Gastro Flashcards
Acute porphyrias
disorders caused by defects in haem synthesis due to alterations in enzyme function or structure.
Acute porphyria types:
Acute intermittent porphyria
Variegate porphyria
ALA deficiency.
Triggers of acute porphyria
Antibiotics - Rifampicin, Isoniazid, Nitrofurantoin Anaesthetic agents - Ketamine, Etomidate Sulfonamides Barbiturates Antifungal agents
Diagnosis of porphyria
Diagnosis can be made on the basis of urinary porphobilinogen levels, which is a product in the pathway of haem metabolism. Urine samples need to be protected from light to prevent the breakdown of PBG.
Management
Treatment of attacks is largely supportive. Haem arginate can also be given intravenously to replenish haem levels.
Indications for inpatient withdrawal
Patients drinking >30 units per day
Scoring over 30 on the SADQ score
High risk of alcohol withdrawal seizures (previous alcohol withdrawal seizures or delirium tremens, or history of epilepsy)
Concurrent withdrawal from benzodiazepines
Significant medical or psychiatric comorbidity
Vulnerable patients
Patients under 18
Management
of alcohol withdrawal
Assisted alcohol withdrawal is required in patients drinking over 15 units per day or in those scoring over 20 on the AUDIT questionnaire.
Chlordiazepoxide prescribed in a reducing regimen in accordance with the CIWA score and local protocol.
In alcohol-withdrawal seizure a patient should be prescribed a rapid-acting benzodiazepine (such as intravenous lorazepam).
Pabrinex (1 pair of ampoules once daily to prevent Wernicke’s encephalopathy).
If there are signs of Wernicke’s encephalopathy (confusion, ataxia, ophthalmoplegia or nystagmus) patients should be prescribed 2 pairs of ampoules TDS.
In delirium tremens (this presents with confusion and visual hallucinations 48-72 hours after abstinence) offer oral lorazepam as first line treatment. If this is declines or symptoms persist offer parenteral lorazepam.
Alpha 1-antitrypsin deficiency
presentation
Alpha 1-antitrypsin deficiency is an inherited condition that affects the lungs, causing emphysema, and the liver, causing cirrhosis and hepatocellular carcinoma.
Presentation
COPD presenting 30-40 years old
Neonatal jaundice at birth
Deranged LFTs in adults with no other identified cause
Alpha 1-antitrypsin deficiency
D and M
investigations
The disease can be tested for with alpha 1 antitrypsin levels, genotyping or liver biopsy (evidence of Periodic acid Schiff positive globules).
Management
The condition has few management options and patients are advised to stop smoking. Intravenous A1AT pooled from human donors is expensive and not widely used. Liver transplant may be required in cases of decompensation.
Causes of a high SAAG in asisties
Cirrhosis Heart failure Budd Chiari syndrome Constrictive pericarditis Hepatic failure A high SAAG (>11g/dL) suggests that the cause of the ascites is due to raised portal pressure.
Causes of a low SAAG (<11g/dL)
Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome
Autoimmune hepatitis
(young middle aged women)
Liver function test results
Liver function test results
Raised ALT and bilirubin with normal/mildly raised ALP. Patients may have an IgG predominant hypergammaglobulinemia.
barrets oesphogous
ass/w GORD
-> leads to a change in the distal oesophagus from the usual squamous epithelium to metaplastic columnar epithelium.
== oesophageal adenocarcinoma.
Cholera treatment
Management
Aggressive fluid replacement: effective therapy can decrease mortality from over 50% to less than 0.2%.
Antibiotics (Doxycycline or co-trimoxazole) decrease volume and duration of diarrhoea by 50% and are recommended for patients with moderate to severe dehydration.
Chronic pancreatitis Clinical Features
Patients present with epigastric pain, classically worse after eating fatty food and relieved by sitting forward.
There may be features of exocrine dysfunction, such as malabsorption and steatorrhoea.
There may be features of endocrine dysfunction (i.e. Type 1 diabetes mellitus) with thirst and polyuria.
On physical examination there may be epigastric tenderness. It is important to check for signs of chronic liver disease (suggestive of alcohol as a cause).
