cavity above and lateral to the pubic tubercle to enter the inguinal canal. This point often confuses finals students, especially as in a thin patient a cough impulse or hernia bulge can be seen or palpated above and lateral to the pubic tuber- cle beneath the external oblique aponeurosis (i.e. it is within the inguinal canal and has not yet emerged from the superficial inguinal ring). Inguinal hernias are classified into direct and indirect. Indirect hernias leave the abdominal cavity through the deep inguinal ring along with the structures of the spermatic cord. Some of these may be due to a patent processus vaginalis (see ‘infantile hernias’) which has not presented until adult life. Direct inguinal hernias enter the inguinal canal ‘directly’ through a weakness or defect in its posterior wall. Both then emerge through the superficial inguinal ring. Indirect hernias, because of their close association with the spermatic cord, often then extend down into the scrotum. Direct hernias rarely extend into the scrotum. Students are often asked in exams to assess whether a groin hernia is inguinal or femoral. The key to this is the position of the pubic tubercle in relation to the point where the hernia emerges into the subcutaneous tissues. A hernia emerg- ing above and medial to the pubic tubercle is an inguinal hernia, whereas a hernia emerging below and lateral is a femoral hernia. Sometimes a hernia is so large that it may appear anywhere in relation to the pubic tubercle. In this case the key is to reduce the hernia, place your finger on the pubic tubercle and ask the patient to cough and see where the lump emerges from.
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how do you determine whether an inguinal hernia is direct or indirect
Your confidence can legitimately be increased by the knowl- edge that your examiner may not be able to get the correct answer himself. The basis of the test is to reduce the hernia, then apply pressure with a fin- ger over the deep inguinal ring. The patient should then be asked to cough or strain. If the hernia is controlled it is probably indirect, but if it comes out anyway it may be a direct hernia (most of those we say are direct are in fact indirect).
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where is the deep inguinal ring
Of some controversy is the actual site of the deep inguinal ring. Most surgical textbooks state that it is about 1.5 cm above the midpoint of the inguinal ligament, which is slightly lateral to the midinguinal point (the site of the femoral artery). However, most anatomy textbooks suggest that the deep inguinal ring is directly above the midinguinal point (i.e. above the femoral pulse), in which case the midpoint of the inguinal ligament becomes redundant as a landmark!
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how do you treat an inguinal hernia
The treatment of an inguinal hernia consists of excision of the sac (herniotomy) and repair of the posterior wall of the inguinal canal and deep inguinal ring (herniorrhaphy). The older operations involve suturing the posterior wall of the inguinal canal with nonabsorbable sutures, but repairs are now being introduced where a nylon mesh is used to close the defect, producing less tension in the sutures and therefore less pain and a lower risk of sutures cutting out leading to a recurrence of the hernia. Such nylon meshes can be inserted either at open operation or by a laparoscopic technique.
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Differential Diagnosis of a Lump in the Groin
hernia • Inguinal lymph nodes (often multiple and usually below the inguinal ligament) • Saphena varix, a dilated varicose vein at the sapheno-femoral junction (disappears on lying flat, and there may be other varicosities in the legs) • Femoral artery aneurysm (pulsatile) • Encysted hydrocoele of the cord (can get above it) • Lipoma of the cord • An incompletely descended testicle (absence of the testicle on that side) Remember you cannot get above a hernia and these other lumps will also not usually exhibit the classical features of hernia: 1. Cough impulse 2. Reducibility 3. Bowel sounds heard over the hernia
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how to examine ‘a lump in the groin’
Although a single enlarged femoral node can sometimes be difficult to distinguish from a strangulated femoral hernia containing omentum, such cases will rarely be seen in the finals. Usually, if care is taken to examine the patient lying down and standing, the diagnosis will become obvious. Remember also to carefully examine both groins (as hernias are often bilateral) and the scrotum as there may be associated epididymal cysts or hydrocoeles to find. This is particularly important for the short case sec- tion of the exam, where questions such as ‘This patient has a lump in his groin — examine him and tell us what you think’ are fairly common. Here is a summary of how to examine ‘a lump in the groin’: 1.Introduceyourselfandaskthepatientifhemindsyourexamininghim. 2. Expose the abdomen, groin and legs. Ask the patient to stand, and inspect for any obvious lumps or scars and comment on your findings (if the patient is already lying it is perfectly reasonable to perform the examination in this position; however, you must stand him at the end of the examination, or you may miss small hernias, saphena varices and varicocoeles). 3.Examinethegenitaliaandbothgroins.Ifyoucanseeanobviouslump feel it gently and ascertain the features of the lump. Ask the patient to cough and feel for a cough impulse, listen over it for bowel sounds and ask him if he is able to reduce it. Once it is reduced find the pubic tubercle and place your index finger on it. Ask the patient to cough and observe where the lump appears from in relation to your finger. An inguinal hernia will come out from the inguinal canal above and medial to your finger, whereas a femoral hernia will protrude below and lateral. If you think this is an inguinal hernia, then state, for example, ‘The patient has a 5 cm smooth lump in his right groin. I think this is an inguinal hernia, because I cannot get above it, it is reducible, exhibits a cough reflex and protrudes above and medial to the pubic tubercle’. The examiner might then ask you to tell if it is direct or indirect. 4. If a scrotal swelling is present determine if it has an upper border, remembering that you cannot get above a hernia. Therefore, a lump with no upper border is likely to be an inguinoscrotal hernia. If you can get above it, then it is likely to be either a cord or a testicular lump. Ask yourself two questions: Is it separate from the testis, and does it trans- illuminate? Do not forget to feel the epididymis and the skin of the scrotum as well (see Figure 12.1).
