Second 1/2 Akt Pm

Front 1

Recommended antibiotic: Exacerbations of chronic bronchitis

Back 1

Amoxicillin or tetracycline or clarithromycin

Front 2

Recommended antibiotic :Uncomplicated community-acquired pneumonia

Back 2

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

Front 3

Recommended antibiotic : Pneumonia possibly caused by atypical pathogens

Back 3

Clarithromycin

Front 4

Recommended antibiotic :Lower urinary tract infection

Back 4

Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin

Front 5

Recommended antibiotic :Acute pyelonephritis

Back 5

Broad-spectrum cephalosporin or quinolone

Front 6

Recommended antibiotic :Acute prostatitis

Back 6

Quinolone or trimethoprim

Front 7

Recommended antibiotic :Impetigo

Back 7

Topical fusidic acid, oral flucloxacillin or erythromycin if widespread

Front 8

Recommended antibiotic :Cellulitis

Back 8

Flucloxacillin (clarithromycin or clindomycin if penicillin-allergic)

Front 9

Recommended antibiotic :Erysipelas

Back 9

Phenoxymethylpenicillin (erythromycin if penicillin-allergic)

Front 10

Recommended antibiotic :Animal or human bite

Back 10

Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic)

Front 11

Recommended antibiotic :Throat infections

Back 11

Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)

Front 12

Recommended antibiotic :Sinusitis

Back 12

Amoxicillin or doxycycline or erythromycin

Front 13

Recommended antibiotic :Otitis media

Back 13

Amoxicillin (erythromycin if penicillin-allergic)

Front 14

Recommended antibiotic :Otitis externa*

Back 14

Flucloxacillin (erythromycin if penicillin-allergic)

*a combined topical antibiotic and corticosteroid is generally used for mild/moderate cases of otitis externa

Front 15

Recommended antibiotic :Gonorrhoea

Back 15

Cefixime or ciprofloxacin**

**there is actually now significant resistance to ciprofloxacin and other guidelines recommend cefixime 400mg PO (single dose) or ceftriaxone 250mg IM

Front 16

Recommended antibiotic :Pelvic inflammatory disease

Back 16

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

Front 17

Recommended antibiotic :Syphilis

Back 17

Benzathinebenzylpenicillin or doxycycline or erythromycin

Front 18

Recommended antibiotic :Bacterial vaginosis

Back 18

Oral or topical metronidazole or topical clindamycin

Front 19

What causes chicken pox?

Back 19

primary infection with varicella zoster virus

Front 20

What is shingles?

Back 20

is reactivation of dormant virus in dorsal root ganglion

Front 21

How is chickenpox spread?

Back 21

- respiratory route
- can be caught from someone with shingles

Front 22

What is the incubation period and infectivity of chickenpox?

Back 22

• infectivity = 4 days before rash, until 5 days after the rash first appeared*
• incubation period = 10-21 days

Front 23

What are the clinical features of chickenpox?

Back 23

• fever initially
• itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular
• systemic upset is usually mild

Front 24

What are the managents and advice given to patients with chickenpox?

Back 24

• keep cool, trim nails
• calamine lotion
• school exclusion: current HPA advice is 5 days from start of skin eruption. They also state 'Traditionally children have been excluded until all lesions are crusted. However, transmission has never been reported beyond the fifth day of the rash.'
• immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops then IV aciclovir should be considered

Front 25

What are the clinical complication of chickenpox?

Back 25

A common complication is secondary bacterial infection of the lesions. Rare complications include
• pneumonia
• encephalitis (cerebellar involvement may be seen)
• disseminated haemorrhagic chickenpox
• arthritis, nephritis and pancreatitis may very rarely be seen

Front 26

Define fetal varicella syndrome and its complications.

Back 26

• risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation
• studies have shown a very small number of cases occurring between 20-28 weeks gestation and none following 28 weeks
• features of FVS include skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning disabilities

Front 27

What is the management plan for preganancy women exposed to chickenpox?

Back 27

• if there is any doubt about the mother previously having chickenpox maternal blood should be checked for varicella antibodies
• if the pregnant women is not immune to varicella she should be given varicella zoster immunoglobulin (VZIG) as soon as possible. RCOG and Greenbook guidelines suggest VZIG is effective up to 10 days post exposure
• consensus guidelines suggest oral aciclovir should be given if pregnant women with chickenpox present within 24 hours of onset of the rash

Front 28

Organism causing chlamydia

Back 28

Chlamydia trachomatis, an obligate intracellular pathogen

Front 29

Clinical features of chlamydia

Back 29

• asymptomatic in around 70% of women and 50% of men
• women: cervicitis (discharge, bleeding), dysuria
• men: urethral discharge, dysuria

Front 30

Potential complication of chlamydia

Back 30

• epididymitis
• pelvic inflammatory disease
• endometritis
• increased incidence of ectopic pregnancies
• infertility
• reactive arthritis
• perihepatitis (Fitz-Hugh-Curtis syndrome)

Front 31

Approximately how young women in UK has chlamydia.

Back 31

1/10

Front 32

incubation period of chlamydia

Back 32

7-21 days

Front 33

Clostridium difficile and its complication

Back 33

Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis.

Front 34

How does clostridium difficile develop? and what medications cause it?

Back 34

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.

Front 35

Clinical features of clostridium difficile

Back 35

• diarrhoea
• abdominal pain
• a raised white blood cell count is characteristic
• if severe toxic megacolon may develop

Front 36

investigation of clostridium difficle

Back 36

detecting Clostridium difficile toxin (CDT) in the stool

Front 37

Management of clostridium difficile

Back 37

• 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

Front 38

Definite traveller's diarrhoea

Back 38

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

Front 39

clinical features of acute food poisoing.

Back 39

sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin.

Front 40

3 organisims most commonly cause acute food poisoning

Back 40

Staphylococcus aureus, Bacillus cereus or Clostridium perfringens.

Front 41

Clinical features of :Escherichia coli

Back 41

Common amongst travellers
Watery stools
Abdominal cramps and nausea

Front 42

Clinical features of :Giardiasis

Back 42

Prolonged, non-bloody diarrhoea

Front 43

Clinical features of :Cholera

Back 43

Profuse, watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers

Front 44

Clinical features of :Shigella

Back 44

Bloody diarrhoea
Vomiting and abdominal pain

Front 45

Clinical features of :Staphylococcus aureus

Back 45

Severe vomiting
Short incubation period

Front 46

Clinical features and complication of :Campylobacter

Back 46

A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody

Complications include Guillain-Barre syndrome

Front 47

Clinical features of Bacillus cereus

Back 47

Two types of illness are seen
• vomiting within 6 hours, stereotypically due to rice
• diarrhoeal illness occurring after 6 hours

Front 48

Clinical features of Amoebiasis

Back 48

Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks

Front 49

Acute food poisioning: incubation period of 1-6 hours

Back 49

Staphylococcus aureus, Bacillus cereus*

*vomiting subtype, the diarrhoeal illness has an incubation period of 6-14 hours

Front 50

Acute food poisioning/ organisms: incubation period of •12-48 hrs

Back 50

: Salmonella, Escherichia coli

Front 51

Acute food poisioning/ organisms: incubation period of 48-72 hrs:

Back 51

Shigella, Campylobacter

Front 52

Acute food poisioning/ organisms: incubation period of 7 days

Back 52

Giardiasis, Amoebiasis

Front 53

alternative name for genital wart

Back 53

condylomata accuminata

Front 54

HPV causing gential wart

Back 54

6 and 11

Front 55

HPV causing cervical cancer

Back 55

16, 18, 33

Front 56

Clinical features of genital wart

Back 56

• small (2 - 5 mm) fleshy protuberances which are slightly pigmented
• may bleed or itch

Front 57

Management of genital wart

Back 57

• topicalpodophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion. Multiple, non-keratinised warts are generally best treated with topical agents whereas solitary, keratinised warts respond better to cryotherapy
• imiquimod is a topical cream which is generally used second line
• genital warts are often resistant to treatment and recurrence is common although the majority of anogenital infections with HPV clear without intervention within 1-2 years

Front 58

Organism causing gonorrhea

Back 58

caused by the Gram negative diplococcus Neisseriagonorrhoea

Front 59

Incubation period of gonorrhoea

Back 59

2-5 days

Front 60

Clinical features of gonorrhoea

Back 60

Acute infection can occur on any mucous membrane surface, typically genitourinary but also rectum and pharynx

• males: urethral discharge, dysuria
• females: cervicitis e.g. leading to vaginal discharge
• rectal and pharyngeal infection is usually asymptomatic

Front 61

Clinical complications of gonorrhea

Back 61

Local complications that may develop include urethral strictures, epididymitis and salpingitis (hence may lead to infertility). Disseminated infection and gonococall arthritis may occur

Front 62

Management of gonorrhea

Back 62

• ciprofloxacin 500mg PO used to be the treatment of choice
• however, there is increased resistance to ciprofloxacin and therefore cephalosporins are now used
• options include cefixime 400mg PO (single dose) or ceftriaxone 250mg IM

Front 63

Define disseminated gonococcal infection

Back 63

- gonococcal infection being the most common cause of septic arthritis in young adults.
- pathophysiology of DGI is not fully understood but is thought to be due to haematogenous spread from mucosal infection (e.g. Asymptomatic genital infection).

Front 64

Complication of of disseminated gonococcal infection

Back 64

septic arthritis, endocarditis and perihepatitis (Fitz-Hugh-Curtis syndrome)

Front 65

classical triad of disseminated gonoccal infection

Back 65

• tenosynovitis
• migratory polyarthritis
• dermatitis (lesions can be maculopapular or vesicular)

Front 66

Define H1N1

Back 66

virus is a subtype of the influenza A virus and the most common cause of flu in humans. The 2009 pandemic was caused by a new strain of the H1N1 virus.

Front 67

H1N1:particularly at risk groups

Back 67

• patients with chronic illnesses and those on immunosuppressants
• pregnant women
• young children under 5 years old

Front 68

Clinical features of H1N1 infection

Back 68

The majority of symptoms are typical of those seen in a flu-like illness:
• fever greater than 38ºC
• myalgia
• lethargy
• headache
• rhinitis
• sore throat
• cough
• diarrhoea and vomiting

Front 69

Complication of H1N1 infection

Back 69

A minority of patients may go on to develop an acute respiratory distress syndrome which may require ventilatory support.

Front 70

2 treatments of H1N1

Back 70

Oseltamivir (Tamiflu)
Zanamivir (Relenza)

Front 71

What is Zanamivir (Relenza)

Back 71

• inhaled medication*
• also a neuraminidase inhibitor
• may induce bronchospasm in asthmatics

*intravenous preparations are available for patients who are acutely unwell

Front 72

What is Oseltamivir (Tamiflu)

Back 72

• oral medication
• a neuraminidase inhibitor which prevents new viral particles from being released by infected cells
• common side-effects include nausea, vomiting, diarrhoea and headaches

Front 73

What is the incidence of HIV + women in london

Back 73

0.4%

Front 74

Factors reducing vertical transmission in HIV pregnancy

Back 74

reduce vertical transmission (from 25-30% to 2%)
• maternal antiretroviral therapy
• mode of delivery (caesarean section)
• neonatal antiretroviral therapy
• infant feeding (bottle feeding)

Front 75

What invesitgation should be screened for all pregnant women?

Back 75

HIV

Front 76

What are the factors that used to reduce HIV vertical transmission during pregancy? Explain each.

Back 76

1 ) Antiretroviral therapy
• all pregnant women should be offered antiretroviral therapy regardless of whether they were taking it previously
• if women are not currently taking antiretroviral therapy the RCOG recommend that it is commenced between 28 and 32 weeks of gestation and should be continued intrapartum. BHIVA recommend that antiretroviral therapy may be started at an earlier gestation depending upon the individual situation

2) Mode of delivery
• elective caesarean section*
• a zidovudine infusion should be started four hours before beginning the caesarean section

3) Neonatal antiretroviral therapy
• zidovudine is usually administered orally to the neonate for four to six weeks

4) Infant feeding
• in the UK all women should be advised not to breast feed

*the 2008 BHIVA guidelines suggest vaginal delivery may be an option for women on HAART who have an undetectable viral load but whether this will translate into clinical practice remains to be seen

Front 77

Opportunistic organisms causing diarrhoea in HIV patients

Back 77

• Cryptosporidium + other protozoa (most common)
• Cytomegalovirus
• Mycobacterium aviumintracellulare
• Giardia

Front 78

Explain role of crytosporidium in HIV + patients

Back 78

the most common infective cause of diarrhoea in HIV patients. It is an intracellular protozoa and has an incubation period of 7 days. Presentation is very variable, ranging from mild to severe diarrhoea. A modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium. Treatment is difficult, with the mainstay of management being supportive therapy*

Front 79

Explain the role of Mycobacterium aviumintracellulare in HIV patients

Back 79

Mycobacterium aviumintracellulare is an atypical mycobacteria seen with the CD4 count is below 50. Typical features include fever, sweats, abdominal pain and diarrhoea. There may be hepatomegaly and deranged LFTs. Diagnosis is made by blood cultures and bone marrow examination. Management is with rifabutin, ethambutol and clarithromycin

Front 80

Which vaccines can be used in all HIV + adults?

Back 80

Hepatitis A
Hepatitis B
Haemophilusinfluenzae B (Hib)
Influenza-parenteral
Japanese encephalitis
Meningococcus-MenC
Meningococcus-ACWY I
Pneumococcus-PPV23
Poliomyelitis-parenteral (IPV)
Rabies
Tetanus-Diphtheria (Td)

Front 81

What vaccines can be used in HIV + if CD4> 200

Back 81

Measles, Mumps, Rubella (MMR)
Varicella
Yellow Fever

Front 82

What vaccines are contraindicated in HIV + adults?

Back 82

Cholera CVD103-HgR
Influenza-intranasal
Poliomyelitis-oral (OPV)
Tuberculosis (BCG)

Front 83

Management of oesophageal candidiasis in HIV + patients

Back 83

Oesophageal candidiasis is the most common cause of oesophagitis in patients with HIV. It is generally seen in patients with a CD4 count of less than 100. Typical symptoms include dysphagia and odynophagia. Fluconazole and itraconazole are first-line treatments

Front 84

Clinical features of HIV seroconversion

Back 84

symptomatic in 60-80% of patients and typically presents as a glandular fever type illness. Increased symptomatic severity is associated with poorer long term prognosis. It typically occurs 3-12 weeks after infection

Features
• sore throat
• lymphadenopathy
• malaise, myalgia, arthralgia
• diarrhoea
• maculopapular rash
• mouth ulcers
• rarely meningoencephalitis

Front 85

What investigations can be used to diagnosis HIV seroconversion?

Back 85

• antibodies to HIV may not be present
• HIV PCR and p24 antigen tests can confirm diagnosis

Front 86

Define Hand, foot, mouth disease.

Back 86

is a self-limiting condition affecting children. It is caused by the intestinal viruses of the Picornaviridae family (most commonly coxsackie A16 and enterovirus 71). It is very contagious and typically occurs in outbreaks at nursery

Front 87

Clinical features of hand, foot, mouth disease.

Back 87

• mild systemic upset: sore throat, fever
• oral ulcers
• followed later by vesicles on the palms and soles of the feet

Front 88

Managment and advice of Hand foot and mouth disease

Back 88

• general advice about hydration and analgesia
• reassurance no link to disease in cattle
• children do not need to be excluded from school*

*The HPA recommends that children who are unwell should be kept off school until they feel better. They also advise that you contact them if you suspect that there may be a large outbreak.

Front 89

Define head lice

Back 89

Head lice (also known as pediculosiscapitis or 'nits') is a common condition in children caused by the parasitic insect Pediculuscapitis, which lives on and among the hair of the scalp of humans

Front 90

Diagnosing headlice

Back 90

• fine-toothed combing of wet or dry hair

Front 91

Management of head lice

Back 91

• treatment is only if living lice are found
• a choice of treatments should be offered - malathion, wet combing, dimeticone, isopropyl myristate and cyclomethicone

School exclusion is not advised for children with head lice

Front 92

Define Hepatitis B

Back 92

a double-stranded DNA virus and is spread through exposure to infected blood or body fluids, including vertical transmission from mother to child. The incubation period is 6-20 weeks.

Front 93

What does hepatitis B vaccination contain?

Back 93

• contains HBsAg adsorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using recombinant DNA technology

Front 94

How often is hepatitis b vaccincation given?

Back 94

• most schedules give 3 doses of the vaccine with a recommendation for a one-off booster 5 years following the initial primary vaccination

Front 95

List the at risk groups who should have hepatitis b vaccination

Back 95

healthcare workers, intravenous drug users, sex workers, close family contacts of an individual with hepatitis B, individuals receiving blood transfusions regularly, chronic kidney disease patients who may soon require renal replacement therapy, prisoners, chronic liver disease patients

Front 96

What is the precentage of adults who fail to respond to hepatitis b vaccination? what are the risk factors?

Back 96

• around 10-15% of adults fail to respond or respond poorly to 3 doses of the vaccine. Risk factors include age over 40 years, obesity, smoking, alcohol excess and immunosuppression

Front 97

Which group of people should have testing for anti-Hbs?

Back 97

only recommended for those at risk of occupational exposure (i.e. Healthcare workers) and patients with chronic kidney disease. In these patients anti-HBs levels should be checked 1-4 months after primary immunisation

Front 98

Anti-Hbs level > 100mIU/ml

Back 98

Indicates adequate response, no further testing required. Should still receive booster at 5 years

Front 99

Anti-Hbs level 100 -10 mIU/ml

Back 99

Suboptimal response - one additional vaccine dose should be given. If immunocompetent no further testing is required

Front 100

Anti-Hbs level <10mIU/ml

Back 100

Non-responder. Test for current or past infection. Give further vaccine course (i.e. 3 doses again) with testing following. If still fails to respond then HBIG would be required for protection if exposed to the virus

Front 101

Complications of hepatitis B infection

Back 101

• chronic hepatitis (5-10%)
• fulminant liver failure (1%)
• hepatocellular carcinoma
• glomerulonephritis
• polyarteritisnodosa
• cryoglobulinaemia

Front 102

Management of Hepatitis B

Back 102

• 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
• however due to the side-effects of pegylated interferon it is now used less commonly in clinical practice. Oral antiviral medication is increasingly used with an aim to suppress viral replication (not in dissimilar way to treating HIV patients) examples include lamivudine, tenofovir and entecavir

Front 103

Managment of hepatitis B in pregnant women

Back 103

• all pregnant women are offered screening for hepatitis B
• babies born to mothers who are chronically infected with hepatitis B or to mothers who've had acute hepatitis B during pregnancy should receive a complete course of vaccination + hepatitis B immunoglobulin
• studies are currently evaluating the role of oral antiviral treatment (e.g. Lamivudine) in the latter part of pregnancy
• there is little evidence to suggest caesarean section reduces vertical transmission

Front 104

Who are included in the human pailloma virus vaccination?