Risk factors for developing CDI
Have been treated with broad-spectrum antibiotics
Common antibiotic risk factors include:
Clindamycin
Ciprofloxacin
Cephalosporins
Penicillins
Have had to stay in a healthcare setting, such as a hospital or care home, for a long time
Are over 65 years old
Have certain underlying conditions, including inflammatory bowel disease (IBD), cancer, or kidney disease
Have a week immune system, as a result of conditions such as diabetes or HIV infection or as side effect of a treatment such as chemotherapy or steroid medication
Are taking a proton pump inhibitor (PPI)
Complications of coeliac
naemia
Hyposplenism (and therefore a susceptibility to encapsulated organisms)
Osteoporosis (a DEXA scan may be required)
Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma).
The likelhood or aquiring this malignancy is directly proportional to the strength of overall adherence to a gluten free diet - i.e. the more a patient breaks adherence, the more likely they are to get EATL.
Enzyme inducers
Reduce the concentration of drugs metabolised by the cytochrome P450 system
Carbamazepine Rifampicin Phenytoin Griseofulvin Phenobarbitone Alcohol (chronic)
Enzyme inhibitors
Increase the concentration of drugs metabolised by the cytochrome P450 system
Valproate Isoniazid Cimetidine Fluclonazole Erythromycin Omeprazole
Gastroenteritis causes
Bacterial causes
The bacteria most commonly implicated are:
Staphylococcus aureus: usually found in cooked meats and cream products.
Bacillus cereus: mainly found in reheated rice.
Clostridium perfringens: usually found in reheated meat dishes or cooked meats.
Campylobacter
E.coli including E.coli 0157 (which can cause haemolytic uraemic syndrome)
Salmonella
Shigella
Viral causes
Rotavirus: most common cause of infantile gastroenteritis
Norovirus: most common cause of viral infectious gastroenteritis in all ages in England and Wales
Adenoviruses: commonly cause infections of the respiratory system but can also cause gastroenteritis, particularly in children.
Specific antibiotics for Gastroenteriti
Salmonella and shigella are treated with ciprofloxacin.
Campylobacter is treatment with a macrolide, such as erythromycin.
Cholera is treated with tetracycline, to reduce transmission.
Food poisoning is a notifiable disease in the UK.
gastroparesis - d n m
Diagnosis
Diagnosis of gastroparesis can be made with a solid meal gastric scintigraphy (Radionuclide studies of gastric emptying)
Management
Dietary modification - low fibre, smaller/more frequent meals, pureed/mashed food
Domperidone - dopamine receptor antagonist
Metoclopramide or Erythromycin (motility agents)
Treatment of H. Pylori
Amoxicillin, clarithromycin and a PPI twice daily for seven days - so-called triple therapy.
After 4-8 weeks patients can be re-tested for H. Pylori to check it has been eradicated.
If still present, NICE recommend another course of triple therapy with metronidazole or clarithromycin - whichever was not used in the initial course - amoxicillin and a PPI. The importance of adherence should also be discussed with the patient.
If the patient has already had courses of clarithromycin and metronidazole, the recommended treatment is a seven day course of a PPI, amoxicillin and either tetracycline or a quinolone.
main types of hiatus hernias
Sliding hiatal hernia (80%): The gastro-oesophageal junction slides up into the chest. A less competent sphincter results in acid reflux. Treatment is similar as for GORD.
Rolling hiatal hernia (20%): The gastro-oesophageal junction remains in the abdomen but part of the stomach protrude into the chest alongside the oesophagus. This type needs more urgent treatment as volvulus can result in ischemia and necrosis.
Clinical features of hiatus hernias
Symptoms include heartburn, dysphagia, regurgitation, odynophagia, shortness of breath, chronic cough and chest pain.