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whats an incisional hernia, how does it develop and how is it managed
These can be simply defined as hernias which arise through a previ- ously made incision. They are often broad-necked and, therefore, have a low risk of strangulation. Factors leading to the development of an incisional hernia include obesity, old age, chronic cough or straining due to constipation or prostatism (i.e. things which increase intra- abdominal pressure), postoperative wound infection or haematoma and poor surgical technique when the wound is closed. In high-risk patients even large incisional hernias are often managed conservatively with an abdominal elastic support corset. Repair may be difficult and require the insertion of a nylon mesh to allow closure of the defect without tension.
147
whats an umbilical hernia
In adults the hernia usually emerges adjacent to the umbilicus (unlike the congenital type) and is usually termed ‘paraumbilical’.
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what is a richter's hernia
This is a hernia where only part of the circumference of the bowel is within the sac. It is most often seen with femoral hernias. This is the only type of hernia which can strangulate without obstructing (other than her- nia which contains only the omentum). Although rather unusual in prac- tice, it seems remarkably common in exam questions, which is why you need to know about it (see Figure 12.1).
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whats an epigastric hernia
This hernia arises in the midline through the linea alba. It is usually small and often difficult to feel, especially in overweight patients. It rarely con- tains bowel but often has extraperitoneal fat. It can cause symptoms out of proportion to its size, however, and patients often undergo unnecessary investigations for other causes of upper abdominal pain before the correct diagnosis is eventually made.
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whats a spigelian hernia
Again, this is very rare but common in exam questions. It is a hernia which occurs into the posterior rectus sheath at the point where the poste- rior sheath becomes deficient (i.e. at the arcuate line of Douglas).
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whats an obturator hernia
This hernia occurs into the obturator foramen and does not usually pro- duce a palpable lump. It is most commonly seen in thin elderly women, and pressure on the obturator nerve gives rise to pain felt on the inner aspect of the thigh. It is usually diagnosed only when obstruction has occurred, often not being suspected prior to laparotomy. The typical pres- entation would be a thin old lady with distention, vomiting, colicky abdominal pain, absolute constipation and pain in the inner thigh.
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what is Whipple's disease
Whipple's disease is a rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men Features malabsorption: diarrhoea, weight loss large-joint arthralgia lymphadenopathy skin: hyperpigmentation and photosensitivity pleurisy, pericarditis neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus Investigation jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules Management guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin
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acute gastroenteritis causes
Gastroenteritis may either occur whilst at home or whilst travelling abroad (travellers' diarrhoea) Travellers' diarrhoea may be defined as at least 3 loose to watery stools in 24 hours with or without one of more of abdominal cramps, fever, nausea, vomiting or blood in the stool. The most common cause is Escherichia coli Another pattern of illness is 'acute food poisoning'. This describes the sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin. Acute food poisoning is typically caused by Staphylococcus aureus, Bacillus cereus or Clostridium perfringens.
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presentation of Giardiasis
Prolonged, non-bloody diarrhoea
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What is the primary mode of action of orilistat?