Back 104

been introduced for girls aged 12-13 years. A number of catch-up programmes are being introduced for older girls.

Front 105

Which vaccination is used in the HPV vaccination program and why?

Back 105

Gardasil- protecting against HPV 16 & 18 it also protects against HPV 6 & 11 (genital warts)

* Cervarix only 16 and 18

Front 106

When and how HPV vaccination are given?

Back 106

For the vaccine to be effective it should be given before sexual activity starts. The vaccine is given as a series of three injections, usually within a 6-month period.

Injection site reactions are particularly common with HPV vaccines.

Front 107

Define infectious mononucleosis

Back 107

caused by the Epstein-Barr virus (also known as human herpesvirus 4, HHV-4). It is most common in adolescents and young adults.

Front 108

Clinical features of infectious mononucleosis

Back 108

• sore throat
• lymphadenopathy
• pyrexia
• malaise, anorexia, headache
• palatal petechiae
• splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
• hepatitis
• presence of 50% lymphocytes with at least 10% atypical lymphocytes
• haemolyticanaemia
• a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

Front 109

Investigation of infectious mononucleosis

Back 109

• heterophil antibody test (Monospot test)

Front 110

Managment of infectious mononucleosis

Back 110

• rest during the early stages, drink plenty of fluid, avoid alcohol
• simple analgesia for any aches or pains
• consensus guidance in the UK is to avoid playing contact sports for 8 weeks after having glandular fever to reduce the risk of splenic rupture

Front 111

Background of influenza

Back 111

- influenza season starts in middle of novemenber
- vaccination begins in sept to early november

Front 112

How many types of influenza virus?

Back 112

There are three types of influenza virus; A, B and C. Types A and B account for the majority of clinical disease. Current vaccines are trivalent and consist of two subtypes of influenza A and one subtype of influenza B.

Front 113

Which group of people should have annual influenza vaccination?

Back 113

annual influenza vaccination for people older than 65 years and those older than 6 months

if they have:
• chronic respiratory disease (including asthmatics who use inhaled steroids)
• chronic heart disease (heart failure, ischaemic heart disease, including hypertension if associated with cardiac complications)
• chronic kidney disease
• chronic liver disease: cirrhosis, biliary atresia, chronic hepatitis
• chronic neurological disease: (e.g. Stroke/TIAs)
• diabetes mellitus (including diet controlled)
• immunosuppression due to disease or treatment (e.g. HIV)
• asplenia or splenic dysfunction
• pregnant women

Children in at risk groups should be vaccinated. Only children aged less than 9 years who have not received influenza vaccine before should receive a second dose of vaccine at least 4 weeks later.

Front 114

Which group of people at at risk of influenza and should be offered vaccination?

Back 114

• health and social care staff directly involved in patient care (e.g. NHS staff)
• those living in long-stay residential care homes
• carers of the elderly or disabled person whose welfare may be at risk if the carer becomes ill (at the GP's discretion)

Front 115

Background of influenza vaccine

Back 115

• it is an inactivated vaccine, so cannot cause influenza. A minority of patients however develop fever and malaise which may last 1-2 days
• should be stored between +2 and +8�C and shielded from light
• contraindications include hypersensitivity to egg protein.
• in adults the vaccination is around 75% effective, although this figure decreases in the elderly
• it takes around 10-14 days after immunisation before antibody levels are at protective levels

Front 116

Define leishmaniasis

Back 116

caused by the intracellular protozoa Leishmania, usually being spread by sand flies. Cutaneous, mucocutaneousleishmaniasis and visceral forms are seen

Front 117

Define Cutaneous leishmaniasis

Back 117

• caused by Leishmaniatropica or Leishmaniamexicana
• crusted lesion at site of bite
• may be underlying ulcer

Front 118

Define Mucocutaneousleishmaniasis

Back 118

• caused by Leishmaniabrasiliensis
• skin lesions may spread to involve mucosae of nose, pharynx etc

Front 119

Define Visceral leishmaniasis (kala-azar)

Back 119

• mostly caused by Leishmaniadonovani
• occurs Mediterranean, Asia, South America, Africa
• fever, sweats, rigors
• massive splenomegaly. hepatomegaly
• poor appetite*, weight loss
• grey skin - 'kala-azar' means black sickness
• pancytopaenia secondary to hypersplenism

*occasionally patients may report increased appetite with paradoxical weight loss

Front 120

Define leoptospirosis

Back 120

Also known as Weil's disease*, leptospirosis is commonly seen in questions referring to sewage workers, farmers, vets or people who work in abattoir. It is caused by the spirochaeteLeptospirainterrogans (serogroup L icterohaemorrhagiae), classically being spread by contact with infected rat urine.

Front 121

Define weil's disease

Back 121

Weil's disease should always be considered in high-risk patients with hepatorenal failure

*the term Weil's disease is sometimes reserved for the most severe 10% of cases that are associated with jaundice

Front 122

Clinical features of leptospirosis

Back 122

• fever
• flu-like symptoms
• renal failure (seen in 50% of patients)
• jaundice
• subconjunctivalhaemorrhage
• headache, may herald the onset of meningitis

Front 123

MRSA stands for

Back 123

Methicillin-resistant Staphylococcus aureus (MRSA) was one of the first organisms which highlighted the dangers of hospital-acquired infections

Front 124

Who should be screened for MRSA?

Back 124

• all patients awaiting elective admissions (exceptions include day patients having terminations of pregnancy and ophthalmic surgery. Patients admitted to mental health trusts are also excluded)
• from 2011 all emergency admissions will be screened

Front 125

How should a patient be screened for MRSA?

Back 125

• nasal swab and skin lesions or wounds
• the swab should be wiped around the inside rim of a patient's nose for 5 seconds
• the microbiology form must be labelled 'MRSA screen'

Front 126

How can MRSA be suppressed in carriers once identified?

Back 126

• nose: mupirocin 2% in white soft paraffin, tds for 5 days
• skin: chlorhexidinegluconate, od for 5 days. Apply all over but particularly to the axilla, groin and perineum

Front 127

Which antibiotics are used to treat MRSA?

Back 127

• vancomycin
• teicoplanin

Front 128

Which antibiotics maybe sensitive but they are generally not used alone because of resistance may develop?

Back 128

• rifampicin
• macrolides
• tetracyclines
• aminoglycosides
• clindamycin

Front 129

Which new antibiotic can be used in treatment of MRSA but reserved for resistant cases?

Back 129

linezolid, quinupristin/dalfopristin combinations and tigecycline

Front 130

How many cases of malaria cases each year in the UK of patients returning from endemic country?

Back 130

1500-2000 cases, majority not taking prophylaxis

Front 131

What protozoa and % cause majority of malaria cases in the UK?

Back 131

Plasmodium falciparum
75%

Front 132

What happens to the innate immunity when move to the Uk from area of high endemic?

Back 132

lost their immunity!

Front 133

Side effects, Start time and end time of malaria prophylaxis: Atovaquone + proguanil (Malarone)

Back 133

GI upset,
Start: 1-2 days
End: 7 days

Front 134

Side effects, Start time and end time of malaria prophylaxis: Doxycycline

Back 134

Side effect: Phtosensitivity, oesophagitis
Start time: 1-2 days
End time: 4 weeks

Front 135

Side effects, Start time and end time of malaria prophylaxis:Chloroquine

Back 135

Side effect: Headache
Start time: 1 week
End time: 4 week

Contraindicated in epilepsy
Taken weekly

Front 136

Side effects, Start time and end time of malaria prophylaxis:Mefloquine (Lariam)

Back 136

Side effect: Dizziness, Neuropsychiatric disturbance
Start time: 2-3 weeks
End time: 4 weeks


Contraindicated in epilepsy
Taken weekly

Front 137

Side effects, Start time and end time of malaria prophylaxis: Proguanil (Paludrine), Proguanil + chloroquine

Back 137

Side effect: GI upset, Headache
Start time:1 week
End time: 4 weeks

Front 138

What are the medical advice and medication for pregnant women travelling to malaria regions?

Back 138

advised to avoid travelling to regions where malaria is endemic. Diagnosis can also be difficult as parasites may not be detectable in the blood film due to placental sequestration. However, if travel cannot be avoided:
• chloroquine can be taken
• proguanil: folate supplementation (5mg od) should be given
• Malarone (atovaquone + proguanil): the BNF advises to avoid these drugs unless essential. If taken then folate supplementation should be given
• mefloquine: caution advised
• doxycycline is contraindicated

Front 139

What are the medical advice and medication for children travelling to malaria regions?

Back 139

avoid travel to malaria endemic regions with children if avoidable. However, if travel is essential then children should take malarial prophylaxis as they are more at risk of serious complications.
• diethyltoluamide (DEET) 20-50% can be used in children over 2 months of age
doxycycline is only licensed in the UK for children over the age of 12 years

Front 140

What investigation should be performed for suspected menigitis?

Back 140

• full blood count
• CRP
• coagulation screen
• blood culture
• whole-blood PCR
• blood glucose
• blood gas

Lumbar puncture if no signs of raised intracranial pressure

Front 141

Management in GP of patient with suspected meningococcal disease.

Back 141

IM benzypenivillin in GP then admit

Front 142

Suspected menigitis antibiotic treatment: aged < 3 months

Back 142

Intravenous cefotaxime + amoxicillin

Front 143

Suspected menigitis antibiotic treatment: aged 3 months - 50 years

Back 143

Intravenous cefotaxime

Front 144

Suspected menigitis antibiotic treatment: aged > 50 years

Back 144

Intravenous cefotaxime + amoxicillin

Front 145

Antibiotic treatment for Meningococcal meningitis

Back 145

Intravenous benzylpenicillin or cefotaxime

Front 146

Antibiotic treatment for Pneuomococcal meningitis

Back 146

Intravenous cefotaxime

Front 147

Antibiotic treatment for Meningitis caused by Haemophilusinfluenzae

Back 147

Intravenous cefotaxime

Front 148

Meningitis caused by Listeria

Back 148

Intravenous amoxicillin + gentamicin

Front 149

Which antibiotic to give to patients with suspsected penicillin allergy or cephalosporin?

Back 149

chloramphenicol.

Front 150

How to manage the contact of confirmed/suspsected menigitis?

Back 150

• prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis
• oral rifampicin or ciprofloxacin may be used
• the risk is highest in the first 7 days but persists for at least 4 weeks
• meningococcal vaccination should be offered when serotype results are available, for close contacts who have not previously been vaccinated

Front 151

What are the complications of mycoplasma pneumoniae infection?

Back 151

• cold agglutins (IgM) may cause an haemolyticanaemia, thrombocytopenia
• erythema multiforme, erythema nodosum
• meningoencephalitis, Guillain-Barre syndrome
• bullous myringitis: painful vesicles on the tympanic membrane
• pericarditis/myocarditis
• gastrointestinal: hepatitis, pancreatitis
• renal: acute glomerulonephritis

Front 152

What does mycoplasma pneumoniae cause?

Back 152

atypical pneumonia which often affects younger patients

Front 153

How many years does epidemic of mycoplama pneumoniae classically happen?

Back 153

Every 4 years

Front 154

Clinical features of mycoplasma pneumoniae.

Back 154

• the disease typically has a prolonged and gradual onset
• flu-like symptoms classically precede a dry cough
• bilateral consolidation on x-ray
• complications may occur as below

Front 155

Investigation of mycoplasma pneumoniae

Back 155

• diagnosis is generally by Mycoplasma serology
• positive cold agglutination test

Front 156

Managment of mycoplasma pneumoniae

Back 156

• erythromycin/clarithromycin
tetracyclines such as doxycycline are an alternative

Front 157

List the UK urgent notifiable diseases

Back 157

- Anthrax
- Cholera
- Diphtheria
- acute infectious hepatitis
- Measles
- Meningitis
- Meningococcal septicaemia
- Plague
- Poliomyelitis
- Rabies
- Invassive group A streptocococcal disease (No to Scarlet fever)
- Smallpox
- SARS
- botulium
- Enteric fever ( typhoid or parathyphoid)
-Viral haemorrhagic fever, including Lassa fever and Marburg virus
- Whooping cough ( acute phase)
- Haemolytic uraemic syndrome
- infectious bloody diarrhoea
- legionnaires' disease

Front 158

List of UK non urgent nortifiable diseases

Back 158

Acute encephalitis
Brucellosis ( unless thought UK acquired_
Food poisoning ( unless clusters)
Leprosy
Malaria (unless UK acquired)
Mumps
Tetanus
TB ( unless HCW, clusters, multi drug resistance)
Typhus
Yellow fever ( unless UK aquired
Scarlet fever

Front 159

How many pneumococal vaccines are currently available?

Back 159

• pneumococcal conjugate vaccine (PCV)
• pneumococcal polysaccharide vaccine (PPV)

Front 160

When is the PCV vaccination given to children?

Back 160

as part of their routine immunisations (at 2, 4 and 13 months).

Front 161

Which group of patients should be vaccinated against pneumococcal infection?

Back 161

• asplenia or splenic dysfunction
• all adults over the age of 65 years
• splenectomy
• chronic respiratory disease: COPD, bronchiectasis, cystic fibrosis, interstitial lung disease.

*Asthma is only included if 'it requires the use of oral steroids at a dose sufficient to act as a significant immunosuppressant'
• chronic heart disease: ischaemic heart disease if requiring medication or follow-up, heart failure, congenital heart disease.

*Controlled hypertension is not an indication for vaccination
• chronic kidney disease
• chronic liver disease: including cirrhosis and chronic hepatitis
• diabetes mellitus if requiring medication
• immunosuppression (either due to disease or treatment). This includes patients with any stage of HIV infection
• cochlear implants
• patients with cerebrospinal fluid leaks

Front 162

How many does of pneumococcal vaccine does an adult receive?

Back 162

1

Front 163

Which group of patients should have pneumococcal booster every 5 years?

Back 163

asplenia, splenic dysfunction or chronic kidney disease

Front 164

What organisms cause community acquired pneumonia?

Back 164

• Streptococcus pneumoniae (accounts for around 80% of cases) - commonest
• Haemophilus influenzae
• Staphylococcus aureus: commonly after the 'flu
• atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
• viruses
• Klebsiella pneumoniae is classically in alcoholics

Front 165

What are the clinical features of pneumococcal pneumonia?

Back 165

• rapid onset
• high fever
• pleuritic chest pain
• herpes labialis
What the BTS recommended treatment for CAP?
• low or moderate severity CAP: oral amoxicillin. A macrolide should be added for patients admitted to hospital
• high severity CAP: intravenous co-amoxiclav + clarithromycin OR cefuroxime + clarithromycin OR cefotaxime + clarithromycin

Front 166

Post-exposure prophylaxis: Hepatitis A

Back 166

• Human Normal Immunoglobulin (HNIG) or hepatitis A vaccine may be used depending on the clinical situation

Front 167

Post-exposure prophylaxis: Hepatitis B

Back 167

• HBsAg positive source: if the person exposed is a known responder to HBV vaccine then a booster dose should be given. If they are in the process of being vaccinated or are a non-responder they need to have hepatitis B immune globulin (HBIG) and the vaccine
•
• unknown source: for known responders the green book advises considering a booster dose of HBV vaccine. For known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine

Front 168

Post-exposure prophylaxis: Hepatitis c

Back 168

• monthly PCR - if seroconversion then interferon +/- ribavirin

Front 169

Post-exposure prophylaxis: HIV

Back 169

• a combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir) as soon as possible (i.e. Within 1-2 hours, but may be started up to 72 hours following exposure) for 4 weeks
• serological testing at 12 weeks following completion of post-exposure prophylaxis
• reduces risk of transmission by 80%

Front 170

Post-exposure prophylaxis: Varicella Zoster

Back 170

• VZIG for IgG negative pregnant women/immunosuppressed

Front 171

What is the estimated transmission risk of hepatitis B after single needlestick injury ?

Back 171

20-30%

Front 172

What is the estimated transmission risk of hepatitis C after single needlestick injury ?

Back 172

0.5-2%

Front 173

What is the estimated transmission risk of HIV after single needlestick injury ?

Back 173

0.3%

Front 174

Explain quinolone and give 2 examples.

Back 174

Quinolones are a group of antibiotics which work by inhibiting DNA synthesis and are bactericidal in nature. Examples include:
• ciprofloxacin
• levofloxacin

Front 175

What is the mechanism of action of quinolones?

Back 175

• inhibit topoisomeras II (DNA gyrase) and topoisomerase IV

Front 176

What are the side effect of quinolones?

Back 176

• lower seizure threshold in patients with epilepsy
• tendon damage (including rupture) - the risk is increased in patients also taking steroids
• cartilage damage has been demonstrated in animal models and for this reason quinolones are generally avoided (but not necessarily contraindicated) in children

Front 177

In what group of patients where a no antibiotic prescribing or delayed antibiotic prescribing approach is generally recommended?

Back 177

acute otitis media, acute sore throat/acute pharyngitis/acute tonsillitis, common cold, acute rhinosinusitis or acute cough/acute bronchitis

Front 178

In what group of patients is an immediate antibiotic prescribing approach may be considered for?

Back 178

• children younger than 2 years with bilateral acute otitis media
• children with otorrhoea who have acute otitis media
• patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present

Front 179

What is the centor criteria?

Back 179

• presence of tonsillar exudate
• tender anterior cervical lymphadenopathy or lymphadenitis
• history of fever
• absence of cough

Front 180

Which group of patients at risk of developing complications, an immediate antibiotic prescribing policy is recommended for?

Back 180

• are systemically very unwell
• have symptoms and signs suggestive of serious illness and/or complications (particularly pneumonia, mastoiditis, peritonsillar abscess, peritonsillar cellulitis, intraorbital or intracranial complications)
• are at high risk of serious complications because of pre-existing comorbidity. This includes patients with significant heart, lung, renal, liver or neuromuscular disease, immunosuppression, cystic fibrosis, and young children who were born prematurely
• are older than 65 years with acute cough and two or more of the following, or older than 80 years with acute cough and one or more of the following:
• - hospitalisation in previous year
• - type 1 or type 2 diabetes
• - history of congestive heart failure
• - current use of oral glucocorticoids

Front 181

How long does an acute otitis media last for?