Hiatal hernias can be diagnosed using barium swallows (upper GI series), which is the most sensitive method, endoscopy and oesophageal manometry.
management of hiatus hernias
Conservative management includes crucial lifestyle changes. Lifestyle advice for patients with hiatal hernia includes
Lose weight
Elevate the head of the bed
Avoid large meals and eat 3-4 hours before bedtime
Avoiding alcohol and acidic foods
Avoid smoking as nicotine relaxes the lower oesophageal sphincter (as can chocolate, peppermint, caffeine, fatty foods, and medications such as calcium-channel blockers, nitrates, and beta-blockers)
Medical management involves PPI use for 4-8 weeks before assessing response.
Surgical management includes Nissen’s fundoplication
Indications for TIPSS
Secondary prophylaxis for oesophageal variceal bleeding
Treatment of refractory ascites
Treating portal hypertension in Budd-Chiari syndrome
Manning criteria for diagnosis of IBS
Abdominal discomfort or pain that is relieved by defecation OR associated with altered bowel frequency or stool form
AND at least 2 of:
Altered stool passage (e.g. straining or urgency)
Abdominal bloating
Symptoms made worse by eating
Passage of mucus
Causes of Prehepatic jaundice
Prehepatic causes of jaundice result in unconjugated hyperbilirubinaemia, which is not water soluble so cannot enter the urine. It is therefore known as acholuric jaundice.
Causes:
Conjugation disorders, such as Gilbert’s disease and Crigler-Naajjar
Haemolysis (such as malaria or haemolytic anaemia)
Drugs, such as contrast or rifampicin
Causes of hepatocelullar dysfunction (‘hepatic jaundice’)
Hepatocellular dysfunction results in a conjugated hyperbilirubinaemia. Causes include:
Viruses (hepatitis, CMV, EBV) Drugs, including paracetamol overdose, halothane, valproate, statins, tuberculosis antibiotics Alcohol Cirrhosis Liver mass (abscess or malignancy) Haemochromatosis Autoimmune hepatitis Alpha-1 antitrypsin deficiency Budd-Chiari Wilson's disease Failure to excrete conjugated bilirubin (Rotor and Dubin-Johnson syndromes)
Causes of post-hepatic jaundice
Impaired excretion of conjugated bilirubin results is cholestasis. Conjugated bilirubin is water soluble, making the urine dark. Less bilirubin reaches the gut, so pale stools also result. Pruritus also suggests an obstructive problem. These so-called post-hepatic causes include:
Primary biliary cirrhosis
Primary sclerosing cholangitis
Common bile duct gallstones or Mirrizi’s syndrome (CBD compression from a gallstone in the cystic duct)
Drugs, including coamoxiclav, flucloxacillin, nitrofurantoin, steroids, sulfonylureas
Malignancy, such as head of the pancreas adenocarcinoma, cholangiocarcinoma
Caroli’s disease
Biliary atresia
Imaging and invasive investigations for cirrhosis
If ascites is present, a peritoneal tap should be taken for microscopy and culture to look for spontaneous bacterial peritonitis.
A Doppler ultrasound would be of use in identifying Budd-Chiari syndrome.
Transient elastography or acoustic radiation force impulse imaging can be used to diagnose non-alcoholic fatty liver disease.
Liver biopsy may be necessary to confirm the underlying diagnosis if still in doubt.
Child-Pugh interpretation
The scores are added and the degree of cirrhosis is classified as Child-Pugh A (<7 points), B (7-9 points) or C (>9 points).
The score can be used as a predictor of mortality, and may also be used to predict the need for a liver transplant.
Management of decompensated liver disease
Good nutrition is essential, with total alcohol abstinence.
Non-steroidal anti-inflammatory drugs, sedatives and opiates should all be avoided.
An ultrasound scan and serum α-fetoprotein every 6 months may be indicated to detect development of hepatocellular carcinoma.
Colestyramine (bile acid sequestrant) can be used to manage pruritus.
Ascites can be managed with fluid restriction (under 1.5L per day) and a low-salt diet. Pharmacological management is with spironolactone; furosemide can be added if necessary. In severe cases, therapeutic paracentesis can be used alongside albumin infusions.
Recurrent episodes of encephalopathy can be reduced in frequency through the use of prophylactic lactulose and rifaximin.