The primary mode of action of orilistat is to inhibit pancreatic lipases, which in turn will decrease the absorption of lipids from the intestine
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Obesity: therapeutic options
The management of obesity consists of a step-wise approach: conservative: diet, exercise medical surgical Orlistat is a pancreatic lipase inhibitor used in the management of obesity. Adverse effects include faecal urgency/incontinence and flatulence. A lower dose version is now available without prescription ('Alli'). NICE have defined criteria for the use of orlistat. It should only be prescribed as part of an overall plan for managing obesity in adults who have: BMI of 28 kg/m^2 or more with associated risk factors, or BMI of 30 kg/m^2 or more continued weight loss e.g. 5% at 3 months orlistat is normally used for
157
cause of dupuytren's contracture
poorly understood vast majority of patients have a family history. associated with epilepsy/antiepileptic therapy. also with alcoholic liver disease. also smoking, trauma and AIDS. and peyronie's disease.
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RLQ pain: differential
``` APPENDICITIS: Appendicitis/ Abscess PID/ Period Pancreatitis Ectopic/ Endometriosis Neoplasia Diverticulitis Intussusception Crohns Disease/ Cyst (ovarian) IBD Torsion (ovary) Irritable Bowel Syndrome Stones ```
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Liver failure (chronic): signs found on the arms
``` CLAPS: Clubbing Leukonychia Asterixis Palmar erythema Scratch marks ```
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Splenomegaly: causes
``` CHICAGO: Cancer Hem, onc Infection Congestion (portal hypertension) Autoimmune (RA, SLE) Glycogen storage disorders Other (amyloidosis) ```
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Left iliac fossa: causes of pain
``` SUPER CLOT: Sigmoid diverticulitis Uteric colic PID Ectopic pregnancy Rectus sheath haematoma Colorectal carcinoma Left sided lower love pneumonia Ovarian cyst (rupture, torture) Threatened abortion/ Testicular torsion ```
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Hepatomegaly: 3 common causes, 3 rarer causes
``` Common are 3 C's: Cirrhosis Carcinoma Cardiac failure Rarer are 3 C's: Cholestasis Cysts Cellular infiltration ```
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CAUSES OF DIARRHOEA
LOCAL GI TRACT 1. gastroenteritis 2. inflammatory bowel disease 3. diverticular disease 4. irritable bowel disease 5. malignancy 6. malabsorption SYSTEMIC CAUSES 1. hyperthyroidism 2. drugs 3. anxiety 4. autonomic neuropathy
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FLUIID REPLACEMENT IN INFECTIOUS DIARRHOEA
1. Rehydrate with oral rehydration therapy (isosomotic electrolyte solutions e.g. dioralyte) 2. Composition of oral rehydration solutions Na 60 mmol, K+ 20 mmol, Cl- 60 mmol glucose 90 mmol 3. If very volume deplete use IV fluids that will replace sodium and potassium initially 0.9% sodium chloride solution; normal saline (150mM NaCL) added potassium, guided by serum electrolytes to replace water losses use 5% dextrose solution
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ANTI-INFECTIVE TREATMENTS for diarrhoea
1. Ciprofloxacinreducesdurationofthe illness by 1-2 days (if bacterial) 2. MetronidazoleorvancomycinforC. Diff 3. Metronidazoleforamoebaorgiardia 4. Loperamide is an opiate that reduces diarrhoea (but may cause constipation)
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TREATING PAIN FROM IRRITABLE BOWEL SYNDROME
``` Pain thought to be due to bowel spasm Muscle relaxants are given with variable results These include antimuscarinic drugs (e.g propantheline) direct acting relaxants (mebeverine, peppermint oil capsules) ```
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initial TREATMENT OF ACUTE INFLAMMATORY BOWEL DISEASE
1. Patients present with bloody diarrhoea, abdo pain, fever, weight loss (usually more than 6 bloody stools per day) 2. Initial treatment is i.v. fluids 3. Stool sample for bacteriology; sigmoidoscopy and biopsy to make diagnosis 4. Specific treatment will be with systemic steroids, aminosalicylates
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Non Pharmacological treatment of dyspepsia
* Weight reduction * Stop smoking * Stop /reduce alcohol intake * Chocolate and caffeine?
