Gastro

Question 1

Acute porphyrias

Answer 1

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.

Question 2

Triggers of acute porphyria

Answer 2

Antibiotics - Rifampicin, Isoniazid, Nitrofurantoin
Anaesthetic agents - Ketamine, Etomidate
Sulfonamides
Barbiturates
Antifungal agents

Question 3

Diagnosis of porphyria

Answer 3

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.

Question 4

Indications for inpatient withdrawal

Answer 4

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

Question 5

Management

of alcohol withdrawal

Answer 5

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.

Question 6

Alpha 1-antitrypsin deficiency

presentation

Answer 6

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

Question 7

Alpha 1-antitrypsin deficiency

D and M

Answer 7

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.

Question 8

Causes of a high SAAG in asisties

Answer 8

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.

Question 9

Causes of a low SAAG (<11g/dL)

Answer 9

Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome

Question 10

Autoimmune hepatitis
(young middle aged women)
Liver function test results

Answer 10

Liver function test results

Raised ALT and bilirubin with normal/mildly raised ALP. Patients may have an IgG predominant hypergammaglobulinemia.

Question 11

barrets oesphogous

Answer 11

ass/w GORD
-> leads to a change in the distal oesophagus from the usual squamous epithelium to metaplastic columnar epithelium.
== oesophageal adenocarcinoma.

Question 12

Cholera treatment

Answer 12

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.

Question 13

Chronic pancreatitis Clinical Features

Answer 13

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).

Question 14

Risk factors for developing CDI

Answer 14

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)

Question 15

Complications of coeliac

Answer 15

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.

Question 16

Enzyme inducers

Answer 16

Reduce the concentration of drugs metabolised by the cytochrome P450 system

Carbamazepine
Rifampicin
Phenytoin
Griseofulvin
Phenobarbitone
Alcohol (chronic)

Question 17

Enzyme inhibitors

Answer 17

Increase the concentration of drugs metabolised by the cytochrome P450 system

Valproate
Isoniazid
Cimetidine
Fluclonazole
Erythromycin
Omeprazole

Question 18

Gastroenteritis causes

Answer 18

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.

Question 19

Specific antibiotics for Gastroenteriti

Answer 19

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.

Question 20

gastroparesis - d n m

Answer 20

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)

Question 21

Treatment of H. Pylori

Answer 21

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.

Question 22

main types of hiatus hernias

Answer 22

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.

Question 23

Clinical features of hiatus hernias

Answer 23

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.

Question 24

management of hiatus hernias

Answer 24

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

Question 25

Indications for TIPSS

Answer 25

Secondary prophylaxis for oesophageal variceal bleeding Treatment of refractory ascites Treating portal hypertension in Budd-Chiari syndrome

Question 26

Manning criteria for diagnosis of IBS

Answer 26

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

Question 27

Causes of Prehepatic jaundice

Answer 27

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

Question 28

Causes of hepatocelullar dysfunction ('hepatic jaundice')

Answer 28

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) ```

Question 29

Causes of post-hepatic jaundice

Answer 29

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

Question 30

Imaging and invasive investigations for cirrhosis

Answer 30

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.

Question 31

Child-Pugh interpretation

Answer 31

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.

Question 32

Management of decompensated liver disease

Answer 32

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.

Question 33

Four stages of hepatic encephalopathy

Answer 33

Altered mood and behaviour, disturbance of sleep pattern and dyspraxia Drowsiness, confusion, slurring of speech and personality change Incoherency, restlessness, asterixis Coma

Question 34

King's College Hospital Criteria for Liver Transplant (paracetamol induced)

Answer 34

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.

Question 35

King's College Hospital Criteria for Liver Transplant (non-paracetamol liver failure)

Answer 35

``` 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. ```

Question 36

Melanosis coli

Answer 36

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

Question 37

Mucosa-associated lymphoid tissue (MALT) lymphoma

Answer 37

``` 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.

Question 38

Candida

Answer 38

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 ```

Question 39

Hairy Leukoplakia

Answer 39

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.

Question 40

Oral ulcers

Answer 40

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.

Question 41

risk factors for duodenal ulcers include:

Answer 41

``` NSIADS Chronic steroid use SSRIs Increase in gastric acid secretion Smoking Blood group O Increased gastric emptying (more acid in the duodenum) ```

Question 42

Risk factors for gastric ulcers

Answer 42

``` NSAIDs H. Pylori Smoking Delayed gastric emptying Severe stress. ```

Question 43

management of petic ulcer disease

Answer 43

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

Question 44

Follow-up of patients with peptic ulcers

Answer 44

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.