Patients at high-risk of spontaneous bacterial peritonitis (such as those who have had previous episodes, or those with low albumin, a high INR and low ascitic albumin) may be treated with prophylactic antibiotics.
Ultimate treatment is a liver transplant. For cases of chronic liver disease scores such as the Model for End-stage Liver Disease (MELD) and UK End-stage Liver Disease (UKELD) are used to help predict severity of disease.
Four stages of hepatic encephalopathy
Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
Drowsiness, confusion, slurring of speech and personality change
Incoherency, restlessness, asterixis
Coma
King’s College Hospital Criteria for Liver Transplant (paracetamol induced)
The criteria for paracetamol induced liver failure are as follows:
Arterial pH <7.3 24h after ingestion OR
Pro-thrombin time >100s
AND creatinine >300µmol/L
AND grade III or IV encephalopathy.
King’s College Hospital Criteria for Liver Transplant (non-paracetamol liver failure)
Prothrombin time >100s OR Any three of: Drug-induced liver failure Age under 10 or over 40 years 1 week from 1st jaundice to encephalopathy Prothrombin time >50s Bilirubin ≥300µmol/L.
Melanosis coli
Melanosis coli is a finding usually associated with chronic laxative abuse, where colonoscopy reveals the presence of dark brown pigmentation of the macrophages in the lamina propria
Mucosa-associated lymphoid tissue (MALT) lymphoma
Clinical features Abdominal pain Nausea and vomiting Symptoms of anaemia Weight loss
Management
The initial treatment for local and disseminated disease is H. Pylori eradication therapy. This can treat the lymphoma in many cases.
If this fails to eradicate the disease, however, other treatment options are chemotherapy and radiotherapy. These may be considered if the disease is progressive or the patient has high risk features, such as being H. Pylori negative at presentation.
In disseminated disease, chemotherapy and rituximab is recommended if there is a threat to vital organ function. Otherwise, a watch and wait approach can be adopted.
Candida
White patches in the mouth are most commonly caused by a fungal infection with Candida; leucoplakia is a generic way to describe white patches found in the mouth.
Old age Diabetes mellitus Immunosuppression Long term corticosteroids Malignancy Antibiotics
Hairy Leukoplakia
Hairy leucoplakia is a benign condition that does not in itself require any treatment, but may lead to medical and psychological issues for the patient given the likely underlying condition. It is caused by Epstein-Barr virus, and is suggestive of underlying HIV infection.
Oral ulcers
Common deficiencies causing oral ulcers include iron, vitamin B12 and folate, which all lead to anaemia. Crohn’s disease can also cause painful oral ulcers.
risk factors for duodenal ulcers include:
NSIADS Chronic steroid use SSRIs Increase in gastric acid secretion Smoking Blood group O Increased gastric emptying (more acid in the duodenum)
Risk factors for gastric ulcers
NSAIDs H. Pylori Smoking Delayed gastric emptying Severe stress.
management of petic ulcer disease
Management
H. Pylori-negative peptic ulcer disease is managed with 4-8 weeks of full dose PPI treatment and lifestyle advise, including:
Stop smoking
Cut down on alcohol
Have more regular, smaller meals and eat 4 hours before bed
Avoid acidic foods, coffee, fatty or spicy foods
Encourage weight loss if obese
Try to avoid stress
Avoid NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs and crack cocaine
Try over the counter antacids
Follow-up of patients with peptic ulcers
Patients with a gastric ulcer should have a repeat endoscopy 6-8 weeks after the start of PPI treatment to ensure ulcer healing and rule out malignancy.
Patients with a duodenal ulcer should be asked about adherence and lifestyle factors should be enforced. If symptoms continue, other rarer causes of duodenal ulcers should be considered, such as malignancy, use of ulcer-promoting drugs, missed H. pylori infection, Zollinger-Ellison syndrome, or Crohn’s disease.
If these are ruled out, a low-dose PPI can be prescribed.