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Pharmacological approach to the treatment of dyspepsia
Neutralising acid Antacids: aluminium and magnesium hydroxide Reduction in acid secretion H2 Rc blockade: eg Ranitidine H+ pump inhibition: eg Lansoprazole Mucosal protection Prostaglandin analogue: eg misoprostol Alignate: eg gaviscon Chelates: eg Sucralfate
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Helicobacter Pylori-Treatment
• Triple therapy: – proton pump inhibitor (standard dose) twice daily + clarithromycin 500 mg twice daily + metronidazole 500 mg twice daily or amoxicillin 1000 mg twice daily, for seven, 10, or 14 days • Quadruple therapy: ( in areas with high clarithromycin resistance) – proton pump inhibitor (standard dose) twice daily + metronidazole 500 mg three times daily + tetracycline 500 mg four times daily + bismuth subcitrate 120 mg four times daily, for seven, 10, or 14 days • Third line treatment (when several attempts have failed) – Proton pump inhibitor (standard dose) twice daily + amoxicillin 1000 mg twice daily + levofloxacin 500 mg twice daily for 10 days be careful of what you give if a PT has CI such as etoh abuse where you shouldn't give metronidazole because of the risk of the disulfiram like reaction.
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what bilirubin leads to detectable jaundice
Jaundice detectable when bilirubin > 60mmol/l
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Bilirubin Metabolism
Haem catabolism - (RES Spleen) to Biliverdin then Unconj bilirubin (Bound to albumin) then Conj bilirubin (by Liver) then Urobilinogen (Colonic bact) then Stercobilinogen
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Liver Function Tests
Liver Synthetic function – Albumin, Clotting (INR), Bilirubin • Liver Damage – Cellular integrity • Alanine/aspartate transaminase - Hepatitic damage – Biliary tract • Alkaline phosphatase • Gamma-glutamyl transferase - Cholestatic damage
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Causes of jaundice (1) | Pre-hepatic
Pre-hepatic • Unconjugated hyperbilirubinaemia • Increased urobilinogen • Gilberts Syndrome − 3% of UK population − AR, glucuronyl transferase ↓ − Normal rest LFTs − No evidence of haemolysis • Haemolysis − spherocytosis − homozygous sickle cell disease − thalassaemia major
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Causes of jaundice (2) | Hepatic
Hepatic • Acute/chronic liver disease • Raised conjugated and unconjugated serum bilirubin • Stools and urine are of normal colour • Causes – Viral hepatitis – Alcoholic cirrhosis/hepatitis – NASH/NAFLD – Primary Biliary cirrhosis – Drug induced jaundice – Autoimmune hepatitis – Cryptogenic
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Causes of jaundice (3) | Post-hepatic
Post-hepatic • Stones / Strictures / Ca Pancreas • Clinical features − Dark Urine (bilirubinuria) as conjugated bilirubin is water soluble & excreted in urine − Absence of bilirubin entering gut results in pale, "putty" coloured stools − Absence of urobilinogen in the urine when measured by dipstick testing
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Investigations of Jaundice | • Pre-Hepatic
Pre-Hepatic – Suggested by absence of liver disease accompanied by anaemia & splenomegaly – Blood film for reticulocytes and abnormal red cell shapes, haemoglobin electrophoresis, red cell antibodies & osmotic fragility
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Investigation of Hepatic Jaundice (Liver disease)
``` Blood tests (liver screen) • HBsAg • Anti–HCV • Ferritin • Caeruloplasmin • α-1-antitrypsin • Autoantibodies / Immunoglobluinsu ```
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what is and what are the common causes of acute liver failure
Development of encephalopathy & coagulopathy within 12 weeks of the onset of jaundice in absence of pre-existing liver disease • Common (55%) – Paracetamol 40% – Acute viral hepatitis 13% (A, B & E) – Idiosyncratic drug reactions 12% (isoniazid, phenytoin, sulphonamides, PTU) Only effective treatment for ALF is Transplantation – Assess & manage appropriately – Referral – Safe transfer
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Investigations of Jaundice | • Post-Hepatic
``` Investigations of Jaundice • Post-Hepatic – Suggested by ALP 3-10>ULN & raised GGT • USS: identifies biliary obstruction, gallstones, liver parenchyma (screen) • Other tests – CT – ERCP – EUS – MRCP – PTC ```
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Cholestatic Jaundice (1)
* Slow onset of Jaundice, with preceding pruritus * Pale stool, dark urine * Absence of urobilinogen * Pain + fever = cholangitis – Treat with abs/drainage • Intrahepatic – Drug induced – PBC – Liver infiltration e.g. tumour, sarcoid – Sepsis / TPN • Extrahepatic – Stones / Strictures
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Intra vs Extra Hepatic cholestasis
``` Intra • Anorexia, malaise • Drug exposure • Ascites • Stigmata of chronic liver disease • Encephalopathy • Raised ALP (Bil late) ``` ``` Extra • Abdo pain • Fever • Middle age/elderly • Abdo tender • Palpable gallbladder • Raised Bil/ALP • Raised INR corrects + vit K ```
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Forms of acute drug-induced liver disease