Back 181

4days

Front 182

How long does acute sore throat/acute pharyngitis/acute tonsillitis last for?

Back 182

1 week

Front 183

How long does common cold last for?

Back 183

1.5 week

Front 184

How long does acute rhinosinusitis last for?

Back 184

2.5weeks

Front 185

How long does acute cough/acute bronchitis last for?

Back 185

3 weeks

Front 186

How many criteria are present for there to be a sore throat caused of Group A beta haemolytic streptococcus? And what percentage?

Back 186

if 3 or more of the criteria are present there is a 40-60% chance the sore throat is caused by Group A beta-haemolytic Streptococcus

Front 187

What are the differentials of genital ulcers?

Back 187

Genital herpes, syphilis, chanroid, lymphogranuloma venereum, Behcet's disease,carcinoma
, granuloma inguinale: Klebsiella granulomatis*

Front 188

Which organism cause chancroid?

Back 188

is a tropical disease caused by Haemophilus ducreyi

Front 189

How does chancroid normally present?

Back 189

causes painful genital ulcers associated with unilateral, painful inguinal lymph node enlargement. The ulcers typically have a sharply defined, ragged, undermined border.

Front 190

Definite Lymphogranuloma venereum

Back 190

caused by Chlamydia trachomatis.
Typically infection comprises of three stages
• stage 1: small painless pustule which later forms an ulcer
• stage 2: painful inguinal lymphadenopathy
• stage 3: proctocolitis

Front 191

School exclusion advice: no exclusion

Back 191

Conjunctivitis
Fifth disease
Roseola
Infectious mononucleosis
Head lice
Threadworms

Front 192

School exclusion advice: 24 hours after commencing antibiotics

Back 192

Scarlet fever

Front 193

School exclusion advice: Four days from onset of rash

Back 193

Measles

Front 194

School exclusion advice: Chickenpox

Back 194

Five days from onset of rash

Front 195

School exclusion advice: Mumps

Back 195

Five days from onset of swollen glands

Front 196

School exclusion advice: Whooping cough

Back 196

Five days after commencing antibiotics

Front 197

School exclusion advice: Rubella

Back 197

Six days from onset of rash

Front 198

School exclusion advice: Diarrhoea & vomiting

Back 198

Until symptoms have settled for 48 hours

Front 199

School exclusion advice: Impetigo

Back 199

Until lesions have crusted over

Front 200

School exclusion advice: Scabies

Back 200

Until treated

Front 201

School exclusion advice: Influenza

Back 201

Until recovered

Front 202

Which organism cause syphilis?

Back 202

caused by the spirochaete Treponema pallidum

Front 203

How many stages do syphilis present?

Back 203

3 stages:
Primary
• chancre - painless ulcer at the site of sexual contact
• local non-tender lymphadenopathy
• often not seen in women (the lesion may be on the cervix)
• A painless ulcer (chancre) is seen in the primary stage.

Secondary (occurs 6-10 weeks after primary infection)
• systemic symptoms: fevers, lymphadenopathy
• rash on trunk, palms and soles
• buccal 'snail track' ulcers (30%)
• condylomata lata

Tertiary stages/latent period
• gummas
• aortic aneurysms
• general paralysis of the insane
• tabes dorsalis

Front 204

What is the incubation period of syphilis?

Back 204

incubation period= 9-90 days

Front 205

What are the clinical features of congenital syphilis?

Back 205

• blunted upper incisor teeth
• keratitis
• saber shins
• saddle nose
• deafness

Front 206

What is tetanus vaccine?

Back 206

a cell-free purified toxin that is normally given as part of a combined vaccine.#

Front 207

When is tetanus vaccine is currently given in the UK as part of the routine immunisation schedule?

Back 207

• 2 months
• 3 months
• 4 months
• 3-5 years
• 13-18 years

This therefore provides 5 doses of tetanus-containing vaccine. Five doses is now considered to provide adequate long-term protection against tetanus.

Front 208

When should tetanus immunoglobulin to given?

Back 208

Intramuscular human tetanus immunoglobulin should be given to patients with high-risk wounds (e.g. Compound fractures, delayed surgical intervention, significant degree of devitalised tissue) irrespective of whether 5 doses of tetanus vaccine have previously been given

If vaccination history is incomplete or unknown then a dose of tetanus vaccine should be given combined with intramuscular human tetanus immunoglobulin for high-risk wounds

Front 209

Rifampicin: side effect and MOA

Back 209

Rifampicin: side effect and MOA

Front 210

Isoniazid : side effect and MOA

Back 210

• mechanism of action: inhibits mycolic acid synthesis
• peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
• hepatitis, agranulocytosis
• liver enzyme inhibitor

Front 211

Pyrazinamide: side effect andMOA

Back 211

• mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
• hyperuricaemia causing gout
• hepatitis

Front 212

Ethambutol:side effect and MOA

Back 212

• mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
• optic neuritis: check visual acuity before and during treatment
• dose needs adjusting in patients with renal impairment

Front 213

What is the standard treatment regime of active TB?

Back 213

Initial phase - first 2 months (RIPE)
• Rifampicin
• Isoniazid
• Pyrazinamide
• Ethambutol (the 2006 NICE guidelines now recommend giving a 'fourth drug' such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected)

Continuation phase - next 4 months
• Rifampicin
• Isoniazid

Front 214

What is the treatment regime of latent TB?

Back 214

isoniazid alone for 6 months

Front 215

How long should meningeal TB be treated for?

Back 215

a prolonged period (at least 12 months) of standard therapy with the addition of steroids

Front 216

Which group of patients should have directly observed therapy with a three times a week dosing regimen of TB medications?

Back 216

• homeless people with active tuberculosis
• patients who are likely to have poor concordance
• all prisoners with active or latent tuberculosis

Front 217

Explain mantoux test and its interpertation

Back 217

• main technique used to screen for latent tuberculosis.
• ml of 1:1,000 purified protein derivative (PPD) injected intradermally
• result read 2-3 days later
In recent years the interferon-gamma blood test has also been introduced. It is used in a number of specific situations such as:
• the Mantoux test is positive or equivocal
• people where a tuberculin test may be falsely negative (see below)

Mantoux test result: <6mm
Negative - no significant hypersensitivity to tuberculin protein
Previously unvaccinated individuals may be given the BCG
Mantoux test result: 6-15 mm
Positive - hypersensitive to tuberculin protein
Should not be given BCG. May be due to previous TB infection or BCG
Mantoux test result: > 15 mm
Strongly positive - strongly hypersensitive to tuberculin protein
Suggests tuberculosis infection.

Front 218

What group of patients may have false negative mantoux test ?

Back 218

• miliary TB
• sarcoidosis
• HIV
• lymphoma
• very young age (e.g. < 6 months)

Front 219

What is the treatment guideline of UTI in non pregnant women?

Back 219

trimethoprim or nitrofurantoin for 3 days

Front 220

What is the treatment guideline of UTI in pregnant women?

Back 220

For symptomatic bacteriuria should be treated with an antibiotic for 7 days. A urine culture should be sent.
For asymptomatic pregnant women:
• a urine culture should be performed routinely at the first antenatal visit
• if positive, a second urine culture should be sent to confirm the presence of bacteriuria
• SIGN recommend to treat asymptomatic bacteriuria detected during pregnancy with an antibiotic
• a 7 day course of antibiotics should be given
• a further urine culture should be sent following completion of treatment as a test of cure

Front 221

What is the treatment of acute pyelonephritis

Back 221

- hospital admission should be considered
- a broad-spectrum cephalosporin or a quinolone for 10-14 days or co-amoxiclav

Front 222

Describe Acanthosis nigricans

Back 222

symmetrical, brown, velvety plaquest that are often found in the axilla, groin, and neck

Front 223

What are the causes of acanthosis nigicans?

Back 223

• gastrointestinal cancer
• diabetes mellitus
• obesity
• polycystic ovarian syndrome
• acromegaly
• Cushing's disease
• hypothyroidism
• familial
• Prader-Willi syndrome
• drugs: oral contraceptive pill, nicotinic acid

Front 224

Define acne rosacea.

Back 224

a chronic skin inflammatory disease of unknown cause
, older patients (30-50), more females

Front 225

Clinical features of acne roasesa

Back 225

Typically affects the nose/cheek/ forehead
Transient erythema (flushing) with burning sensation is common
Telangiectasia is common
Persistant erythema can cause papules and pustules
Rhinophyma ( red nose)
Blepharitis

Front 226

Management of acne rosacea

Back 226

1) Topical metronidazole ( mild disease)
2) Oral metronidazole, oxytetracycline, erythromycin
3) Camouflage cream
4) High SFF
5) Laser therapy( prominent telangiectasia)
6) Avoid steriod
7) Avoid exacerbating factors ( heat, cold, wind, sun, stress, drinking hot liquid, alcohol, caffiene, spices )

Front 227

Define Acne Vulgaris

Back 227

- A common inflammatory disease of pilosebaceous follicles caused by keratin plugs.
- Increased sebum production which is converted to FFA by anearobic propionibacterium acne --> irritant causing inflammation and delayed hypersensitivity causing papules, comdeones, and pustules
- affecting mostly adolescence ( 80-90%, with 60 % seeking help)
- Adults > 25y: 10-15% female, 5% male

Front 228

Exacerbating factors of Acne vulgaris

Back 228

menstruation/ hormonal factors ( androgen increases sebum production )
OCP
Topical acngenic agents ( steroids, taqrs, ointments, greasy cometics )
Systemic meds: lithium, phenytoin, steroids, halogens, androgens, iodides, bromides, danzol

Front 229

How many types of Acne Vulagris are there?

Back 229

4 types:
1) Type 1 (mild)- comedones ( dilated sebaceous follicles, Open- black head, closed- white heads)
2) Type 2 (moderate)- papules ( inflammatory lesions form and follicles bursts and release irritant ) +/- scarring
3) Type 3 ( Moderate)- pustular ( as above) + scarring
4) Type 4 (Severe) -nodules and cysts ( excessive inflammatory response) + severe scarring

Front 230

What is characteristic about drug induced acne?

Back 230

monomorphic appearance

Front 231

What type of acne does steroid induced acne cause?

Back 231

pustules

Front 232

What is acne fulminans?

Back 232

Severe acne with systemic upset. Ususally require hospitalization and responds to steroid.

Front 233

What is the treatment of acne vulgaris?

Back 233

1) mild - topical single therapy ( Topical retinoids, BZP )
2) moderate - topical combination therapy ( topical abx erythromycin/clindamycin, BZP, topical retinoid - retinion)
3) severe - oral antibiotics ( oxytetracycline, doxycycline, trimethoprim, erythromycin-safe in pregana, tetracycline )
4) very severe- oral isotretinion ( unsafe in pregnancy and breastfeeding)

* COCP can also be used- dianette
* oral treatment takes 3-4 months to see effect
* no role of dietary modication in patients with acne

Front 234

Why is minocycline less used in the management of acne vulgaris?

Back 234

potentially causes irreversible pigementation

Front 235

What is a potential complication of long term antibiotic use in acne vulagris? Whats the treatment?

Back 235

gram negative follicultis, can be treated with oral trimethoprim

Front 236

Define actinic keratoses (aka. solar keratoses)

Back 236

a common premalignant skin lesions that develops as result of chronc sun exposure
more common in elderly
more males
1-10% can transform to SCC

Front 237

What is the Sx of actinic keratoses?

Back 237

Normally found in sun exposed areas
small crusty scaly pink/brown/flesh coloured lesions

Front 238

What are the management of actinic keratoses?

Back 238

1) Advice: avoid sun, SPF
2) Fluorouracil cream : 2-3 weeks course, can cause inflammation of skin, which can be treated with topical hydrocortisone
3) Topical diclofenac ( mild disease, moderate efficacy but few side effects)
4) Topical imiquimoid (Aldara) applied for 8-10 weeks
5) Cryotherapy
6) Curettage and cautery

* biopsy lesions that are resistant to treatment.

Front 239

How many types of allergy testing?

Back 239

Skin prick test
Radioallergosorbent rest (RAST)
Skin patch testing

Front 240

Explain skin prick test

Back 240

commonest because easy to perform, quick 15mins to read, and inexpensive
Procedure: skin pricked with needles, diluted allergen applied, wheal develops if allergic and compared to control (sterile water)
Useful for food allergies and pollen

Front 241

Explain RAST testing

Back 241

Useful for food allergies, inhaled allergen (eg. pollen), and wasp/bee venom
Results graded from 0 ( negative) to 6 ( strong)
Determines amount of IgE in blood that reacts to specific known or suspected allergen
used when skin prick test unsuitable (eg. extensive ezcema or patient taking antihistamine)

Front 242

Explain skin patch testing

Back 242

Useful for contact dermatiis
30-40 allergens and irritants placed on the back --> removed 48 hours later, read by dermatologist

Front 243

What causes scarring alopecia (ie. destruction of hair follicle?

Back 243

Trauma/burn
radiotherapy
lichen planus
discoid lupus
untreated tinea capitis --> kerion

Front 244

What causes non scarring alopecia ( ie. preservation of hair follicles ) ?

Back 244

Male pattern baldness
tchicotillomania
telogen effluvium ( hair loss following stressful event)
autoimmune ( alopecia areata)
Fe/zinc deficiency
Rx: COCP, colchichine, heparin, carbimazole, cytotoxic drugs

Front 245

Define alopecia areata.

Back 245

autoimmune condition characterized by patches of complete hair loss ( localised , well demarcated ) localized to scalp, eyebrowns, beard, eyelashes
If hair loss is at hairline, there maybe "exclamation mark" pattern.

Front 246

How long does patient with alopecia areata take to regrow hair without treatment?

Back 246

50% regrows at 1 y, 80-90% grows eventually

* worse prognosis if young and extensive losses
* frequent recurrence that can be precipated by emotional distress

Front 247

What are the treatment options for patients with alopecia areata?

Back 247

1) reassurance
2) Wigs
3) Topical or intralesional corticosterioids
4) Topical minoxidil
5) phototherapy
6) dithranol
7) contact immunotherapy

* treatments are usually unsatisfactory

Front 248

Define antiphospholipid (antibody) syndrome.

Back 248

an not understood acquired disorder that causes an increased risk of venous and aterial thromboses formation.
It can be a primary condition or secondary condition
It is associated with SLE, autoimmune diseases, lymphoproliferative disorders, phenothiazine (rare)

Front 249

What lab investigations can be done for patient with suspected antiphospholipid syndrome?

Back 249

Anticardiolipin and lupus anticoagulant antibodies

Front 250

What are the features associated with antiphsopholipid syndrome?

Back 250

Venous/aterial thrombosis
recurrent spontaneous fetal loss
thombocyctopenia
prolonged APPT ( but ex vivo reation of lupus anticoagulant autoantibodies with phsopholips results in transient paradoxical rise in APTT)
livedo reticularis (purplish mottling of the skin)
pre-eclampsia
pulmonary hypertension

Front 251

What is the anticoagulation management of patients with antiphospholid syndrome?

Back 251

Arterial thrombosis (INR 2-3) and recurrent venous thrombosis (INR 3-4) - lifelong warfarin
Initial venous thrombosis (INR 2-3)- 6/12 warfarin

Front 252

Explain Athele's foot ( aka: tinea pedis) .

Back 252

Fungal infection of the foot caused by Trichophyton

Front 253

What are the clinical features of tinea pedis ( athlete's foot)?

Back 253

typically scaling, flaking, itching between toes
exacerbated by heat, humidity, occlusive footwear

Front 254

What is the treatment for tinea pedis?

Back 254

First line : Topical imidazole ( clotrimazole 1%, 2% miconazole) , undecenoate ( Mycota) , terbinafine

Front 255

Explain Basal Cell Carcinoma.

Back 255

maligant proleration of basal cells of the epidermis
one of the 3 main types of skin cancer
commonest skin cancer in the western world
There are 4 subtypes but most common is nodular BCC
Lesions are also known as rodent ulcers characterized by slow growth and local invasion
Mets are extremely rare
More male

Front 256

What are the causes of BCC?

Back 256

scar formation, radiation, trauma, arsenic exposure, genetic predisposition ( Gorlin syndrome)
Most commonly sun exposure

Front 257

What are the clinical features of basal cell carcinoma?

Back 257

normally over sun exposed area ( eg. head and neck)
initially pearly, flesh-coloured papule with telangiectasia which may ulcerate leaving a central crater.

Front 258

What are the treatment options fo basal cell carcinoma?

Back 258

1) topical cream if surgery not appropriate: imiquimod, fluorouracil
2) Radiotherapy
3) cryotherapy
4) curettage
5) surgical removal

* lifelong follow up
*95% cure rate if lesion is less than 2cm

Front 259

Define blepharitis.

Back 259

inflammation of the eyelid margins

Front 260

What are the causes of blepharitis?

Back 260

1) Posterior blephritis (Common) : meibomian gland dysfunction
2) Anterior blephritis ( uncommon ): seborrhoeic dermatitis, staphylococcal infection

* more common with acne rosacea patients

Front 261

What are the clinical features and complications of blephritis?

Back 261

usually bilateral
sticky morning eyes
grittness and discomfort
red and swollen ( esp,. staphylococcal blepharitis)

Complications: styes and chalazion, secondary conunctivitis, keratitis, corneal ulveration and neovascularization

Front 262

Why does meibomian dysfunction causes blephritis?

Back 262

meibomian glands secretes oil onto eye surface--> prevent tears film evaporating rapidly T4 if lack --> drys eyes and irritation.

Front 263

What is the management plan for blepharitis?

Back 263

1) softening of lid margins using hot compression BD
2) Mechanical removal of debris from lid margin with diluated baby shampoo (4:1 with cooled boil water). Can also use sodium bicarbonate.
3) Artificial tears
4) topical and systemic abx +/- referral ? steroid.

Front 264

Explain bowen's disease.

Back 264

Aka: SCC in situ
more common in female
3% chance of developing into invasive skin cancer

Front 265

Clinical features of bowen's disease

Back 265

red, scaly patches with sharply demarcated red and scaly border
often found in the lower limbs

Front 266

Treatment options fo bowen's disease

Back 266

1) biopsy for diagnosis
2) as per BCC,
topical cream if surgery not appropriate: imiquimod, fluorouracil
Radiotherapy
cryotherapy
curettage
surgical removal

Front 267

What are the causes of bullous skin disorders?