Causes of Vitamin B12 Deficiency
Gastric causes – pernicious anaemia, chronic severe atrophic gastritis
Pancreatic – any cause of pancreatic insufficiency
Small bowel bacterial overgrowth (since bacteria utilize vitamin B12), terminal ileal resection, severe terminal ileal disease (i.e. Crohn’s disease)
Tuberculosis
Metformin therapy
Zollinger-Ellison syndrome
Primary biliary cirrhosis
Clinical features
Clinical features
Patients commonly present with the following symptoms:
Extreme fatigue Itching Dry skin Dry eyes Jaundice
Positive Anti-mitochondrial antibodies in >90% of individuals
Primary biliary cirrhosis
Management
Management
Treatment is largely supportive and includes the following:
Ursodeoxycholic acid
Cholestyramine
Vitamin supplements
Liver transplantation (NB: May recur after transplantation)
Primary sclerosing cholangitis
Clinical features
Clinical features Can be asymptomatic with abnormal LFTs of hepatomegaly Jaundice Right upper quadrant pain Fatigue, weight loss, fevers and sweats.
Primary sclerosing cholangitis
Diagnosis
Deranged LFTs - cholestatic picture
Positive anti-smooth muscle and antinuclear antibodies and myeloperoxidase antineutrophil cytoplasmic antibody (ANCA)
Multiple beaded biliary strictures are seen on magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP).
Primary sclerosing cholangitis
Increased cancer risk
hepatobiliary cancer (cholangiocarcinoma), w
Primary sclerosing cholangitis
Management
Management
Avoid alcohol
Pruritis can be managed with cholestyramine
Supplement fat soluble vitamines (A,D,E,K)
Strictures can be dilated via ERCP
Liver transplantation may be indicated in cases complicated by chronic liver disease and/or hepatobiliary malignancies.
Vitamin B1 deficiency features
Patients with thiamine (vitamin B1) deficiency typically present with:
Wernicke’s encephalopathy (confusion, ataxia, and ocular abnormalities)
Wet beriberi (high output cardiac failure)
Dry beriberi (peripheral neuropathy)
Risk factors include chronic alcohol use and malabsorption.
Treatment is with intravenous thiamine.
Vitamin B3 deficiency (pellagra) features
This is more common in underdeveloped countries and countries in which the diet consistent predominantly of corn and maize.
Symptoms can be remembered according to the 3 Ds:
Diarrhoea
Dermatitis
Dementia
Treatment is with nicotinamide (vitamin B3).
Treatment for UC - Mild-moderate disease
topical aminosalicylate as first-line treatment.
If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate
consider steroids
Treatment for UC
Acute severe disease
Step 1: IV corticosteroids (if contraindicated or not tolerated, use IV ciclosporin).
Step 2: If no improvement in 72 hours or worsening symptoms, add IV ciclosporin or consider surgery (if IV ciclosporin contraindicated or not tolerated, consider infliximab).
Indications for emergency surgery:
Surgery should be considered in patients with:
Acute fulminant ulcerative colitis
Toxic megacolon who have little improvement after 48-72 hours of intravenous steroids
Symptoms worsening despite intravenous steroids
complications for UC
short-term/acute complications
Toxic megacolon: this describes a severe form of colitis, and is seen in around 15% of ulcerative colitis patients.
Massive lower gastrointestinal haemorrhage: this occurs in up to 3% of patients.
Long-term complications
Colorectal cancer: this occurs in 3-5% of patients. There is a higher risk with disease duration, severity and extent of colitis, and concomitant primary sclerosing cholangitis (PSC).
ICE guidance suggests offering colonoscopy surveillance to high risk patients.
Cholangiocarcinoma: ulcerative colitis approximately doubles the risk of cholangiocarcinoma.
Strictures: these can cause large bowel obstruction.
Whipple’s disease
Investigations
Whipple’s disease is more common in males. Diagnosis is with a small bowel biopsy, which shows the presence of acid-Schiff (PAS)-positive macrophages, which are seen to contain the causative bacteria on electron microscopy.
Management
Treatment is with a long term course of co-trimoxazole.
Brucellosis
Brucellosis is caused by the gram-negative, aerobic and intracellular bacillus of Brucella spp.
Brucellosis transmission
ransmission
In travelers, this is commonly via consumption of untreated milk/dairy (especially unpasteurized) products, as well as raw meat or liver.