Hepatocellular Necrosis - Diclofenac Steatosis - Tetracycline Cholestasis Hepatocanalicular - Augmentin Canalicular - Chlorpromazine, OCP Mixed - Phenytoin
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Oesophageal cancer | overview
Metaplastic columnar epithelium would be seen with Barrett's but this is not consistent with the obstructive lesion seen on endoscopy. Oesophageal cancer Until recent times oesophageal cancer was most commonly due to a squamous cell carcinoma but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's. The majority of tumours are in the middle third of the oesophagus. ``` Risk factors smoking alcohol GORD Barrett's oesophagus achalasia Plummer-Vinson syndrome rare: coeliac disease, scleroderma ```
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most common cancers causing bone mets
Bone metastases Most common tumour causing bone metastases (in descending order) prostate breast lung ``` Most common site (in descending order) spine pelvis ribs skull long bones ```
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Gastric cancer | overview, associations and investigation
Epidemiology overall incidence is decreasing, but incidence of tumours arising from the cardia is increasing peak age = 70-80 years more common in Japan, China, Finland and Colombia than the West more common in males, 2:1 Histology signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis ``` Associations H. pylori infection blood group A: gAstric cAncer gastric adenomatous polyps pernicious anaemia smoking diet: salty, spicy, nitrates may be negatively associated with duodenal ulcer ``` Investigation diagnosis: endoscopy with biopsy staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT
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normal LFTs
``` Bilirubin 3-17 umol/l Alanine transferase (ALT) 3-40 iu/l Aspartate transaminase (AST) 3-30 iu/l Alkaline phosphatase (ALP) 30-100 umol/l Gamma glutamyl transferase (yGT) 8-60 u/l Albumin 35-50 g/l ```
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Causes of hepatosplenomegaly
Commonest causes - Infections (acute viral hepatitis, glandular fever, AMV, malaria) - Infiltration (leukaemia, lymphoma, myeloproliferative disorders) - Chronic liver disease with portal hypertension - Others (amyloidosis, sarcoidosis)
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what is faecal elastase used for
raised in chronic pancreatitis
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Spontaneous bacterial peritonitis
The most likely diagnosis here is spontaneous bacterial peritonitis. The fever indicates a likely infective cause, and the lack of diarrhoea points away from gastroenteritis. A history of liver failure is also suggested by the chronic alcohol abuse and diffuse oedema, predisposing to spontaneous bacterial peritonitis. Spontaneous bacterial peritonitis Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis. Diagnosis paracentesis: neutrophil count > 250 cells/ul Management intravenous cefotaxime is usually given Antibiotic prophylaxis should be given if: patients who have had an episode of SBP patients with fluid protein
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presentation of ascending cholangitis
An infection of the bile ducts commonly secondary to gallstones. Classically presents with a triad of: fever (rigors are common) RUQ pain jaundice
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things that helicobacter pylori is associated with
Helicobacter pylori is a Gram negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease Associations peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers) gastric cancer B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients) atrophic gastritis
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Iron deficiency anaemia | features
``` Features koilonychia atrophic glossitis post-cricoid webs angular stomatitis ``` Blood film target cells 'pencil' poikilocytes if combined with B12/folate deficiency a 'dimorphic' film occurs with mixed microcytic and macrocytic cells
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Wernicke's encephalopathy
Pabrinex, a yellow coloured fluid which you might have seen on the wards, contains vitamins B and C. It does not vitamin D. Vitamin B1, also called thiamine, is essential for glial cells of the nervous system, as well as other bodily systems. Deficiency can cause Wernicke's encephalopathy and if left untreated can lead to irreversible Korsakoff's syndrome. Vitamin B12 deficiency is linked to pernicious anaemia. Wernicke's encephalopathy Wernicke's encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics. Rarer causes include: persistent vomiting, stomach cancer, dietary deficiency. A classic triad of nystagmus, ophthalmoplegia and ataxia may occur. In Wernicke's encephalopathy petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls ``` Features nystagmus (the most common ocular sign) ophthalmoplegia ataxia confusion, altered GCS peripheral sensory neuropathy ``` Investigations decreased red cell transketolase MRI Treatment is with urgent replacement of thiamine Relationship with Korsakoff syndrome If not treated Korsakoff's syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms.