Back 267

• congenital: epidermolysis bullosa
• autoimmune: bullous pemphigoid, pemphigus
• insect bite
• trauma/friction
• drugs: barbiturates, furosemide

Front 268

Define bullous pemphigoid.

Back 268

a chronice autoimmune skin condition causing sub-epidermal blistering of skin. ( ie. IgG antibodies againist hemidesmosomal protien at dermal-erpidermal basement membrane)
Elderly female most common

Front 269

Clinical features of bullous pemphigoid

Back 269

itchy, tense blisters typically around flexures
mouth usually spared ( 10-50% patient with involvement)
blisters heal without scarring

Front 270

How is bullous pemphigoid diagnosed ( ie. invesgation ) ?

Back 270

skin biopsy: immunofluorescence shows IgG and C3 at basement membrane
blood test: anti-basement membrane antibodies (IgG)

Front 271

Management of bullous pemphigoid.

Back 271

1) referral to dermatologist
2) oral steroid +/- azathioprine
3) Topical steroid ( ie . clobetasol )
4) Topical antibiotic ( tetracycline +/- nicotinamide)
5) dapsone ( mild cases)

Front 272

Management of cellulitis.

Back 272

1) flucloxacillin oral ( mild/moderate) or clarithromycin/clindamycin (if pen allergic)
2) oral clindamycin if fail to responds to flucloxacillin
3) IV benpen ( severe) + admit

Front 273

Define cherry haemangioma ( aka: campbell demorgan spot).

Back 273

benign vacular neoplasm/lesion
abnormal proliferation of capillaries
Male=female
more elderly
can increase in size

Front 274

Clinical features and treatment of cherry haemangioma.

Back 274

dome shaped erythmatous papule
1-3 mm in size
non blanching
not found on mucous membrane
NO treatment needed ( comestic: laser or excision)

Front 275

Define chondrodematitis nodularis helicis.

Back 275

common and begnin
characterized by development of painful nodule on ear
usually secondary to friction, cold, trauma and persistent pressure ( eg. headset)
More men
Elderly

Front 276

Management of chondrodermatitis nodularis helicis.

Back 276

1) reducing pressure
2) ear protectors
3) surgical- but with high recurrence
4) cyrotherapy, steroid injfection, collagen injection.

Front 277

Define contact dermatitis and how many types?

Back 277

cutaneous inflammation between interaction of external agent and skin. There are 2 types: 1) allergic contact dermatitis 2) irritant contact dermatitis

Front 278

Explain/Sx/Mx irritant contact dermatitis.

Back 278

non immune mediated
irritant to skin ( weak acids or alkalis-detergent)
comon, esp amongst hand
erythema ( common)
crusting/ vesicles (rare)
Mx: avoidance, moisturiers, topical +/- oral steroids

Front 279

Explain/Sx/Mx allergic contact dermatitis.

Back 279

immune cell mediated type 4 hypersentivity
uncommon
Eg. hair dye
Presents with weeping eczema
Mx: patch testing, avoidance, topical steroid +/- oral steroid

Front 280

What material can cause allergic contact dermatitis and irritant contact dermatitis?

Back 280

cement!
Alkaline nature-irriatnt
dichromates in cement- allergic

Front 281

Explain dermatitis herpetiformis

Back 281

Autoimmune blistering skin disorder.
Deposition of IgA in dermis
Associated with coeliac disease (80%), thyroid disease, intestinal lymphoma, iron and folate deficiency

Front 282

Sx of dermatitis herpetiformis.

Back 282

intensely itchy grounped of papules, vesicles, urticarial wheals on extensor surfaces of skin ( eg. elbow, knee, buttocks)
Bilateral symmetrical
almost always excoriated, rarely blisters

Front 283

What is seen on skin biopsy for dermatitis herpetitformis?

Back 283

direct immunofluorescence - deposition of IgA in granular pattern in the upper dermis

Front 284

Mx for dermatitis herpetiformis

Back 284

Gluten free diet
dapsone for itch

Front 285

Explain dermatomyositis

Back 285

idopathic or associated with CTD or underlying malignancy ( eg. lung cancer- about 20-25%, more if older)
an inflammatory disorder causing symmetrical, proximal muscle weakness, and characteristic skin lesions.

Front 286

What is the name of the condition that is similar to dermatomyositis but skin manifestiation isn't prominent?

Back 286

polymyositis

Front 287

Clinical features of dermatomyositis.

Back 287

Photosensitive
Macular rash over back and shoulder
Nail fold capillary dilatation
Heliotrope rash-in periorbital region ( red rash)
Gottron's papules - roughenged red papules over extensor surfaces of fingers.

Front 288

What are the associated features systemic complications of dermatomyositis?

Back 288

proximal muscle weakness +/- tenderness
Raynaud's
Respiratory muscle weakness
interstitial lung disease ( fibrosising alveolitis or organising pneumonia)
Dysphagia and dyphonia

Front 289

What drugs causes photosensitivity?

Back 289

Amiodarone
Doxycycline, tetracycline, sulphonamide, ciprofloxacin
Thiazides
NSAID ( eg. piroxicam)
Sulphonylureas
Psoralens

Front 290

What is ezcema herpeticum?

Back 290

occurs in patients with severe atopic ezcema and infected with HSV 1/2
Hospitalization and IV aciclovir

Front 291

Define and explain atopic ezcema.

Back 291

an acute and chornic inflammation of the skin
IgE mediated ( Type 1 hypersensitivity)

Front 292

How many children in the UK has atopic ezcema? How many % clear for 5 and how many clear by 10?

Back 292

15-30%
by 5y- 50%
by 10y-75 %

Front 293

What is the clinical features of atopic eczema? infant? younger children? older children/adult?

Back 293

Infant (2-6m): face, scalp, trunk
Younger children: extensor surfaces
Older children/adults: flexures surfaces and creases of face/neck

Front 294

What is the treatment options for atopic eczema?

Back 294

1) Avoid irritant
2) Abundance of emollient ( 250 gram/week, cream soaks better then ointments, BD)
3) Topical steroids- applied 30 mins after emollients
4) Severe cases- wet wraps/ oral ciclosporin/steroids, topical immunomodulators- pimecrolimus and tacrolimus ( safe for face and neck)

* topical0 fuscidic acid /oral antibiotics- cephalexin, antiseptic body waters dermol 500.

Front 295

What is the UK working Party diagnostic criteria for atopic ezcema?

Back 295

any itchy skin condition in the last 12 months + 3 or more of the following
1) visible flexural dermatitis
2) PmHX of atopic dsease ( or if under 4y, first degree relative with atopic disease)
3) history of dry skin
4) history of flexural involvement ( or if under 18m, dermatitis on cheeks+/- extensor areas)
5) onset below age of 2y ( not used if child is under 4y)

Front 296

List the mild topical steroids.

Back 296

Hydrocortisone 0.5-2.5%

Front 297

List the moderate topical steroid

Back 297

betamethasone valerate 0.025% ( Betnovate RD)
clobestasone butyrate 0.05% ( Eurmovate)

Front 298

List the potent topical steroids

Back 298

FLuticasone propionate 0.05% ( Cutivate)
Betamethasone valerate 0.1% ( Betonovate)

Front 299

List the very potent topical steroid.

Back 299

Clobestasol priopionate 0.05% (Dermovate)

Front 300

Define erythema ab igne and explain its clinical features and managment

Back 300

a skin disorder that occurs due to prolonged exposure to infared radiation
commonly seen in elderly women sitting beside a heater/open fire
Sx: retiuclated, erythematous patches with hyperpigmentation and telangiectasia.
Can develop into SCC
treated via avoidance, if not better then biopsy +/- 5-fluorouracil cream , topical tretinoin or laser

Front 301

Define erythema multiforme and its clinical features.

Back 301

a skin disorder that cause be caused by many things.
Presents with target "bull eyed" lesions, bilateral symmetrical
macules/papules with central vesicles
all lesions appear with 3 days
Initially on back of hands/feet before spreading to torso
Upper limbs more affected than lower limbs
Pruitius
weakness malasie

Front 302

List the causes of erythema multiforme

Back 302

idiopathic
Viruses: HSV ( commonest), Orf ( skin disease of sheep/goat caused by parapox virus)
Bacteria: mycoplasma and streptococcus, histoplasma capsulatum
rx: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, COCP, nevirapine
Disease: sarcoidosis, malignancy, CTD- SLE.

Front 303

Mx of erythema multiforme

Back 303

1) symptomatic treatment ( oral antihistamines)
2) ? steriod if unwell ( controversial)

* usually heals without complications within 2 weeks

Front 304

Define and explain erythema nodosum.

Back 304

acute or chronic inflammation of subcutanesous fat ( aka: panniculitis)

Front 305

Clinical features of erythema nodosum

Back 305

tender, erythematous, round, poorly demarcated nodular lesions
usually over shin, but can be anywhere ( thigh, arms)
usually resolves with 6 weeks
lesions heal without scarring
more female
assocaited arthralgia, fever, malaise
asymmetrical

Front 306

Causes of erythema nodosum.

Back 306

NO (no causes in 40%) D- drugs ( sulfonamides, OCP, penicillin) S- sarcodisis U- ulcerative colitis and Crohn's (More C than U), Malignancy ( leukaemia, hodgkin's, lymphoma)

Infection: streptococci, TB, brucellosis,
Bechcet's disease
Pregnancy

Front 307

Investigation of eyrthema nodosum

Back 307

CXR- ? chest infection ? sarcoidosis
throat culture
Antistreptolysin test

Front 308

Managment of erythema nodosum

Back 308

1) symptomatic : bed rest, compressive bandages, wet dressing
2) NSAID
3) treat underlying

Front 309

What is the definition of erythroderma? what are its causes?

Back 309

it is a generalised term used when there are more than 95% of the skin involvement in any kind of rashes.

Causes:
idiopathic
eczema
psoriasis
lymphoma and leukaemia
Rx: gold

Front 310

What is erythromdermic psoriasis?

Back 310

Its a condition when a chonic skin condition progress to an exfoliative phase with plaque conver most of the body. (eg. acute withdrawal of steroid)
Associated with systemic upset
Hospitalised

Front 311

What causes fungal nail infection (aka: onychomycosis) ?

Back 311

dermatophytes- mainly trichophyton rumbrum ( accounts for 90% of cases)
yeasts- candida
non-dermatophyte moulds

Front 312

How does onychomycosis present?

Back 312

unsightly nails that are thickened, rough, opaque

Front 313

How to diagnose onychomycosis?

Back 313

nail clipping, scarping of affected nails.

Front 314

What are the treatment options of onychomycosis?

Back 314

1) investigated first before treatment
2) candida infection- topical antifungal for mild disease ( amorolfine) or oral itraconazole for severe disease for 3 months
3) dermatophyte infection- first line oral terbinafine, alternative itraconazole. Fingers- 6 wks to 3 months and toes- 3 m to 6m.

* treatment only successful in 50 -80% of patients.

Front 315

What is geographic tongue? How does it present? Treatment?

Back 315

a benign, chronic condition of the tongue of an unknown cause.
more in female
looks like a map on tongue ( erythematous smooth areas with irregular border)
1-3% of population
Mx: reassurance
Can present with burning tongue after eating

Front 316

What is granuloma annulare?

Back 316

papular lesions that are often slightly hyperpigmented and depressed centrally
usually asymptomatic
typicaly on dorsal of surfaces of hands and feets, extensor aspects of arms and legs
? weak link to diabetes mellitus

Front 317

What is Kaposi sarcoma thats related to HIV? Complication? Management? Presentation?

Back 317

It is causes by Human herpes virus 8
it usually presents with purple papules or plaques on skin or mucosa (eg. GI and resp) which may ulcerate
Complication: respiratory involvement causing massive haemoptysis and pleural effusion
Management: radiotherapy and resection

Front 318

What is hereditary haemorrhagic telangiectasia?

Back 318

Aka: Osler-Weber- Rendu sundrome
Autosomal dominant or idiopathic ( 20%)
Presents with multiple telangiectasia over skin and mucosa

Front 319

What is the diagnostic criteria for hereditary haemorrhagic telangiectasia?

Back 319

There are 4 main diagnostic criteria ( more than 3 definite, 2 is possible)
1) telangiectases: multiple at characteristic site ( lips, oral cavity, fingers, nose)
2) Visceral lesions: ateriovenous malformation ( pulmonary, hepatic, cerebral, spinal ) and GI telangiectasia ( with/without bleeding)
3) positive first relative family history
4) recurrent/spontanesous nose bleeds ( epistaxis)

Front 320

Explain HSV.

Back 320

There are 2 types: HSV 1 ( coldsore) and HSV ( genital herpes). There is overlap.
Painful vesicular grouped lesions.

Front 321

How does a patient with HSV infection present and its management?

Back 321

cold sore ( topical aciclovir)
severe gingivostomatitis ( oral aciclovir, chlorhexidine MW)
painful genital ulceration ( oral aciclovir )

Front 322

What is herpes zoster and its treatment.

Back 322

Aka: shingles

reactivation of varicella zoster virus--> acute painful blistering in the same dermatome

managed with oral aciclovir

Front 323

Definition of hirsutism

Back 323

describes androgen dependent hair growth in women

Front 324

Definition of hypertrichosis

Back 324

describes androgen independent hair growth in women

Front 325

What causes hypertrichosis?

Back 325

Anorexia nervosa
porphyria cutanea tarda
congenital hypertrichosis lanuginosa
congenital hypertrichosis terminalis
Rx: minoxidil, ciclosporin, diazoxide

Front 326

Whats causes hirsutism?

Back 326

PCOS
Cushing's syndrome
Congential adrenal hyperplasia
androgen therapy
Obesity ( because peripheral conversion of oestrogens to androgens)
adrenal tumor
androgen secreting ovarian tumor
Rx: phenytoin

Front 327

What scoring system is used to assess hirsutism?

Back 327

Ferriman-gallwey scoring system: body divided into 9 parts and scored out of 4, > 15 is moderate/severe hirsutism.

Front 328

How can hirsutism be managed?

Back 328

1) advise weight loss if high BMI
2) aesthetic management ( laser, wax etc)
3) facial hirsutim ( topical elfornithine- contraindicated in pregnancy and breastfeeding)
4) COCP ( eg. dianette- co-cyprindiol or Yasmin- ethinylestradiol and drospirenone ). Not for long term use.

Front 329

What is hyperhidrosis?

Back 329

term to describe excessive sweating

Front 330

What are the treatment options fo hypertrichosis?

Back 330

1) topical aluminium- first line, but can cause skin irritation
2) iontophresis- plates, particularly useful for palmar, plantar and axillary hyperhidrosis
3) botox injection- currently liscensed for axillary symptoms
4) surgery - ( eg. endoscopic transthoracic sypathectomy)- but at risk of over compensatory sweating post procedure.

Front 331

What is xanthomata?

Back 331

- deposition of yellowish cholesterol-rich material.
- cutaneous manifestations of lipidosis in which there is an accumulation of lipids in large foam cells within the skin

Front 332

In which condition can you see palmar xanthoma?

Back 332

remnant hyperlipidaemia
familial hypercholesterolaemia ( less common)

Front 333

What are eurptive xanthoma?

Back 333

presents as multiple red/yellow vesicles on the extensor surfaces ( eg. elbows, knees) secondary to high triglyceride level

Front 334

What causes eruptive xanthoma?

Back 334

familial hypertriglyceridaemia
lipoprotien lipase deficiency

Front 335

Out of tendon xanthoma ( yellow) , tuberous xanthoma, xanthelasma ( eyes), which one can be seen in patients without lipid abnormalitis

Back 335

xanthelasma

Front 336

Which condition is associated with tendon xanthoma, tuberous xanthoma, xanthelasma?

Back 336

familial hypercholesterolaemia
remnant hyperlipidaemia

Front 337

What are the management options of xanthelasma?

Back 337

1) electrodesiccation
2) laser therapy
3) topical trichloroacetic acid
4) surgical excision

Front 338

What is the Gell and coombs classication of hypersensitivity?

Back 338

type 1- anaphyalctic
type 2- cell bound
type 3- immune complex
type 4- delayed hypersensitivity
type 5- stimulated hypersensitivity

Front 339

Explain and give examples of type 1- anaphyalctic

Back 339

IgE bound to mast cells and antigen reacts with it
Eg: anapylaxis an atopy

Front 340

Explain and give examples of type 2 cell bound

Back 340

IgG and IgM binds to antigen on cell surface
Eg: autoimmune haemolytic anaemia, ITP, Good pasture's

Front 341

Explain and give examples of type 3 immune complex

Back 341

fee atigen and antibody (IgG and IgA) combine
Eg. serum sickness, SLE, post streptococcal glomerulonephritis, extrinsic allergic alveolitis ( esp, during acute phase)

Front 342

Explain and give examples of type 4 delayed hypersensitivity

Back 342

T cell mediated
Eg. TB, tuberculin skin reaction, graft versus hot disease, allergic contact dermatitis, scabies, extrinsic allergic alveolitis ( es, chronic phase)

Front 343

Explain and give examples of type 5 stimulated hypersensitivity

Back 343

IgG antibodies stimulate cells they are directed against
Eg. Grave's disease, myasthenia gravis

Front 344

Define impetigo vulgaris and its presentation.

Back 344

acute purulent infection
Vesicular--> golden yellow honey crusted lesions with surrounding erythema
face,arms, legs, buttocks
young school children

Front 345

What causes impetigo vulgaris?

Back 345

GroupA B haemolytic streptococcus, S. aureus

Front 346

How to treat impetigo vulgaris?

Back 346

1) localised disease
- remove crust
- topical mupirocin or fusdic acid ( first line)
2) extensive disease
- oral flucloxacillin
- oral erythromycin ( if pen allergic)

Front 347

What are the side effects of oral isotretinoin?

Back 347

1) hair thinning
2)dry skin, eyes, lips ( commonest), nasal mucosa ( nosebleeds)
3)low mood
4)benign intracranial HTN ( not to be given with tetracycline,which will worsen symptoms)
5) raised triglycerides
6) teratogenicity (should ideally be using 2 forms of contraception eg. COCP and condomes)
* 2/3 of patients have long term remission or cure of severe acne following a course of oral isotretinoin

Front 348

What are keloid scars?