Abbatoir workers, meat packers, vets, and hunters can also acquire it through the skin or mucous membrane contact (e.g.conjunctiva from eye splashes, or needlestick injury).
The most common mode of transmission in farmers is via inhalation.
It is very important to inquire about animal exposure and consumption of unpasteurized dairy products in any returning traveler with possible signs/symptoms consistent with brucellosis.
Clinical Features of Brucellosis
often non-specific, with fever, weight loss, night sweats, lymphadenopathy and joint pain/myalgia or spinal tenderness.
Hepatosplenomegaly occurs in about 1/3 of patients, and patients often look pale and unwell on presentation.
fevers that are classically remittent (temperature remains normal throughout the day and fluctuates more than 1 degree over 24 hours).
Brucellosis Complications
Complications
Endocarditis Sacroiliitis or osteomyelitis Epididymo-orchitis ITP CNS involvement: spinal syndromes, peripheral neuropathy, cerebellar ataxia. Abscess formation, usually hepatic
Brucellosis investigation and management
Investigations
Gold standard: blood cultures with the isolation of Brucella spp using Casteneda’s medium
Antibody testing if culture not possible (particularly towards O-polysaccharide).
Raised serum brucella agglutinins or Rose Bengal Test - need additional confirmatory testing in addition to this.
CSF culture or PCR
MRI scanning for brucellar spondylodiscitis
Liver or bone marrow biopsy in certain cases.
Management
Treat with Doxycyclin, Rifampicin and Gentamicin (or just Doxycyclin and Gentamicin)
Prevention depends on public health measures and control of infection in animals via vaccination and surveillance.
Cellulitis
risk factors
Advancing age
Immunocompromised e.g. diabetic
Predisposing skin condition e.g. ulcers, pressure sores, trauma, lymphoedema
Erysipelas refers to infection of the dermis and upper subcutaneous tissue
Erysipelas Clinical Features
Borders are sharply defined and affected skin is raised, swollen, firm, erythematous and pruritic.
Commonly affects the lower limbs. If face involved can have ‘butterfly’ distribution over the cheeks and the bridge of the nose.
Almost all are caused by group A beta-hemolytic streptococci (unlike cellulitis).
If face affected, this source of infection is usually the nasopharynx (possibly recent nasopharyngeal infection).
Pseudomembranous colitis Definition
An antibiotic-associated colitis caused by C difficile.
Pseudomembranous colitis risk factors
ntibiotics most commonly associated include quinolones (ciprofloxacin), macrolides (clarithromycin), clindamycin and cephalosporins. Other risk factors: Prolonged courses Multiple antibiotics Immunocompromise Use of PPIs Increasing age Severe comorbidity
Investigations for Pseudomembranous colitis
and management
Investigations for Pseudomembranous colitis
Plan abdominal Xray and CT can be useful in severe disease, for detecting perforation or toxic megacolon.
Avoid barium enemas.
Management of Pseudomembranous colitis
Rx: stop causative antibiotic. Supportive + oral metronidazole (oral vancomycin if not effective).
Consider surgical intervention if any complications occur
Differentials for Cavitating Lung Lesions
Infective Bacterial: S. aureus, TB, Klebsiella, S. pneumoniae Fungal: histoplasmosis, coccidiomycosis, candida (not aspergillomas, as these grow in pre-formed cavities) Malignancy Primary Secondary Rheumatological Vasculitis: Granulomatosis with polyangiitis Rheumatoid nodules Other: Sarcoidosis Pulmonary embolism
Incubation Periods of Common Infections
<1 week: Meningococcus, Diphtheria, Influenza, Scarlet Fever
1-2 weeks: Malaria, Dengue Fever, Typhoid, Measles.
2-3 weeks: Mumps, Rubella, Chickenpox
> 3 weeks: Infectious mononucleosis, CMV, Viral Hepatitis, HIV
Campylobacter jejuni type of bacteria
Most common cause of food poisoning in the UK.
Gram-negative rods with characteristic ‘seagull’ shape, which release enterotoxin in the gut and also invades the mucosa.