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relationship between wernicke's and korsakoff's
``` wernicke's encephalopathy is: Features nystagmus (the most common ocular sign) ophthalmoplegia ataxia confusion, altered GCS peripheral sensory neuropathy ``` If not treated Korsakoff's syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms. due to thiamine deficiency = B1
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what happens in bulbar palsy
palsy of the lower motor neurones 9-12, often with slurred speech, nasal regurgitation of food, difficulty chewing and chocking on fluids. signs include tongue fasciculation and absence of a gag reflex. coughing mid swallow indicates difficulty making the movement.
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most common reaction to bisphosphonates
irriatation, inflammation or ulceration of the oesophagus. should be taken 30 mins before food e.g. breakfast, and they should not lie down for at least 30 mins afterwards.
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isolated raised ALP ?
if GGT is normal then this suggests a bone source of the ALP.
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ALARM symptoms in dyspepsia
``` Anaemia Loss of weight Anorexia Recent onset of symptoms Melena or haematemesis. ```
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hoarse voice and odynophagia?
cancers in the upper part of the oesophagus are associated with a hoarse voice.
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if a pt presents with cognitive dysfunction on a background of liver damage what is likely happening and what do you need to do
suggestive of hepatic encephalopathy 1 - nutritional management - reduce the protein intake while still receiving the maximum tolerable = about 1.2grams per 24 hour 2 - reduction in nitrogenous load - this can be achieved via bowel cleansing (enemas) and lactulose . for acute encephalopathy give lactulose 45ml PO followed by an hourly dose until there is a bowel movement. after this the target is 2-3 soft bowel movements per day = 15-45ml /8-12hours.
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effect of steroids on the gastric mucosa
can cause gastric ulcers so watch out for bleeds and give PPIs
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if someone doesn't have capacity to consent to a procedure but it needs to be done i.e. its in their best interests , what needs to be done?
the op has to go ahead but a member of the medical team has to sign a form saying that they don't have capacity and one member of the team needs to act as proxy consent giver and to explain why the procedure is necessary
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how does terlipressin work
apparently it narrows the blood vessels to the small intestines thus reducing venous pressure?
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meds before having an OGD
PPI and H2 antagonists should be stopped for at least 2 weeks before the endoscopy.
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SE of cyclizine
its an antihistamine so dry mouth and drowsy
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se of ondansentron
headache and constipation.
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when can a doctor treat a patient against their wishes
under common law - first have to prove that the PT lacks capacity to make the decision and then that it is in their best interests. - in an emergency - where the doctor feels that the patient is at immediate harm or at risk of harming others, or to prevent a crime.
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PBC vs PSC presentation
they often present in a similar manner e.g. pruritis and obstructive jaundice, but PSC is more likely to fluctuate, is associated with inflammatory bowel disease and is more common in men cf PBC which is more common in women (middle aged). ANA is more likely to be positive in PSC and AMito Ab in PBC.
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Rx of a patient with wernicke's
2 doses of vitamins B and C = Pabrinex IV TDS. give this before giving any glucose e.g. dextrose as the glucose can precipitate wernicke's encephalopathy if its not already there. benzos for withdrawal PPIs for alcoholic gastritis Pancreatin to replace liver enzymes if needed orla vitamin B on discharge.
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overview of the Rockall score
defines a number of risk factors that independently predict death. 4 areas = age, comorbidities, shock and endoscopic findings. obviously this is why it is used after endoscopy to inform decision making.
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what happens in re-feeding syndrome
consider in alcoholics that go off after eating food. due to prolonged starvation, they are largely dependent on fats and protein catabolism for energy and lose intracellular electrolytes especially phosphate. when food is suddenly available again the shift back to carbohydrates and rise in insulin drives cellular uptake of phosphate. can cause profound hypophosphataemia. early features are non specific but PTs can go on to cardioresp failure, arrhythmia, rhabdomyal, seizures and coma and sudden death. do U and Es and phosphate.
213
oesophageal spasm
loss of normal propulsion. chest pain, re-gurg, dysphagia. treat with CCB or nitrates.
214
cancers that commonly metastasise to bone
Any cancer can spread to any organ however the commonest sites of primary cancer that can spread to bone are thyroid, breast, lung, renal and prostate
215
Iron Deficiency Anaemia + Weight Loss = ?
Iron Deficiency Anaemia + Weight Loss = Colon Cancer until proven otherwise.
216
recurrent dyspepsia mx
He should have an OGD – his age makes pathology other than GORD more common, this is the recommended course of action for all those over 45 years of age. The correct answer is: oesophagogastroduodenoscopy (OGD)