Back 348

- they are tumour like lesions tha arise from the connective tissue of a scar and extend beyond the healed wound site

Front 349

What are the predisposing factors of keloid scars?

Back 349

1) more common in young than old
2) ethnicity ( eg. people with darker skin)
3) common sites:
- sternum ( most)
- shoulder
- neck
-face
- extensor surgace of limbs
- truck ( least)

* keloid scarsare less likely along langerlines ( ie. along relaxed skin tension lines)

Front 350

What is keratocanthoma?

Back 350

benign epithelial neoplasm with atypical keratinocytes in epidermis
middle age, but not increase number in age

Front 351

What is kertocanthoma associated with?

Back 351

HPV, UV radiation, chemical carcinogen ( tar and mineral oil)

Front 352

Which skin cancer does keratocanthoma look like?

Back 352

SCC therefore remove urgently

Front 353

What are the clinical features of keratoacanthoma?

Back 353

erupting "volcano " lesion
initially smooth dome shaped papule--> rapidly grows and become a crater centrally filled with keratin ( usually over 6 weeks)
- spontaneous regression within 3 months is common
- often resulting in disfiguring scar
- usually found in sun exposed skin
- tender

Front 354

What is lentigo maligna?

Back 354

- a type of melanoma in situ ( ie. normal and maligant melanocytes confined to epidermis)
- pre malignant lesion
- progresses slowly-->eventually become lentigo maligna melanoma ( 15% of all melanomas)

Front 355

What is leukoplakia?

Back 355

- commonest oral premalignant condition
- white hard spot/plaque on the oral mucous membranes ( doesn't rub off)
- strongly associated with tobacoo use and alcohol consumption
- M>F
- peak at 50

Front 356

What are the differential of leukoplakia?

Back 356

candidiasis and lichen planus, oral hairy leukoplakia

Front 357

Once leukoplakia is diagnosed, what is the investigation performed and why ?

Back 357

- Biopsy because premalignant lesion and exclude SCC
- regular follow up is required to exclude malignant transformation to SCC ( 1% of patients)

Front 358

What is lichen planus?

Back 358

- an acute or chronic inflammtory skin/mucosa condition of unknown aetiology, most likely immune mediated
- characterized by violaceous papules, esp on flexural surfaces

Front 359

What is lichen planus associated with and what can trigger it?

Back 359

- associated with hepatitis C
- can be triggered by severe emotional distress

Front 360

Which medications cause lichenoid drug eruptions?

Back 360

gold, quinine, thiazide

Front 361

What are the clinical features of lichem planus?

Back 361

- intensely itchy flat topped shiny papular rash
- resolves with hyperpigmented macules
- rash are often polygonal in shape with a white-lace pattern on surface ( aka: Wickham's striae)
-sites: wrists, ankles, genitalia, nails, scalp, mucous membranes ( mouth/vulva/glans)
- nails: longitudinal ridging, dystrophic
- mucous membrane: lacy,whitish reticular network, milky white ( 50% of patients)

Front 362

What phenomenon is associated with lichen planus?

Back 362

Koebner phenomenon following trauma

Front 363

What is the treatment of lichen planus?

Back 363

1) topical corticosteroids ( mainstay)
2) extensive may require oral steroids or immunosuppression
3) photochemotherapy for generalised or resistant cases
4) oral retinoids for erosive lesion in mouth

Front 364

What is lichen sclerosus?

Back 364

inflammatory condition of the skin
ususally found in elderly female
affecting genitalia
leads to atrophy of the epidermis with white plaques forming

Front 365

What is the prominent clinical feature of lichen sclerosus?

Back 365

itch!

Front 366

How is lichen sclerosus usually invesitgated? why?

Back 366

- biopsy to exclude other diagnoses
- increased risk of vulval cancer

Front 367

What is the main stay management of lichen sclerosus?

Back 367

topical steroids and emollients

Front 368

What is lyme disease?

Back 368

- spread by ticks
- caused by the spirochaete Borrelia burgdorferi

Front 369

What are the clinical features of lyme disease?

Back 369

Early: erythema chronicum migrans ( widespread area of surrounding erythema) + fever + arthralgia
CVS: heart block, myocarditis
Neuro: cranial nerve palsies, meningitis

Front 370

What is the investigation for lyme disease?

Back 370

blood test: antibodies to Borrelia burgdorfei

Front 371

What is the management of lyme disease?

Back 371

early disease ( doxycycline)
disseminated disease ( ceftriaxone)

Front 372

What is Jarisch-Herxheimer reaction?

Back 372

patient presents with fever, rash, tachycardia after first dose antibiotic
most commonly seen in syphillis- spirochaetal disease

Front 373

What is the breslow thickness and 5 year survival for malignant melanoma?

Back 373

- measures the invasion depth of a tumour
- single most important factor in determine prognosis

< 1mm (95-100%)
1-2 mm ( 80-96%)
2.1-4 mm ( 60-75%)
>4 mm ( 50%)

Front 374

What is melasma ( aka: chloasma)?

Back 374

a hyperpigmented macular skin condition in sun exposed area, particularly around face

Front 375

What causes the development of melasma?

Back 375

Pregnancy and COCP

Front 376

Who is are risk of developing melasma?

Back 376

women and dark skin people

Front 377

What is milia?

Back 377

- small benign keratin filled cyts
- typically on face
- any age but more new born

Front 378

What is molluscum contagiosum?

Back 378

highly infectious skin condition caused by DNA pox virus

Front 379

What is the characteristic rash of molluscum contagiosum?

Back 379

small, dome like, pearly, umbilicated lesions

Front 380

What are the treatment options of mollusum contagiosum?

Back 380

1) conversative ( esp. early phrase as begnin)- usually resolve within 1 year
2) avoid direct contact with others to prevent spread
3) surgical ( aldara, curettage, cryotherapy, topical cantharidin)

Front 381

What type of hypersensitivity reaction is nickle reaction?

Back 381

It is an allergic contact dermatitis ie. type 4 hypersensitivity reaction

Front 382

What is onycholysis?

Back 382

seperation of nail plate from nail bed

Front 383

What causes onycholysis?

Back 383

-idiopathic
- trauma ( eg. excessive manicuring)
- infection ( esp. fungal )
- skin disease ( psoriasis, dermatitis )
- impaired peripheral circulation ( PVD, Raynaud's)
- Hyper and hypo thyroidism

Front 384

What orf?

Back 384

- skin lesion found in sheep and goats but can be transmitted to humans.
- caused by parapox virus

Front 385

What is the clinical presentation of orf in humans?

Back 385

initially small, raised, red-blue papules ---> grow to 2-3 cm and become flat topped and haemorrhagic
usually self limiting disease

Front 386

What is the clinical features of pemphigus vulgaris?

Back 386

-presenting symptoms with mucosal ulceration ( 50-60% pt) then skin lesions over 6-12 months
-heals with hyperpigmentation but no scars

Front 387

What is pemphigus vulgaris?

Back 387

- autoimmune blistering disease

- more common amongst mediterranean, asian, Jewish population

Front 388

Describe the rash of pemphigus vulgaris.

Back 388

- painful, easily rupture, flaccid, non-pruritic epidermal bullae/vesicles on an erythematous or normal skin base
- superficial bullae as compared to bullous pemphigus

Front 389

What is the pathophysiology of pemphigus vulgaris? skin biopsy?

Back 389

- IgG antibodies directed against epidermal desmoglein 3 leading to intraepidermal bullae
- skin biopsy shows acantholysis ( ie. loss of intracellular connection), immunoflurescence shows IgG and C3 deposition intraepidermally.

Front 390

which conditions are pemphigus vulgaris associated with?

Back 390

thymoma, myasthenia gravis, malignancy, use of D-penicillamine

Front 391

What is the Nikolsky's sign of pemphigus vulgaris?

Back 391

sliding and rubbing pressure on skin causes the seperation of epidermis (ie. spread of bullae)

Front 392

What is the treatment option of pemphigus vulgaris?

Back 392

1) prednisolone until no new blisters
2) immunosuppressant

Front 393

What is pityriasis versicolor?

Back 393

-aka: tinea versicolor
-superficial cutaneous fungal infection caused by malassezia furfur

Front 394

What are the predisposing factors to pityriasis versicolor?

Back 394

-none
- immunosuppression
- malnutrition
- cushing's

Front 395

What are the clinical features of pityriasis versicolor?

Back 395

-area of hypopigmentation, pink or brown patches
- mostly affecting trunk
-scale
- mild pruritus

Front 396

What are the treatment options of pityriasis versicolor?

Back 396

1) topical antifungal ( terbinafine or selenium sulphide)
2) extensive disease ( oral itraconazole)

Front 397

What is pompholyx?

Back 397

- aka: dyshidrotic dermatitis
- a type of ezcema that affects both hands (cheiropompholyx) and feet ( pedopompholyx)

Front 398

What are the clinical features of pompholyx?

Back 398

pruritic small blisters forming on palms and soles --> burst--> dry and cracked

Front 399

What are the treatments for pompholyx?

Back 399

- cool compression
- emollient
- topical steroid + wrap
- intralesional triamcinoclone
- oral steroid in severe cases

Front 400

What is porphyria cutanea tarda?

Back 400

-inherited defect in uroporphyrinogen decarboxylase OR
caused by hepatocyte damage secondary to alcohol and oestrogens
- commonest hepatic porphyria

Front 401

What are the clinical features of porphyria cutanea tarda?

Back 401

- commonest- photosensitive rash with blistering and skin fragility on face/ dorsal aspect of hands
- hypertrichosis ( abnormal hair overgrowth)
- hyperpigmentation

Front 402

What the porphyria cutanea tarda investigated?

Back 402

urine- elevated uroporphyrinogen and pink flourescence of urine under Wood's lamp

Front 403

How is porlyria cutanea tarda treated?

Back 403

chloroquine and venesection

Front 404

What are at risk of developing pressure ulcers?

Back 404

- lack of mobility ( age, paralysis, body illness, pain )
- malnourishment
- incontinence
- elderly

Front 405

Where does pressure usually develop?

Back 405

over bony prominences ( sacrum/heel)

Front 406

How many gradings are there of the European Pressure Ulcer Advisory Panel criteria?

Back 406

4 grades

Front 407

What is European Pressure Ulcer Advisory Panel criteria grade 1?

Back 407

- non - blanchable erythema of intact skin
- indicators : discolouration of skin, warmth, induration, hardness ( particluarly useful in darker skin)

Front 408

What is European Pressure Ulcer Advisory Panel criteria grade 2?

Back 408

- abrasion or blister, superficial ulcer
- partical thickness skin loss involving epidermis or dermis or both

Front 409

What is European Pressure Ulcer Advisory Panel criteria grade 3?

Back 409

- full thickness skin loss
- damage to or necrosis of subcutaneous tissue that extend ( not through) underlying fascia

Front 410

What is the European Pressure Ulcer Advisory Panel criteria grade 4?

Back 410

- extensive destruction
- tissue necrosis
-damage to muscle/bone/supporting structure
-with or without full skin loss

Front 411

What is the management plan for a patient with pressure ulcer?

Back 411

1) referral to tissue viability nurse
2) consider referral for surgical debridement
3) hydrocolloid dressing and hydrogels- promote ulcer healing in a moist enviroment

* dont use soap
* would swab shouldn't be routinely done useless look infected ( ie. with surround erythema)

Front 412

What are the 5 conditions that most commonly cause pruritus?

Back 412

1) Liver disease
2) Iron deficiency anaemia
3) Polycythaemia
4) Chronic kidney disease
5) lymphoma

Front 413

What other conditions cause pruritus?

Back 413

Hyper-/hypo thyrodism
Diabetes
Pregnancy
"senile" pruritus
urticaria
Skin disorder: eczema, scabies, psoriasus, pityriasis roasea

Front 414

What is pyoderma gangrenosum?

Back 414

a condition that causes small red papule then becoming deep,red, necrotic ulcers with violaceous border

Front 415

What are the clinical features of pyoferma gangrenosum?

Back 415

- typically affecting the lower limbs
- maybe with systemic upset ( eg. myalgia and fever)

Front 416

What conditions are associated with pyoderma gangrenosum?

Back 416

- idiopathic in 50% of cases
- IBD ( UC, Crohn's)
- RA
- SLE
- myeloproliferative disorders
- lymphoma
- leukaemias
- primary biliary cirrhosis
- monoclonal gammapathy (IgA)
- DM II (rare)

Front 417

What are the treatments of pyoderma gangrenosum?

Back 417

Rapid progression therefore steroid asap
consider other immunosupressants ( eg. ciclosporin or infliximab)

Front 418

What is pyogenic granuloma?

Back 418

it is a common benign skin lesion.

Front 419

What conditions are associated with pyogenic granuloma?

Back 419

Trauma
Pregnancy

Front 420

What are the clinical features of pyrogenic granuloma?

Back 420

- more common in young adults and female
- small red/brown spot--> raised red/brown spherican lesions +/- bleeding and ulcerating ( over days to weeks)
- common site: head/neck, upper trunk, and hands, oral mucosa ( particularly in pregnancy)

Front 421

What is the treatment option with pyogenic granuloma?

Back 421

1) normally resolves post partum
2) curettage and cauterisation
3) cryotherapy
4) excision

Front 422

What is reactive arthritis?

Back 422

-one of the HLA-B27 associated seronegative spondyloarthopathies.
- an arthritis that develop following an infection where the organism can't not isolated in the joint fluid.

Front 423

What is reiter's sydrome?

Back 423

- Post STI
- classic triad of urethritis, conjunctivitis, arthritis

Front 424

What are the clinical features of reactive arthritis/Reiter's syndrome?

Back 424

-asymmetrical oiligoarthritis of lower limbs
- dactylitis
- urethritis
- conjunctivitis (50%), anterior uveitis
- Skin:
circinate balanitis (painless vesicles on the coronal margin of prepuce),
keratoderma,
blenorrhagica ( waxy yellow/brown papules on palms
and soles)

* 25% develop recurrent episodes
* 10% develop chronic disease
* typically develops over 4 weeks from initial infection
* above symptoms can last for 4-6 months

Front 425

What is scabies?

Back 425

-caused by parasite mite Sarcoptes scabiei
-mite burrows into the skin and laying its eggs in stratum corneum
- transmitted via contact

Front 426

What are the clinical features of scabies?

Back 426

- incubation : intensely widespread itch after 1 month from initial infection
- linear burrows on sides of finger, interdigital webs and flexor aspect of wrist, usually sparing od head and neck ( except infants)
- prone to secondary infection because of excoriation and infection
- can remain itchy for 4 -6 weeks after clearing infection ( prolonged hypersensitvity)

Front 427

What type of hypersensitvitiy reaction is scabies infection?

Back 427

Type 4 delayed reaction to mites and effects

Front 428

What is the management plan for a patient who has been infected with scabie?

Back 428

1) avoid lose physical contact until all contacts treated, even if asymptomatic
2) wash all clothing, bedding etc at 40c because mites can remain alive 2-3 days on them
3) permethrin 5% (first line) - apply to dry skin, left on whole body for 8-12 hours, repeat 1 week
4) malathion 0.5% ( second line) -left on 24 hrs, repeat 1 week later
5) antihistamine

Front 429

Whatis seborrhoeic dermatitis?

Back 429

thought to be caused by inflammatory reaction to proliferation of normal skin fungus inhabitant known as malassezia furfur

Front 430

How many % of the general population is affected by seborrhoeic dermatitis?

Back 430

2 %

Front 431

What kind of problems does seborrhoeic dermatitis cause? Adult and children.

Back 431

- eczematous lesion on sebum rich areas: scalp ( dandruff), periorbital, auricular, chest, nasolabial folds, +/- otitis externa and blepharitis
- greasy, erythematous, yellow, non pruritic scaling papules, plaques
- Children: cradle cap, nappy area, face and limb flexures

Front 432

What is cradle cap?

Back 432

seborric dermatitis in scalp of babies.
normally develop in first few weeks of life
erythematous rash with coarse yellow scales
tends to spontaneously resolve by 8 months

Front 433

What is the management of cradle cap and seborhoeic dermatitis in children?

Back 433

1) mild -moderate ( baby shampoo, baby oil)
2) severe- mild topical steroids ( eg 1 % hydrocortisone)

Front 434

What conditions are seborrheic dermatitis associated with?

Back 434

-immunocompromised patients ( eg. HIV)
- Parkinson's disease

Front 435

What is the scalp management of seborrheic dermatitis in adult?

Back 435

First line ( zinc pyrithione- Head & shoulder) or ( tar ( Neutrogena T gel)
second line ketoconazole
Selenium sulphide and topical corticosteroid maybe useful

Front 436

What is the body and face treatment for an adult with seborrheic dermatitis?

Back 436

Difficult to treat. recurrence common.
1) Topical antifungal ( Ketoconazole)
2) Topical steroids ( short term)

Front 437

What is seborrhoeic keratoses?

Back 437

benign epidermal skin lesion seen in elderly patients
autosomal dominant

Front 438

What are the clinical features of seborrhoeic keratoses?

Back 438

-Large variation in colour ( flesh to light brown)
- stuck on appearance
- may look warty over time

Front 439

What is the management of seborrhoeic keratoses?

Back 439

Reassurance as benign
comestic: curettage, cryosurgery, shave biopsy

Front 440

What are the differential for shin lesions?

Back 440

Erythema nodosum
pretibial myxoedema
pyoderma gangrenosum
necrobiosis lipoidica diabeticorum

Front 441

What is pretibial myxoedema?

Back 441

Shiny orange peel skin symmetrical erythematous lesions seen in Grave's disease

Front 442

What is necrobiosis lipoidica diabeticorum?

Back 442

Shiny painless areas of yellow/red skin typically on skin of diabetics
associated telangiectasia

Front 443

What are the differential of skin disorders affecting the soles of feet?

Back 443

Verrucas
Tinea pedis
Corn and calluses
Keratoderma
Pitted keratolysis
Palmoplantar pustulosis
Juvenile plantar dermatosis

Front 444

What is verrucas?

Back 444

Secondary to the human papilloma virus
Firm, hyperkeratotic lesions
Pinpoint petechiae centrally within the lesions
May coalesce with surrounding warts to form mosaic warts

Front 445

What is tinea pedis?

Back 445

More commonly called Athlete's foot
Affected skin is moist, flaky and itchy

Front 446

What is corn calluses?