Incubation period of 16-48 hours, with chicken being a common source (classically during summer BBQs!).
Vomiting is rare
Can cause bloody diarrhoea
Salmonella enteritidis/typhimurium
Second most common cause of food poisoning in the UK.
Gram-negative bacteria that multiply locally in the small and large intestines, invade the mucosa and cause inflammation.
Incubation period of 16-48 hours, with common sources being eggs and foods contaminated on kitchen preparation surfaces
Bacillus cereus
Gram-positive rods that produce 2 toxins, an emetic pre-formed enterotoxin that is absorbed into the blood-stream from the stomach, and a diarrhoea-causing enterotoxin that acts on receptors in the small intestine and large bowel.
Symptoms start 30 minutes to 6 hours after eating contaminated food (due to the pre-formed toxin), and profuse vomiting is a common feature. Fever is usually absent.
Rice is a common source, as it provides the carbohydrate for the bacteria to produce the toxins.
These are heat stable, so when the rice is reheated they remain active
Leprosy
Leprosy manifests in a number of different ways due to a range of factors, most important being host immunology and bacterial virulence/initial infectious load.
At one end of the spectrum is disseminated lepromatous/ multibacillary leprosy;
Where the host immune system cannot contain the bacteria and it becomes widely disseminated
Causes peripheral nerve inflammation and damage, as well as dermatological lesions including nodules, hypoesthetic patches and the development of ‘leonine’-like facial appearance.
Nerve thickening may be felt on palpation, with the most commonly affected nerves being the ulnar, median, radial cutaneous, greater auricular, common peroneal and posterior tibial nerves.
At the other end of the spectrum is tuberculoid/paucibacillary leprosy;
Where the immune system is able to control the infection and a milder form of nerve damage and dermatological manifestations occur.
The nerve damage in all forms can lead to contractures, ulceration and deformity in the long term.
Leprosy Treatment
Treatment of multibacillary leprosy involves the use of dapsone, rifampicin and clofazimine (an immunosuppressive agent, not needed in paucibacillary disease) for 12-24 months.
Thalidomide is another treatment option for non-pregnant individuals.
Patients commenced on medications need to be monitored closely throughout the course of treatment for immunological complications known as type I and II (erythema nodosum lepromum) reactions, which require hospital in-patient treatment.
Side-effects of dapsone include methaemoglobinaemia, agranulocytosis, Stevens-Johnson Syndrome and the DRESS syndrome, and it can also trigger a haemolytic crisis is G6PD deficiency.
Clofozamine can cause abnormal skin pigmentation.
Mumps
Paramyxovirus.
1) Parotitis:
The parotid glands are almost always affected, usually bilaterally (though can be unilateral). Swelling can be severe enough to prevent the mouth from being opened and usually lasts 3-4 days. Prior to parotitis, there may be flu-like symptoms such as headache, malaise and myalgia.
2) Orchitis: Epididymo-orchitis is the second most common extra-salivary symptom of Mumps, which presents as severely painful swelling of one or both testicles and/or backache. It usually develops 4-5 days after onset of parotitis. 7% of post-pubertal females get oophoritis, with rare cases of infertility and premature menopause as a result.
3) Aseptic meningitis:
A relatively common complication in 4-25% of cases. Usually mild and self-limiting
4) Encephalitis:
Rare complication presenting as headache, vomiting, seizures, unconsciousness.
5) Deafness:
A rare cause of acute or insidious sensorineural hearing loss (usually unilateral) in children.
6) Other: Pancreatitis, nephritis, arthritis, thyroiditis, pericarditis.
Pseudomonas
Pseudomonas aeruginosa is a gram-negative rod that is an important cause of infections in immunocompromised or severely ill patients.