Question 45

Causes of Vitamin B12 Deficiency

Answer 45

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

Question 46

Primary biliary cirrhosis | Clinical features

Answer 46

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

Question 47

Primary biliary cirrhosis | Management

Answer 47

Management Treatment is largely supportive and includes the following: Ursodeoxycholic acid Cholestyramine Vitamin supplements Liver transplantation (NB: May recur after transplantation)

Question 48

Primary sclerosing cholangitis | Clinical features

Answer 48

``` Clinical features Can be asymptomatic with abnormal LFTs of hepatomegaly Jaundice Right upper quadrant pain Fatigue, weight loss, fevers and sweats. ```

Question 49

Primary sclerosing cholangitis | Diagnosis

Answer 49

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).

Question 50

Primary sclerosing cholangitis Increased cancer risk

Answer 50

hepatobiliary cancer (cholangiocarcinoma), w

Question 51

Primary sclerosing cholangitis | Management

Answer 51

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.

Question 52

Vitamin B1 deficiency features

Answer 52

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.

Question 53

Vitamin B3 deficiency (pellagra) features

Answer 53

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).

Question 54

Treatment for UC - Mild-moderate disease

Answer 54

topical aminosalicylate as first-line treatment. If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate consider steroids

Question 55

Treatment for UC | Acute severe disease

Answer 55

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

Question 56

complications for UC

Answer 56

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.

Question 57

Whipple's disease

Answer 57

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.

Question 58

Brucellosis

Answer 58

Brucellosis is caused by the gram-negative, aerobic and intracellular bacillus of Brucella spp.

Question 59

Brucellosis transmission

Answer 59

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.

Question 60

Clinical Features of Brucellosis

Answer 60

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).

Question 61

Brucellosis Complications

Answer 61

Complications ``` Endocarditis Sacroiliitis or osteomyelitis Epididymo-orchitis ITP CNS involvement: spinal syndromes, peripheral neuropathy, cerebellar ataxia. Abscess formation, usually hepatic ```

Question 62

Brucellosis investigation and management

Answer 62

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.

Question 63

Cellulitis | risk factors

Answer 63

Advancing age Immunocompromised e.g. diabetic Predisposing skin condition e.g. ulcers, pressure sores, trauma, lymphoedema

Question 64

Erysipelas refers to infection of the dermis and upper subcutaneous tissue

Answer 64

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).

Question 65

Pseudomembranous colitis Definition

Answer 65

An antibiotic-associated colitis caused by C difficile.

Question 66

Pseudomembranous colitis risk factors

Answer 66

``` 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 ```

Question 67

Investigations for Pseudomembranous colitis | and management

Answer 67

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

Question 68

Differentials for Cavitating Lung Lesions

Answer 68

``` 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 ```

Question 69

Incubation Periods of Common Infections

Answer 69

<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

Question 70

Campylobacter jejuni type of bacteria

Answer 70

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

Question 71

Salmonella enteritidis/typhimurium

Answer 71

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

Question 72

Bacillus cereus

Answer 72

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

Question 73

Leprosy

Answer 73

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.

Question 74

Leprosy Treatment

Answer 74

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.

Question 75

Mumps

Answer 75

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.

Question 76

Pseudomonas

Answer 76

Pseudomonas aeruginosa is a gram-negative rod that is an important cause of infections in immunocompromised or severely ill patients.

Question 77

Antibiotics which are effective against Pseudomonas:

Answer 77

``` Ciprofloxacin or levofloxacin (but not moxifloxacin) - note, this is the only oral anti-pseudomonal Tazocin Ceftazidime Meropenem Gentamicin ```

Question 78

Pyrexia of Unknown Origin | Causes

Answer 78

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%)

Question 79

Schistosomiasis features

Answer 79

'Swimmer's itch' after cercariae penetration of the dermis. 'Katayama fever': d

Question 80

Schistosomiasis diagnosis and management

Answer 80

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.

Question 81

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).

Answer 81

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.

Question 82

antibiotic - Exacerbations of chronic bronchitis

Answer 82

Amoxicillin or tetracycline or clarithromycin

Question 83

antibiotic. - Uncomplicated community-acquired pneumonia

Answer 83

Amoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)

Question 84

antibiotic - Pneumonia possibly caused by atypical pathogens

Answer 84

Clarithromycin

Question 85

antibiotic- Hospital-acquired pneumonia

Answer 85

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)

Question 86

antibiotic-Lower urinary tract infection

Answer 86

Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin

Question 87

antibiotic - Acute pyelonephritis

Answer 87

Broad-spectrum cephalosporin or quinolone

Question 88

antibiotic Clostridium difficile

Answer 88

First episode: metronidazole | Second or subsequent episode of infection: vancomycin

Question 89

antibiotic for Campylobacter enteritis, salmoella and shigellosis

Answer 89

Campylobacter enteritis Clarithromycin Salmonella (non-typhoid) Ciprofloxacin Shigellosis Ciprofloxacin

Question 90

antibiotic for Gonorrhoeaq

Answer 90

Intramuscular ceftriaxone

Question 91

antibiotic for Chlamydia

Answer 91

Doxycycline or azithromycin

Question 92

antibiotic for Pelvic inflammatory disease

Answer 92

Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole

Question 93

antibiotic for Syphilis

Answer 93

Benzathine benzylpenicillin or doxycycline or erythromycin

Question 94

antibiotic for Bacterial vaginosis

Answer 94

Oral or topical metronidazole or topical clindamycin

Question 95

antibiotic for Throat infections

Answer 95

Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)

Question 96

antibiotic for Sinusitis

Answer 96

Phenoxymethylpenicillin

Question 97

antibiotic for Otitis media

Answer 97

Otitis media Amoxicillin (erythromycin if penicillin-allergic)

Question 98

antibiotic for Otitis externa**

Answer 98

Otitis externa** Flucloxacillin (erythromycin if penicillin-allergic)

Question 99

antibiotic for Periapical or periodontal abscess

Answer 99

Periapical or periodontal abscess Amoxicillin

Question 100

antibiotic for Gingivitis: acute necrotising ulcerative

Answer 100

Gingivitis: acute necrotising ulcerative Metronidazole