Back 446

A corn is small areas of very thick skin secondary to a reactive hyperkeratosis
A callus is larger, broader and has a less well defined edge than a corn

Front 447

What is keratoderma?

Back 447

May be acquired or congenital
Describes a thickening of the skin of the palms and soles
Acquired causes include reactive arthritis (keratoderma blennorrhagica)

Front 448

What is pitted keratolysis?

Back 448

Affects people who sweat excessively
Patients may complain of damp and excessively smelly feet
Usually caused by Corynebacterium

Front 449

What is plamoplanta pustulosis?

Back 449

Crops of sterile pustules affecting the palms and soles
The skin is thickened, red. Scaly and may crack
More common in smokers

Front 450

What is Junvenile planta dermatosis?

Back 450

Affects children. More common in atopic patients with a history of eczema
Soles become shiny and hard. Cracks may develop causing pain
Worse during the summer

Front 451

What are the skin manifestation of SLE?

Back 451

• photosensitive 'butterfly' rash
• discoid lupus
• alopecia
• livedo reticularis: net-like rash

Front 452

What are the skin disorder associated with DMII?

Back 452

pyoderma gangrenosum
Necrobiosis lipoidica
Candidiasis and staphlococcal infection
Neuropathic ulcers
Vitiligo
Lipoatrophy
Granuloma annulare

Front 453

What skin disorder is Gastric cancer associated with?

Back 453

Acanthosis nigricans

Front 454

What skin disorder is Lymphoma associated with?

Back 454

Acquired ichthyosis

Front 455

What skin disorder is Gastrointestinal and lung cancer associated with?

Back 455

Acquired hypertrichosis lanuginosa

Front 456

What skin disorder is Ovarian and lung cancer associated with?

Back 456

Dermatomyositis

Front 457

What skin disorder is Lung cancer associated with?

Back 457

Erythema gyratum repens

Front 458

What is skin disorder is Lymphoma associated with?

Back 458

Erythroderma

Front 459

What skin disorder is Pancreatic cancer associated with?

Back 459

Migratory thrombophlebitis

Front 460

What skin disorder is Glucagonoma associated with?

Back 460

Necrolytic migratory erythema

Front 461

What skin disorder is Myeloproliferative disorders associated with?

Back 461

Pyoderma gangrenosum (bullous and non-bullous forms)

Front 462

What skin disorder is Haematological malignancy e.g. Myelodysplasia - tender, purple plaques associated with?

Back 462

Sweet's syndrome

Front 463

What skin disorder is Oesophageal cancer associated with?

Back 463

Tylosis

Front 464

What is spider naevi?

Back 464

describe a central red papule with surrounding capillaries. The lesions blanch upon pressure
- AKA:spider angiomas

Front 465

Where are spider naevi most found?

Back 465

upper part of the body

Front 466

How many % of people will have idopathic spide naevi?

Back 466

Around 10-15%

Front 467

What conditions are spider navi associated with?

Back 467

• liver disease
• pregnancy
• combined oral contraceptive pill

Front 468

What is stevens-johnson syndrome?

Back 468

severe form of erythema multiforme associated with mucosal involvement and systemic symptoms

Front 469

How does Stevens-Johnsons syndrome usually present?

Back 469

• rash is typically maculopapular with target lesions being characteristic. May develop into vesicles or bullae
• mucosal involvement
• systemic symptoms: fever, arthralgia

Front 470

What are the causes of stevens-johnson's syndrome?

Back 470

• idiopathic
• bacteria: Mycoplasma, Streptococcus
• viruses: herpes simplex virus, Orf
• drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill
• connective tissue disease e.g. SLE
• sarcoidosis
• malignancy

Front 471

What are strawberry naevus?

Back 471

aka: capillary haemangioma
erythematous, raised and multilobed tumours
-present in around 10% of white infants

Front 472

When are strawberry naevus usually develope and regress?

Back 472

- usually not present at birth but may develop rapidly in the first month of life.
- Typically they increase in size until around 6-9 months before regressing over the next few years (around 95% resolve before 10 years of age).

Front 473

What is a potential complication of having strawberry naevus ?

Back 473

• mechanical e.g. Obstructing visual fields or airway
• bleeding
• ulceration
• thrombocytopaenia

Front 474

Where are strawberry naevus usually found?

Back 474

face, scalp and back

Front 475

Which babies are most likely to have strawberry naevus?

Back 475

Female infants, premature infants and those of mothers who have undergone chorionic villous sampling

Front 476

What is cavernous haemangioma?

Back 476

deep capillary haemangioma

Front 477

If treatment is needed, what is used to treat strawberry naevi?

Back 477

steroid
? BB

Front 478

What is systemic sclerosis?

Back 478

a condition of unknown aetiology characterised by hardened, sclerotic skin and other connective tissues

Front 479

What is more likely to have systemic sclerosis? and why how much?

Back 479

women, 4x

Front 480

What are the 3 patterns of disease for sysemic sclerosis?

Back 480

Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis
Scleroderma (without internal organ involvement)

Front 481

What is Limited cutaneous systemic sclerosis

Back 481

• Raynaud's may be first sign
• scleroderma affects face and distal limbs predominately
• associated with anti-centromere antibodies
• a subtype of limited systemic sclerosis is CREST syndrome: Calcinosis, Raynaud's phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia

Front 482

What is
Scleroderma (without internal organ involvement)?

Back 482

• tightening and fibrosis of skin
• may be manifest as plaques (morphoea) or linear

Front 483

What is Diffuse cutaneous systemic sclerosis

Back 483

• scleroderma affects trunk and proximal limbs predominately
• associated with scl-70 antibodies
• hypertension, lung fibrosis and renal involvement seen
• poor prognosis

Front 484

What antibodies are associated with systemic sclerosis?

Back 484

• ANA positive in 90%
• RF positive in 30%
• anti-scl-70 antibodies associated with diffuse cutaneous systemic sclerosis
• anti-centromere antibodies associated with limited cutaneous systemic sclerosis

Front 485

What is tinea?

Back 485

a term given to dermatophyte fungal infections

Front 486

What are the 3 main types of tinea infection?

Back 486

• tinea capitis - scalp
• tinea corporis - trunk, legs or arms
• tinea pedis - feet

Front 487

What is tinea capitis?

Back 487

- scalp ringworm

Front 488

Whats causes scarring alopecia in children?

Back 488

• a cause of scarring alopecia mainly seen in children

Front 489

What happens is tinea capitis isn't treated?

Back 489

pustular, spongy/boggy mass called a kerion may form

Front 490

What is the most common dermatophytes cauing tinea capitis in US and UK?

Back 490

Trichophyton tonsurans

Front 491

What other organisim cause tinea capitis?

Back 491

Microsporum canis acquired from cats or dogs

Front 492

How is tinea capitis diagnosed?

Back 492

lesions due to Microsporum canis green fluorescence under Wood's lamp.
most useful investigation is scalp scrapings

*lesions due to Trichophyton species do not readily fluoresce under Wood's lamp

Front 493

How is tinea capitis treated?

Back 493

oral antifungals:
-terbinafine for Trichophyton tonsurans infections - -griseofulvin for Microsporum infections.

-Topical ketoconazole shampoo should be given for the first two weeks to reduce transmission

Front 494

What is tinea corporis?

Back 494

dermatophytes infection of the skin.

Front 495

What rash does tinea corporis cause?

Back 495

• well-defined annular, erythematous lesions with pustules and papules

Front 496

What organisms cause tinea corporis?

Back 496

Trichophyton rubrum and Trichophyton verrucosum (e.g. From contact with cattle)

Front 497

How is tinea corporis treated?

Back 497

• may be treated with oral fluconazole

Front 498

What is toxic epidermal necrolysis?

Back 498

life-threatening skin disorder that is most commonly seen secondary to a drug reaction

Front 499

How does the skin present with toxic epidermal necrolysis?

Back 499

the skin develops a scalded appearance over an extensive area.

Front 500

What are clinical features of toxic epidermal necrolysis?

Back 500

• systemically unwell e.g. pyrexia, tachycardic
• positive Nikolsky's sign: the epidermis separates with mild lateral pressure

Front 501

What drugs are known to induce toxic epidermal necrolysis?

Back 501

• phenytoin
• sulphonamides
• allopurinol
• penicillins
• carbamazepine
• NSAIDs

Front 502

What is the managment of toxic epidermal necrolysis?

Back 502

• stop precipitating factor
• supportive care, often in intensive care unit
• intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
• other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis

Front 503

What is tuberous sclerosis?

Back 503

- genetic condition of autosomal dominant inheritance-
-majority of features seen in TS are neuro-cutaneous

Front 504

What are the cutaneous features of tuberous sclerosis?

Back 504

• depigmented 'ash-leaf' spots which fluoresce under UV light
• roughened patches of skin over lumbar spine (Shagreen patches)
• adenoma sebaceum: butterfly distribution over nose
• fibromata beneath nails (subungual fibromata)
• caf�u-lait spots* may be seen

Front 505

What are the neurological features of tuberous sclerosis?

Back 505

• developmental delay
• epilepsy (infantile spasms or partial)
• intellectual impairment

Front 506

Other than neuro-cutaneous manifestation of tuberous sclerosis, what other manifestations can there be?

Back 506

• retinal hamartomas: dense white areas on retina (phakomata)
• rhabdomyomas of the heart
• gliomatous changes can occur in the brain lesions
• polycystic kidneys, renal angiomyolipomata

Front 507

What is urticaria?

Back 507

describes a local or generalised superficial swelling of the skin

Front 508

What is the most common cause of urticaria?

Back 508

Allergy more than non allergic causes

Front 509

What are the clinical features of urticaria?

Back 509

• pale, pink raised skin. Variously described as 'hives', 'wheals', 'nettle rash'
• pruritic

Front 510

What is the mangement of urticaria?

Back 510

• non-sedating antihistamines are first-line
• prednisolone is used for severe or resistent episodes

Front 511

What conditions causes large vessel vaculitis?

Back 511

• temporal arteritis
• Takayasu's arteritis

Front 512

What conditions causes medium vessel vaculitis?

Back 512

• polyarteritis nodosa
• Kawasaki disease

Front 513

What conditions causes small vessel vaculitis?

Back 513

• ANCA-associated vasculitides (Wegener's*, Churg-Strauss*, microscopic polyangiitis)
• Henoch-Schonlein purpura
• cryoglobulinaemic vasculitis

Front 514

What is venous lake?

Back 514

Angiomas on the lips

Front 515

What is the treatment of venous lake?

Back 515

is usually clinical and no treatment is required except for cosmetic reasons

Front 516

Where is venous ulceration usually seen?

Back 516

above the medial malleolus

Front 517

What is the most important investigation in non healing ulcers?

Back 517

• ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing

'normal' ABPI may be regarded as between 0.9 - 1.2.

below 0.9 indicate arterial disease. Interestingly, values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)

Front 518

What is the management of venous ulcers?

Back 518

• compression bandaging, usually four layer (only treatment shown to be of real benefit)
• oral pentoxifylline, a peripheral vasodilator, improves healing rate
• small evidence base supporting use of flavinoids
• little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression

Front 519

What is vitiligo?

Back 519

an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.

Front 520

What is the clinical features of vitiligo?

Back 520

• well demarcated patches of depigmented skin
• the peripheries tend to be most affected
• trauma may precipitate new lesions (Koebner phenomenon)

Front 521

What conditions are vitiligo associated with?

Back 521

• type 1 diabetes mellitus
• Addison's disease
• autoimmune thyroid disorders
• pernicious anaemia
• alopecia areata

Front 522

What is the management of vitligo?

Back 522

• sun block for affected areas of skin
• camouflage make-up
• topical corticosteroids may reverse the changes if applied early
• there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients

Front 523

What does zinc deficiency cause?

Back 523

• perioral dermatitis: red, crusted lesions
• acrodermatitis
• alopecia
• short stature
• hypogonadism
• hepatosplenomegaly
• geophagia (ingesting clay/soil)
• cognitive impairment

Front 524

What is psoriasis?

Back 524

- multifactorial and not yet fully understood
- common and chronic skin disorder
-• genetic: associated HLA-B13, -B17, and -Cw6. Strong concordance (70%) in identical twins
• immunological: abnormal T cell activity stimulates keratinocyte proliferation. There is increasing evidence this may be mediated by a novel group of T helper cells producing IL-17, designated Th17. These cells seem to be a third T-effector cell subset in addition to Th1 and Th2
• environmental: it is recognised that psoriasis may be worsened (e.g. Skin trauma, stress), triggered (e.g. Streptococcal infection) or improved (e.g. Sunlight) by environmental factors

Front 525

What are the complications of having psoriasis?

Back 525

• psoriatic arthropathy (around 10%)
• increased incidence of metabolic syndrome
• increased incidence of cardiovascular disease
• psychological distress

Front 526

How does psoriatic rash present?

Back 526

red, scaly patches on the skin

Front 527

What are recognised substypes of psoriasis?

Back 527

• plaque psoriasis:
• flexural psoriasis:
• guttate psoriasis
• pustular psoriasis:

Front 528

What is plaque psoriasis?

Back 528

most common sub-type resulting in the typical well demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp

Front 529

What is flexural psoriasis?

Back 529

in contrast to plaque psoriasis the skin is smooth

Front 530

What is guttate psoriasis?

Back 530

- transient multiple red, teardrop lesions appear on the body
- more common in children and adolescents
- may be precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing

Front 531

What is pustular psoriasis?

Back 531

commonly occurs on the palms and soles

Front 532

What are the exacerbating factors of psoriasis?

Back 532

• trauma
• alcohol
• drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors
• withdrawal of systemic steroids

Front 533

What is the management of guttate psoriasis?

Back 533

• most cases resolve spontaneously within 2-3 months
• there is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
• topical agents as per psoriasis
• UVB phototherapy
• tonsillectomy may be necessary with recurrent episodes

Front 534

What is the managment of chronic plaque psoriais?

Back 534

• regular emollients may help to reduce scale loss and reduce pruritus

• for acute control SIGN recommend: 'Short term intermittent use of a potent topical corticosteroid or a combined potent corticosteroid plus calcipotriol ointment is recommended to gain rapid improvement in plaque psoriasis.'

• 'For long term topical treatment of plaque psoriasis a vitamin D analogue (e.g. Calcipotriol) is recommended.'

• 'If a vitamin D analogue is ineffective or not tolerated then consider coal tar (solution, cream or lotion), tazarotene gel, or short contact dithranol (30 minute exposure in patients with a small number of relatively large plaques of psoriasis).

Front 535

What is the role of steroids use in psoriasis?

Back 535

• topical steroids are commonly used in flexural psoriasis and there is also a role for mild steroids in facial psoriasis. If steroids are ineffective for these conditions vitamin D analogues or tacrolimus ointment should be used second line
• SIGN caution against the long term use of potent or very potent topical steroids due to the risk of side-effects

Front 536

How do you manage scalsp psoriasis?

Back 536

• for short term control SIGN recommend either the use of potent topical corticosteroids or a combination of a potent corticosteroid and a vitamin D analogue
• 'For patients with thick scaling of the scalp, initial treatment with overnight application of salicylic acid, tar preparations, or oil preparations (eg olive oil, coconut oil) to remove thick scale is recommended.

Front 537

What is the role of phototherapy in managing psoriasis in secondary care ?

Back 537

• narrow band ultraviolet B light (311-313nm) is now the treatment of choice
• photochemotherapy is also used - psoralen + ultraviolet A light (PUVA)
• adverse effects: skin ageing, squamous cell cancer (not melanoma)

Front 538

What is the role of systemic therapy in managing psoriasis in secondary care ?

Back 538

• methotrexate: useful if associated joint disease
• ciclosporin
• systemic retinoids
• biological agents: infliximab, etanercept and adalimumab
• ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials

Front 539

What is the MOA of coal tar commonly used drugs in psoriasis?

Back 539

probably inhibit DNA synthesis

Front 540

What is the MOA of calcipotriol commonly used drugs in psoriasis?

Back 540

vitamin D analogue which reduces epidermal proliferation and restores a normal horny layer

Front 541

What is the MOA of dithranol commonly used drugs in psoriasis?

Back 541

: inhibits DNA synthesis, wash off after 30 mins, SE: burning, staining

Front 542

What are the nail changes seen in psoriasis?

Back 542

• pitting
• onycholysis
• subungual hyperkeratosis
• loss of nail


* Psoriatic nail changes affect both fingers and toes and do not reflect the severity of psoriasis but there is an association with psoriatic arthropathy

Front 543

What is amiodarone and its MOA?

Back 543

a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias.

main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

Front 544

What factors limits the use of amiodarone?

Back 544

• long half-life (20-100 days)
• should ideally be given into central veins (causes thrombophlebitis)
• has proarrhythmic effects due to lengthening of the QT interval
• interacts with drugs commonly used concurrently e.g. Decreases metabolism of warfarin ( increase plasma level of warfarin)

Front 545

What are the side effects of amiodarone?

Back 545

• thyroid dysfunction
• corneal deposits
• pulmonary fibrosis/pneumonitis
• liver fibrosis/hepatitis
• peripheral neuropathy, myopathy
• photosensitivity
• 'slate-grey' appearance
• thrombophlebitis and injection site reactions
• bradycardia

Front 546

What monitoring is needed for patients started on amiodarone?

Back 546

• TFT, LFT, U&E, CXR prior to treatment
• TFT, LFT every 6 months

Front 547

Angina pectoris: What 3 medications should a patient recieve in the absence of contraindication?

Back 547

• all patients should receive aspirin and a statin in the absence of any contraindication
• sublingual glyceryl trinitrate to abort angina attacks

Front 548

What is the stepwise medication management of angina pectoris?

Back 548

• NICE recommend using either a beta-blocker or a calicum channel blocker first-line based on 'comorbidities, contraindications and the person's preference'
• if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used.
• If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)

• if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
• if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
• if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine
• if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

Front 549

What is a common problem with nitrate medications and what can be done about it to prevent it?

Back 549

• many patients who take nitrates develop tolerance and experience reduced efficacy
• the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness
• this effect is not seen in patients who take modified release isosorbide mononitrate

Front 550

What is Ivabradine?

Back 550

• a new class of anti-anginal drug which works by reducing the heart rate
• acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity
• adverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due to the mechanism of action, may also be seen
• there is no evidence currently of superiority over existing treatments of stable angina

Front 551

Explain angiotensin II receptor blockers. Give 3 examples.