Antibiotics which are effective against Pseudomonas:
Ciprofloxacin or levofloxacin (but not moxifloxacin) - note, this is the only oral anti-pseudomonal Tazocin Ceftazidime Meropenem Gentamicin
Pyrexia of Unknown Origin
Causes
Causes
Abscesses - particularly liver, lung and kidney
Bacterial infections - Infective endocarditis, brucellosis, typhus, Lyme disease
Parasitic and fungal infections - malaria, schistosomiasis
Malignancy - particularly Hodgkin’s lymphoma, renal hydronephromas and some other solid organ tumours
Drug reactions - often accompanied with eosinophilia
Connective tissue disorders - SLE, vasculitides, Kawasaki’s etc
Thromboembolic disease
Autoimmune inflammatory syndromes - such as FMF, TRAPs and hyper Ig-D syndrome
Cause not identified (20%)
Schistosomiasis features
‘Swimmer’s itch’ after cercariae penetration of the dermis.
‘Katayama fever’: d
Schistosomiasis diagnosis and management
Diagnosis
Identification of eggs on microscopic examination of urine or stool.
Serology if within 2 months of exposure, as eggs may not be detected this early
Histopathological analysis of affected tissue, not often used.
Management
Praziquantel is the drug of choice.
Kills adults but not the eggs or migrating schistosomula
Hence needs to be given again 2-3 months after exposure to allow for the development of the worms.
Steroids are needed in acute Katayama Fever to suppress hypersensitivity reaction.
Problem gram +ve organisms:
MRSA: resistant to flucloxacillin
Coagulase -ve Staph: commonly cause infection of hospital lines and prostheses. Most are resistant to flucloxacillin.
VRE: Vancomycin resistent enterococci (most also resistant to amoxicillin), including E. faecalis and E. faecium. Normal flora of the gut, but often colonize diabetic ulcers and sacral sores, as well as causing infections in immunocompromised patients (particularly meningitis, septicemia, wound infections and endocarditis).
Treatment options for problem gram +ves:
1st line - Glycopeptides: vancomycin (but not for VRE or VRSA) or Teicoplanin. Narrow spectrum agents, only available IV and cannot penetrate blood-brain barrier as they are large molecules. Vancomycin is nephrotoxic so levels need to be measured.
For VRE - treat with oxazolidinone e.g. linezolid. Narrow spectrum gram-positive agent with excellent penetration into skin and brain. However, can cause bone marrow suppression, peripheral neuropathy and optic neuritis.
Other options: Tazocin, daptomycin, tigecycline.
antibiotic - Exacerbations of chronic bronchitis
Amoxicillin or tetracycline or clarithromycin
antibiotic. - Uncomplicated community-acquired pneumonia
Amoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)
antibiotic - Pneumonia possibly caused by atypical pathogens
Clarithromycin
antibiotic- Hospital-acquired pneumonia
Within 5 days of admission: co-amoxiclav or cefuroxime
More than 5 days after admission: piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g. ceftazidime) OR a quinolone (e.g. ciprofloxacin)
antibiotic-Lower urinary tract infection
Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin
antibiotic - Acute pyelonephritis
Broad-spectrum cephalosporin or quinolone
antibiotic Clostridium difficile
First episode: metronidazole
Second or subsequent episode of infection: vancomycin
antibiotic for Campylobacter enteritis, salmoella and shigellosis
Campylobacter enteritis Clarithromycin
Salmonella (non-typhoid) Ciprofloxacin
Shigellosis Ciprofloxacin
antibiotic for Gonorrhoeaq
Intramuscular ceftriaxone
antibiotic for Chlamydia
Doxycycline or azithromycin
antibiotic for Pelvic inflammatory disease
Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole
antibiotic for Syphilis
Benzathine benzylpenicillin or doxycycline or erythromycin
antibiotic for Bacterial vaginosis
Oral or topical metronidazole or topical clindamycin
antibiotic for Throat infections
Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)
antibiotic for Sinusitis
Phenoxymethylpenicillin
antibiotic for Otitis media
Otitis media Amoxicillin (erythromycin if penicillin-allergic)
antibiotic for Otitis externa**
Otitis externa** Flucloxacillin (erythromycin if penicillin-allergic)
antibiotic for Periapical or periodontal abscess
Periapical or periodontal abscess Amoxicillin
antibiotic for Gingivitis: acute necrotising ulcerative
Gingivitis: acute necrotising ulcerative Metronidazole