Back 551

- are generally used in situations where patients have not tolerated an ACE inhibitor, usually due to the development of a cough.
-Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-effects include hypotension and hyperkalaemia.
- Evidence base
• shown to reduce progression of renal disease in patients with diabetic nephropathy
• evidence base that losartan reduces CVA and IHD mortality in hypertensive patients
- Mechanism
• block effects of angiotensin II at the AT1 receptor
- Examples
• candesartan
• losartan
• irbesartan


-

Front 552

When are ACEi used?

Back 552

- first-line treatment in younger patients with hypertension ( known to be less effective in treating hypertensive Afro-Caribbean patients)
- treat heart failure
- used to treat diabetic nephropathy
- secondary prevention of ischaemic heart disease

Front 553

What is the MOA of ACEi?

Back 553

• inhibit the conversion angiotensin I to angiotensin II

Front 554

What are the side effects of ACEi?

Back 554

• cough: occurs in around 15% of patients and may occur up to a year after starting treatment. Thought to be due to increased bradykinin levels
• angioedema: may occur up to a year after starting treatment
• hyperkalaemia
• first-dose hypotension: more common in patients taking diuretics

Front 555

What are the cautions and contraindications for ACEi?

Back 555

• pregnancy and breastfeeding - avoid
• renovascular disease - significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
• aortic stenosis - may result in hypotension
• patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension
• hereditary of idiopathic angioedema

Front 556

What are the NICE suggested acceptable ranges of creatinine and eGFR changes?

Back 556

The NICE CKD guidelines suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable

Front 557

What are the monitoring thats required for ACEi patients?

Back 557

• urea and electrolytes should be checked before treatment is initiated and after increasing the dose
• a rise in the creatinine and potassium may be expected after starting ACE inhibitors. Acceptable changes are an increase in serum creatinine, up to 30%* from baseline and an increase in potassium up to 5.5 mmol/l*.

Front 558

What are the clinical features of severe aortic stenosis?

Back 558

• narrow pulse pressure
• slow rising pulse
• delayed ESM
• soft/absent S2
• S4
• thrill
• duration of murmur
• left ventricular hypertrophy or failure

Front 559

What are the causes of aortic stenosis?

Back 559

• degenerative calcification (most common cause in older patients > 65 years)
• bicuspid aortic valve (most common cause in younger patients < 65 years)
• William's syndrome (supravalvular aortic stenosis)
• post-rheumatic disease
• subvalvular: HOCM

Front 560

What is the management of patients with asymptomatic and symptomatic aortic stenosis?

Back 560

• if asymptomatic then observe the patient is general rule
• if symptomatic then valve replacement
• if asymptomatic but valvular gradient > 50 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
• balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

Front 561

What is the CHA2DS2-VASc sore?

Back 561

to determine the most appropriate anticoagulation strategy in AF patients


C Congestive heart failure
H Hypertension (or treated hypertension)
A2 Age >= 75 years
D Diabetes
S2 Prior Stroke or TIA
V Vascular disease (including ischaemic heart disease and peripheral arterial disease)
A Age 65-74 years
S Sex (female)

Front 562

What is the anticoagulation strategy based on the CHA2DS2-VASc score?

Back 562

Score Anticoagulation
0 No treatment is preferred to aspirin
1 Oral anticoagulants preferred to aspirin; dabigatran is an alternative
2 or more Oral anticoagulants; dabigatran is an alternative

*the wording in the guidelines ('is preferred to') can be slightly confusing. It basically means that, say for a score of 0, whilst aspirin is an acceptable management option the weight of the clinical evidence would support no treatment instead

Front 563

What is the management of patients with <48hr history of atrial fibrillation

Back 563

If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either:
• electrical - 'DC cardioversion'
• pharmacology - amiodarone if structural heart disease, flecainide in those without structural heart disease

Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary

Front 564

What is the management of patients with AF > 48 hours?

Back 564

If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately.

If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion

Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

Front 565

What is the management guideline on the management of patients with AF who developed a stroke or TIA?

Back 565

• following a stroke or TIA warfarin should be given as the anticoagulant of choice. Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities
in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

Front 566

What are the agents used to control rate in patients with AF?

Back 566

• beta-blockers
• calcium channel blockers
• digoxin (not considered first-line anymore as they are less effective at controlling the heart rate during exercise. However, they are the preferred choice if the patient has coexistent heart failure)

Front 567

What are the agents used to maintain sinus rhytm in patients with history of AF?

Back 567

• sotalol
• amiodarone
• flecainide
• others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine

Front 568

Which group of AF patients favour rate control?

Back 568

Older than 65 years
History of ischaemic heart disease

Front 569

What group of AF patients favour rhythm control?

Back 569

Younger than 65 years
Symptomatic
First presentation
Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol)
Congestive heart failure

Front 570

What is atrial flutter?

Back 570

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

Front 571

What are the ECG findings of atrial flutter?

Back 571

• 'sawtooth' appearance
• as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
• flutter waves may be visible following carotid sinus massage or adenosine

Front 572

What is the management of atrial flutter?

Back 572

• is similar to that of atrial fibrillation although mediction may be less effective
• atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
• radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

Front 573

What is B-type natriuretic peptide ?

Back 573

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.

Front 574

What factors increase level of BNP?

Back 574

- heart failure
- any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels.
- reduced excretion in patients with chronic kidney disease

Front 575

What factors decrease level of BNP?

Back 575

ACE inhibitors, angiotensin-2 receptor blockers and diuretics.

Front 576

What are the clinical uses of BNP?

Back 576

Diagnosing patients with acute dyspnoea
• a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
• NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure

Prognosis in patients with chronic heart failure
• initial evidence suggests BNP is an extremely useful marker of prognosis

Guiding treatment in patients with chronic heart failure
• effective treatment lowers BNP levels

Front 577

Where are beta blockers used?

Back 577

• angina
• post-myocardial infarction
• heart failure: beta-blockers were previously avoided in heart failure but there is now strong evidence that certain beta-blockers improve both symptoms and mortality
• arrhythmias: beta-blockers have now replaced digoxin as the rate-control drug of choice in atrial fibrillation
• hypertension: the role of beta-blockers has diminished in recent years due to a lack of evidence in terms of reducing stroke and myocardial infarction.
• thyrotoxicosis
• migraine prophylaxis
• anxiety

Front 578

What are the examples of beta blocker?

Back 578

• atenolol
• propranolol: one of the first beta-blockers to be developed. Lipid soluble therefore crosses the blood-brain barrier

Front 579

What are the side effects of beta blocker?

Back 579

• bronchospasm
• cold peripheries
• fatigue
• sleep disturbances, including nightmares

Front 580

What are the contraindication of beta blocker use?

Back 580

• uncontrolled heart failure
• asthma
• sick sinus syndrome
• concurrent verapamil use: may precipitate severe bradycardia

Front 581

Explain its indication, notes and side effects of CCB: verpamil.

Back 581

Angina, hypertension, arrhythmias

Highly negatively inotropic

Should not be given with beta-blockers as may cause heart block

S/E: Heart failure, constipation, hypotension, bradycardia, flushing

Front 582

Explain its indication, notes and side effects of CCB: Diltiazem

Back 582

Angina, hypertension

Less negatively inotropic than verapamil but caution should still be exercised when patients have heart failure or are taking beta-blockers


S/E:Hypotension, bradycardia, heart failure, ankle swelling

Front 583

Explain its indication, notes and side effects of CCB: Nifedipine, amlodipine, felodipine
(dihydropyridines)

Back 583

Hypertension, angina, Raynaud's

Affects the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of heart failure

S/E: Flushing, headache, ankle swelling

Front 584

Characteristic exam features of: Myocardial infarction

Back 584

Cardiac-sounding pain
• heavy, central chest pain they may radiate to the neck and left arm
• nausea, sweating
• elderly patients and diabetics may experience no pain

Risk factors for cardiovascular disease

Front 585

Characteristic exam features of: Pneumothorax

Back 585

History of asthma, Marfan's etc
Sudden dyspnoea and pleuritic chest pain

Front 586

Characteristic exam features of: Pulmonary embolism

Back 586

Sudden dyspnoea and pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy

Front 587

Characteristic exam features of: Pericarditis

Back 587

Sharp pain relieved by sitting forwards
May be pleuritic in nature

Front 588

Characteristic exam features of: Dissecting aortic aneurysm

Back 588

'Tearing' chest pain radiating through to the back
Unequal upper limb blood pressure

Front 589

Characteristic exam features of: Gastro-oesophageal reflux disease

Back 589

Burning retrosternal pain
Other possible symptoms include regurgitation and dysphagia

Front 590

Characteristic exam features of: Musculoskeletal chest pain

Back 590

One of the most common diagnoses made in the Emergency Department. The pain is often worse on movement or palpation.
Pain often precedes the rash
May be precipitated by trauma or coughing
Shingles

Front 591

what is the management of patients presenting with acute chest pain?

Back 591

Immediate management of suspected acute coronary syndrome (ACS)
• glyceryl trinitrate
• aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel) outside of hospital
• do not routinely give oxygen, only give if sats < 94%*
• perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does not exclude ACS

Referral
• current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission
• chest pain 12-72 hours ago: refer to hospital the same-day for assessment
• chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

*NICE suggest the following in terms of oxygen therapy:
• do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
• people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
• people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Front 592

What is NICE's definition of anginal pain?

Back 592

NICE define anginal pain as the following:
• 1. constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
• 2. precipitated by physical exertion
• 3. relieved by rest or GTN in about 5 minutes

• patients with all 3 features have typical angina
• patients with 2 of the above features have atypical angina
• patients with 1 or none of the above features have non-anginal chest pain

If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further diagnostic testing is required. It should be noted that all men over the age of 70 years who have typical anginal symptoms fall into this category.

For patients with an estimated risk of 10-90% the following investigations are recommended. Note the absence of the exercise tolerance test:

Front 593

what is the diagnostic testing for paitents with anginal patient and an estimated likelihood of CAD of 61-90%?

Back 593

Coronary angiography

Front 594

what is the diagnostic testing for paitents with anginal patient and an estimated likelihood of CAD of 30-60%?

Back 594

Functional imaging, for example:
• myocardial perfusion scan with SPECT
• stress echocardiography
• first-pass contrast-enhanced magnetic resonance (MR) perfusion
• MR imaging for stress-induced wall motion abnormalities.

Front 595

what is the diagnostic testing for paitents with anginal patient and an estimated likelihood of CAD of 61-90%?

Back 595

CT calcium scoring

Front 596

What are the clinical features of complete heart block?

Back 596

• syncope
• heart failure
• regular bradycardia (30-50 bpm)
• wide pulse pressure
• JVP: cannon waves in neck
• variable intensity of S1

Front 597

What are the 3 different types of heart block?

Back 597

First degree heart block
• PR interval > 0.2 seconds

Second degree heart block
• type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
• type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Third degree (complete) heart block
• there is no association between the P waves and QRS complexes

Front 598

When is digoxin mainly used?

Back 598

Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.

Front 599

What is the MOA of digoxin?

Back 599

• decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
• increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve

Front 600

What are the clinical features of digoxin toxicity?

Back 600

• generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
• arrhythmias (e.g. AV block, bradycardia)

Front 601

What are the precipitating factors of digoxin toxicity?

Back 601

• classically: hypokalaemia*
• increasing age
• renal failure
• myocardial ischaemia
• hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
• hypoalbuminaemia
• hypothermia
• hypothyroidism
• drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (compete for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

*hyperkalaemia may also worsen digoxin toxicity, although this is very small print

Front 602

What is the managment of digoxin toxicity?

Back 602

• Digibind
• correct arrhythmias
• monitor potassium

Front 603

Coronary artery and its ECG changes: anteroseptal

Back 603

LAD, V1-V4

Front 604

Coronary artery and its ECG changes:inferior

Back 604

RCA, II/ III/ aVF

Front 605

Coronary artery and its ECG changes:Anterolateral

Back 605

Left anterior descending or left circumflex, V4-6, I, aVL

Front 606

Coronary artery and its ECG changes:Lateral

Back 606

Left circumflex, I, aVL +/- V5-6

Front 607

Coronary artery and its ECG changes: Posterior

Back 607

Usually left circumflex, also right coronary, Tall R waves V1-2

Front 608

What are the causes of LBBB?

Back 608

• ischaemic heart disease
• hypertension
• aortic stenosis
• cardiomyopathy
• idiopathic fibrosis

Front 609

ECG and coronary arteries

Back 609

Anteroseptal: V1-V4, Left anterior descending
Inferior: II, III, aVF, Right coronary
Anterolateral: V4-6, I, aVL, Left anterior descending or left circumflex
Lateral:I, aVL +/- V5-6, Left circumflex
Posterior:Tall R waves V1-2,Usually left circumflex, also right coronary

Front 610

What are the causes of RBBB?

Back 610

• normal variant - more common with increasing age
• chronically increased right ventricular pressure - e.g. cor pulmonale
• pulmonary embolism
• myocardial infarction
• cardiomyopathy or myocarditis

Front 611

What are the normal ECG variants in an athlete?

Back 611

• sinus bradycardia
• junctional rhythm
• first degree heart block
• Wenckebach phenomenon

Front 612

What are the ECG changes in acute MI?

Back 612

• hyperacute T waves are often the first sign of MI but often only persists for a few minutes
• ST elevation may then develop
• the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
• pathological Q waves develop after several hours to days. This change usually persists indefinitely

Definition of ST elevation*
• new ST elevation at the J-point in two contiguous leads with the cut-off points: >=0.2 mV in men or >= 0.15 mV in women in leads V2-V3 and/or >= 0.1 mV in other leads

Front 613

What is hypertrophic obstructive cardiomyopathy ?

Back 613

an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500.

Front 614

What are the clinical features of hypertrophic obstructive cardiomyopathy?

Back 614

• often asymptomatic
• dyspnoea, angina, syncope
• sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
• jerky pulse, large 'a' waves, double apex beat
• ejection systolic murmur: increases with Valsalva manoeuvre and decreases on squatting

Front 615

What conditions are associated with hypertrophic obstructive cardiomyopathy?

Back 615

• Friedreich's ataxia
• Wolff-Parkinson White

Front 616

What are the clinical features seen on Echo for patients with hypertrophic obstructive cardiomyopathy?

Back 616

• mitral regurgitation (MR)
• systolic anterior motion (SAM) of the anterior mitral valve leaflet
• asymmetric hypertrophy (ASH)

Front 617

What are the clinical features of ECG changes for patients with hypertrophic obstructive cardiomyopathy?

Back 617

• left ventricular hypertrophy
• progressive T wave inversion
• deep Q waves
• atrial fibrillation may occasionally be seen

Front 618

What determines the choice of investigation for suspected heart failure patients?

Back 618

Previous myocardial infarction
• arrange echocardiogram within 2 weeks

No previous myocardial infarction
• measure serum natriuretic peptides (BNP)
• if levels are 'high' arrange echocardiogram within 2 weeks
• if levels are 'raised' arrange echocardiogram within 6 weeks

Front 619

What is B-type natriuretic peptide?

Back 619

a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis

Front 620

What is the the classication for BNP level?

Back 620

BNP
High levels > 400 pg/ml (116 pmol/litre)
Raised levels 100-400 pg/ml (29-116 pmol/litre)
Normal levels < 100 pg/ml (29 pmol/litre)

Front 621

What increases BNP levels?

Back 621

Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis

Front 622

What decreases BNP level?

Back 622

Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists

Front 623

What are the key changes of NICE hypertension 2011 guidelines?

Back 623

• classifying hypertension into stages
• recommending the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM)
• calcium channel blockers are now considered superior to thiazides
• bendroflumethiazide is no longer the thiazide of choice

Front 624

What is the criteria for stage 1 hypertension?

Back 624

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

Front 625

What is the criteria for stage 2 hypertension?

Back 625

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

Front 626

What is the criteria for severe hypertension?

Back 626

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg

Front 627

How is hypertension diagnosed?

Back 627

If a BP reading is >= 140 / 90 mmHg patients should be offered ABPM to confirm the diagnosis.

Patients with a BP reading of >= 180/110 mmHg should be considered for immediate treatment.

Ambulatory blood pressure monitoring (ABPM)
• at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00)
• use the average value of at least 14 measurements

If ABPM is not tolerated or declined HBPM should be offered.

Home blood pressure monitoring (HBPM)
• for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
• BP should be recorded twice daily, ideally in the morning and evening
• BP should be recorded for at least 4 days, ideally for 7 days
• discard the measurements taken on the first day and use the average value of all the remaining measurements

Front 628

What is the management plan for hypertensive patients?

Back 628

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)
• treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greater

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
• offer drug treatment regardless of age

For patients < 40 years consider specialist referral to exclude secondary causes.

Step 1 treatment
• patients < 55-years-old: ACE inhibitor (A)
• patients > 55-years-old or of Afro-Caribbean origin: calcium channel blocker

Step 2 treatment
• ACE inhibitor + calcium channel blocker (A + C)

Step 3 treatment
• add a thiazide diuretic (D, i.e. A + C + D)
• NICE now advocate using either chlorthalidone (12.5-25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide

NICE define a clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated doses as resistant hypertension. They suggest step 4 treatment or seeking expert advice

Step 4 treatment
• consider further diuretic treatment
• if potassium < 4.5 mmol/l add spironolactone 25mg od
• if potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic treatment
• if further diuretic therapy is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker

If BP still not controlled seek specialist advice.

Front 629

What is the blood pressure managment target for patient < 80y and > 80y?

Back 629

Clinic BP ABPM / HBPM
Age < 80 years 140/90 mmHg 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg

Front 630

What is direct renin inhibitor ( eg. aliskiren- named rasilez)

Back 630

• by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
• no trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
• adverse effects were uncommon in trials although diarrhoea was occasionally seen
• only current role would seem to be in patients who are intolerant of more established antihypertensive drugs

Front 631

What are the causes of secodnary hypertension?

Back 631

Renal - accounts for 80% of secondary hypertension
• glomerulonephritis
• pyelonephritis
• adult polycystic kidney disease
• renal artery stenosis

Endocrine disorders
• Cushing's syndrome
• primary hyperaldosteronism including Conn's syndrome
• Liddle's syndrome
• congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
• phaeochromocytoma
• acromegaly

Others
• pregnancy
• coarctation of the aorta
• the combined oral contraceptive pill
• steroids
• MAOI

Front 632

Infective endocarditis: prophylaxis

Back 632

NICE recommends the following procedures do not require prophylaxis:
• dental procedures
• upper and lower gastrointestinal tract procedures
• genitourinary tract; this includes urological, gynaecological and obstetric procedures and childbirth
• upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy

The guidelines do however suggest:
• any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
• if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis

Front 633

Isolated systolic hypertension

Back 633

Isolated systolic hypertension (ISH) is common in the elderly, affecting around 50% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH reduced both strokes and ischaemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is contradicated by the 2011 NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension.

Front 634

What is long QT syndrome?

Back 634

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.

Front 635

What causes prolonged QT syndrome?

Back 635

1) Congenital
• Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
• Romano-Ward syndrome (no deafness)

2) Drugs*
• amiodarone, sotalol, class 1a antiarrhythmic drugs
• tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
• methadone
• chloroquine
• terfenadine**
• erythromycin
• haloperidol

**a non-sedating antihistamine and classic cause of prolonged QT in a patient, especially if also taking P450 enzyme inhibitor, e.g. Patient with a cold takes terfenadine and erythromycin at the same time

3) Other
• electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
• acute myocardial infarction
• myocarditis
• hypothermia
• subarachnoid haemorrhage

Front 636

what are the clinical features of long QT syndrome?

Back 636

• may be picked up on routine ECG or following family screening
• Long QT1 - usually associated with exertional syncope, often swimming
• Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
• Long QT3 - events often occur at night or at rest
• sudden cardiac death

Front 637

What is the management of long QT syndrome?

Back 637

• avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
• beta-blockers***
• implantable cardioverter defibrillators in high risk cases

***note sotalol may exacerbate long QT syndrome

Front 638

What is the NICE guideline for the management of patients following a MI?

Back 638

All patients should be offered the following drugs:
• ACE inhibitor
• beta-blocker
• aspirin
• statin

Clopidogrel
• ST-segment-elevation MI: patients treated with a combination of aspirin and clopidogrel during the first 24 hours after the MI should continue this treatment for at least 4 weeks
• non-ST segment elevation myocardial infarction (NSTEMI): following the 2010 NICE unstable angina and NSTEMI guidelines clopidogrel should be given for the first 12 months if the 6 month mortality risk* is > 1.5%

Aldosterone antagonists
• patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

*this can be calculated using scoring systems such as GRACE

Front 639

What are nitrates and its side effects?

Back 639

Nitrates are a group of drugs which have vasodilating effects. The main indications for their use is in the management of angina and the acute treatment of heart failure. Sublingual glyceryl trinitrate is the most common drug used in patients with ischaemic heart disease to relieve angina attacks.

Mechanism of action
• cause release of nitric oxide in smooth muscle, increasing cGMP which leads to a fall in intracellular calcium levels
• in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

Side-effects
• hypotension
• tachycardia
• headaches

Front 640

What are the indications for permanent pacemaker insertion?

Back 640

• persistent symptomatic bradycardia e.g. sick sinus syndome
• complete heart block
• Mobitz type II AV block
• persistent AV block after myocardial infarction

Front 641

Define pre-eclampsia.

Back 641

Pre-eclampsia is a condition seen after 20 weeks gestation characterised by pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours). Oedema used to be third element of the classic triad but is now often not included in the definition as it is not specific

Front 642

What are the associated complications of pre-eclampsia?

Back 642

• fetal: prematurity, intrauterine growth retardation
• eclampsia
• haemorrhage: placental abruption, intra-abdominal, intra-cerebral
• cardiac failure
• multi-organ failure

Front 643

What are the risk factors of pre-eclampsia?

Back 643

• > 40 years old
• nulliparity (or new partner)
• multiple pregnancy
• body mass index > 30 kg/m^2
• diabetes mellitus
• pregnancy interval of more than 10 years
• family history of pre-eclampsia
• previous history of pre-eclampsia
• pre-existing vascular disease such as hypertension or renal disease

Front 644

What are the clinical features of severe pre-eclampsia?

Back 644

• hypertension: typically > 170/110 mmHg and proteinuria as above
• proteinuria: dipstick ++/+++
• headache
• visual disturbance
• papilloedema
• RUQ/epigastric pain
• hyperreflexia
• platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome

Front 645

What is the management of patients with pre-eclampsia?

Back 645

• consensus guidelines recommend treating blood pressure > 160/110 mmHg although many clinicians have a lower threshold
• oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used
• delivery of the baby is the most important and definitive management step. The timing depends on the individual clinical scenario

Front 646

Which medications may exacerbate heart failure?

Back 646

• thiazolidinediones*: pioglitazone is contraindicated as it causes fluid retention
• verapamil: negative inotropic effect
• NSAIDs**/glucocorticoids: should be used with caution as they cause fluid retention
• class I antiarrhythmics; flecainide (negative inotropic and proarrhythmic effect)

*pioglitazone is now the only thiazolidinedione on the market

**low-dose aspirin is an exception - many patients will have coexistent cardiovascular disease and the benefits of taking aspirin easily outweigh the risks

Front 647

Define biological ( bioproesthetic) valves.

Back 647

Usually bovine or porcine in origin

Major disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve

Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.

Front 648

Define mechanical valves.

Back 648

The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays

Mechanical valves have a low failure rate

Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed. Aspirin is normally given in addition unless there is a contraindication.

Target INR
• aortic: 2.0-3.0
• mitral: 2.5-3.5

Front 649

What is the therapetic drug monitoring for lithum?

Back 649

• range = 0.4 - 1.0 mmol/l
• take 12 hrs post-dose

Front 650

What is the therapetic drug monitoring for ciclopsorin?

Back 650

• trough levels immediately before dose

Front 651

What is the therapetic drug monitoring for digoxin?

Back 651

• at least 6 hrs post-dose

Front 652

What is the therapetic drug monitoring for phenytoin?

Back 652

trough levels immediately before dose

Front 653

Define syncope.

Back 653

Syncope may be defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.

Front 654

What are the investigations/examination for evaluating causes of syncope?

Back 654

• cardiovascular examination
• postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
• ECG
• carotid sinus massage
• tilt table test
• 24 hour ECG

Front 655

What conditions cause syncope and how are they caterogized?

Back 655

Reflex syncope (neurally mediated)
• vasovagal: triggered by emotion, pain or stress. Often referred to as 'fainting'
• situational: cough, micturition, gastrointestinal
• carotid sinus syncope

Orthostatic syncope
• primary autonomic failure: Parkinson's disease, Lewy body dementia
• secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
• drug-induced: diuretics, alcohol, vasodilators
• volume depletion: haemorrhage, diarrhoea

Cardiac syncope
• arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
• structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
• others: pulmonary embolism

Reflex syncope is the most common cause in all age groups although orthostatic and cardiac causes become progressively more common in older patients.

Front 656

signs of life threatening asthma

Back 656

� PEFR < 33% best or predicted
� Oxygen sats < 92%
� Silent chest, cyanosis or feeble respiratory effort
� Bradycardia, dysrhythmia or hypotension
� Exhaustion, confusion or coma

Front 657

signs of severe asthma

Back 657

� PEFR 33 - 50% best or predicted
� Can't complete sentences
� RR > 25/min
� Pulse > 110 bpm

Front 658

Signs of moderate asthma

Back 658

� PEFR > 50% best or predicted
� Speech normal
� RR < 25 / min
� Pulse < 110 bpm

Front 659

Management of moderate asthma

Back 659

• beta 2 agonists such as salbutamol, either nebulised or via a spacer (4-6 puffs, given one at a time and inhaled separately, repeated at intervals of 10-20 minutes)
• if PEFR between 50-75% then prednisolone 40-50mg

Front 660

Management of severe asthma

Back 660

• consider admission
• oxygen to hypoxaemic patients to maintain a SpO2 of 94-98%
• beta 2 agonists such as salbutamol, either nebulised or via a spacer (4-6 puffs, given one at a time and inhaled separately, repeated at intervals of 10-20 minutes)
• prednisolone 40-50mg
• if no response then admit

Front 661

Management of life threatening asthma

Back 661

• arrange immediate admission (999 call)
• oxygen to hypoxaemic patients to maintain a SpO2 of 94-98%
• nebulised beta 2 agonists (e.g. Salbutamol) + ipratropium
• prednisolone 40-50mg or IV hydrocortisone 100mg

Front 662

signs of increase possibility of asthma during examination and history

Back 662

� Wheeze, breathlessness, chest tightness and cough, worse at night/early morning
� History of atopic disorder
� Wheeze heard on auscultation
� Unexplained peripheral blood eosinophilia

Front 663

signs of decreased possibility of asthma during examination and history

Back 663

� Prominent dizziness, light-headedness, peripheral tingling
� Chronic productive cough in the absence of wheeze or breathlessness
� Repeatedly normal physical examination
� Significant smoking history (i.e. > 20 pack-years)
� Normal PEF or spirometry when symptomatic

Front 664

If FEV1/FVC < 0.7 ( asthma), what is the treatment management?
If FEV1/FVC > 0.7 ( asthma), what is the treatment management?

Back 664

• FEV1/FVC < 0.7: trial of treatment
• FEV1/FVC > 0.7: further investigation/consider referral

Front 665

What value of improvement in FEV1 is considered significant?

Back 665

A > 400 ml improvement in FEV1 is considered significant
• before and after 400 mcg inhaled salbutamol in patients with diagnostic uncertainty and airflow obstruction present at the time of assessment
• if there is an incomplete response to inhaled salbutamol, after either inhaled corticosteroids (200 mcg twice daily beclometasone equivalent for 6-8 weeks) or oral prednisolone (30 mg once daily for 14 days)

Front 666

What value of peak flow is considered significant?

Back 666

It is now advised to interpret peak flow variability with caution due to the poor sensitivity of the test
• diurnal variation % = [(Highest - Lowest PEFR) / Highest PEFR] x 100
• assessment should be made over 2 weeks
greater than 20% diurnal variation is considered significant

Front 667

What are the common causes of occupational asthma?

Back 667

• isocyanates - the most common cause. Example occupations include spray painting and foam moulding using adhesives
• platinum salts
• soldering flux resin
• glutaraldehyde
• flour
• epoxy resins
• proteolytic enzymes

Front 668

How is occupational asthma diagnosed?

Back 668

• specific recommendations are made in the 2007 joint British Thoracic Society and SIGN guidelines
serial measurements of peak expiratory flow are recommended at work and away from work

Front 669

What is the step 1 of asthma?

Back 669

Inhaled short-acting B2 agonist as required

Front 670

What is the step 2 of asthma management?

Back 670

Add inhaled steroid at 200-800 mcg/day*

400 mcg is an appropriate starting dose for many patients. Start at dose of inhaled steroid appropriate to severity of disease

*beclometasone dipropionate or equivalent

Front 671

What is step 3 of asthma management?

Back 671

1. Add inhaled long-acting B2 agonist (LABA)

2. Assess control of asthma:
• good response to LABA - continue LABA
• benefit from LABA but control still inadequate: continue LABA and increase inhaled steroid dose to 800 mcg/day* (if not already on this dose)
• no response to LABA: stop LABA and increase inhaled steroid to 800 mcg/ day.* If control still inadequate, institute trial of other therapies, leukotriene receptor antagonist or SR theophylline



*beclometasone dipropionate or equivalent

Front 672

What is step 4 of asthma management?

Back 672

Consider trials of:
• increasing inhaled steroid up to 2000 mcg/day*
• addition of a fourth drug e.g. Leukotriene receptor antagonist, SR theophylline, B2 agonist tablet



*beclometasone dipropionate or equivalent

Front 673

What is step 5 of asthma management?

Back 673

Use daily steroid tablet in lowest dose providing adequate control. Consider other treatments to minimise the use of steroid tablets

Maintain high dose inhaled steroid at 2000 mcg/day*

Refer patient for specialist care

*beclometasone dipropionate or equivalent

Front 674

What are leukotriene receptor antagonists? Medication example.

Back 674

• e.g. Montelukast, zafirlukast
• have both anti-inflammatory and bronchodilatory properties
• should be used when patients are poorly controlled on high-dose inhaled corticosteroids and a long-acting b2-agonist
• particularly useful in aspirin-induced asthma
• associated with the development of Churg-Strauss syndrome

Front 675

What medication is more lipophillic than beclometasone?

Back 675

fluticasone

Front 676

What is long acting B2 agonists better than doubling inhaled steroid?

Back 676

Long acting B2-agonists acts as bronchodilators but also inhibit mediator release from mast cells. Recent meta-analysis showed adding salmeterol improved symptoms compared to doubling the inhaled steroid dose

Front 677

What is bronchiectasis?

Back 677

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation

Front 678

What is the management of bronchiectasis?

Back 678

. After assessing for treatable causes (e.g. immune deficiency) management is as follows:
• physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
• postural drainage
• antibiotics for exacerbations + long-term rotating antibiotics in severe cases
• bronchodilators in selected cases
• immunisations
• surgery in selected cases (e.g. Localised disease)

Front 679

What organisms are most commonly isolated from patients with bronchiectasis?

Back 679

Most common organisms isolated from patients with bronchiectasis:
• Haemophilus influenzae (most common)
• Pseudomonas aeruginosa
• Klebsiella spp.
• Streptococcus pneumoniae

Front 680

Who should be considered for diagnosis of COPD?

Back 680

NICE recommend considering a diagnosis of COPD in patients over 35 years of age who are smokers or ex-smokers and have symptoms such as exertional breathlessness, chronic cough or regular sputum production.

Front 681

What investigations are recommended in patients with suspected COPD?

Back 681

• post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
• chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
• full blood count: exclude secondary polycythaemia
• body mass index (BMI) calculation

Front 682

Categorise severity of COPD using FEV1

Back 682

Post-bronchodilator FEV1/FVC, FEV1 (of predicted), Severity
< 0.7 > 80% Stage 1 - Mild**
< 0.7 50-79% Stage 2 - Moderate
< 0.7 30-49% Stage 3 - Severe
< 0.7 < 30% Stage 4 - Very severe



*note that the grading system has changed following the 2010 NICE guidelines. If the FEV1 is greater than 80% predicted but the post-bronchodilator FEV1/FVC is < 0.7 then this is classified as Stage 1 - mild

**symptoms should be present to diagnose COPD in these patients

Front 683

Why is measuring peak expiratory flow limted value in COPD patients?

Back 683

it may underestimate the degree of airflow obstruction

Front 684

How many hours per day should COPD patient on LTOT use it for?

Back 684

15 hours

Front 685

What is used to supply oxygen for LTOT?

Back 685

Oxygen concentrators are used to provide a fixed supply for LTOT.

Front 686

in which group of patients should LTOT be assessed for?

Back 686

• very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be 'considered' for patients with severe airflow obstruction (FEV1 30-49% predicted)
• cyanosis
• polycythaemia
• peripheral oedema
• raised jugular venous pressure
• oxygen saturations less than or equal to 92% on room air

Front 687

How is a patient who is considered for LTOT assessed? and when is LTOT offered?

Back 687

Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.

Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
• secondary polycythaemia
• nocturnal hypoxaemia
• peripheral oedema
• pulmonary hypertension

Front 688

What organisms most commonly cause infective exacerbation of COPD?

Back 688

The most common bacterial organisms that cause infective exacerbations of COPD are:
• Haemophilus influenzae (most common cause)
• Streptococcus pneumoniae
• Moraxella catarrhalis

Respiratory viruses account for around 30% of exacerbations, with the human rhinovirus being the most important pathogen.

Front 689

How to manage the exacerbation of COPD?

Back 689

• increase frequency of bronchodilator use and consider giving via a nebuliser
• give prednisolone 30 mg daily for 7-14 days
it is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE do not support this approach. They recommend giving oral antibiotics 'if sputum is purulent or there are clinical signs of pneumonia'

Front 690

What is the management of stable COPD?

Back 690

General management
• smoking cessation advice
• annual influenza vaccination
• one-off pneumococcal vaccination


Bronchodilator therapy
• a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
• for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1

FEV1 > 50%
• long-acting beta2-agonist (LABA), for example salmeterol, or:
• long-acting muscarinic antagonist (LAMA), for example tiotropium

FEV1 < 50%
• LABA + inhaled corticosteroid (ICS) in a combination inhaler, or:
• LAMA

For patients with persistent exacerbations or breathlessness
• if taking a LABA then switch to a LABA + ICS combination inhaler
• otherwise give a LAMA and a LABA + ICS combination inhaler

Oral theophylline
• NICE only recommends theophylline after trials of short an long-acting bronchodilators or to people who cannot used inhaled therapy
• the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed

Mucolytics
• should be 'considered' in patients with a chronic productive cough and continued if symptoms improve

Front 691

Define cor pulmonale and its management.

Back 691

• features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
• use a loop diuretic for oedema, consider long-term oxygen therapy
• ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

Front 692

What are the factors that may increase the survival in patients with COPD?

Back 692

• smoking cessation - the single most important intervention in patients who are still smoking
• long term oxygen therapy in patients who fit criteria
• lung volume reduction surgery in selected patients

Front 693

Define cystic fibrosis.

Back 693

Cystic fibrosis (CF) is an autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

In the UK 80% of CF cases are due to delta F508 on the long arm of chromosome 7. Cystic fibrosis affects 1 per 2500 births, and the carrier rate is c. 1 in 25

Front 694

What are the organisms which may colonise in CF patients?

Back 694

• Staphylococcus aureus
• Pseudomonas aeruginosa
• Burkholderia cepacia*
• Aspergillus

*previously known as Pseudomonas cepacia

Front 695

What are the clinical features of cystic fibrosis?

Back 695

Presenting features
• neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
• recurrent chest infections (40%)
• malabsorption (30%): steatorrhoea, failure to thrive
• other features (10%): liver disease

Other features of cystic fibrosis
• short stature
• diabetes mellitus
• delayed puberty
• rectal prolapse (due to bulky stools)
• nasal polyps
• male infertility, female subfertility

Front 696

What is the management of cystic fibrosis?

Back 696

Management of cystic fibrosis involves a multidisciplinary approach

Key points
• regular (at least twice daily) chest physiotherapy and postural drainage. Parents are usually taught to do this. Deep breathing exercises are also useful
• high calorie diet, including high fat intake*
• vitamin supplementation
• pancreatic enzyme supplements taken with meals
• heart and lung transplant

*this is now the standard recommendation - previously high calorie, low-fat diets have been recommended to reduce the amount of steatorrhoea

Front 697

What drugs can cause lung fibrosis?

Back 697

Causes
• amiodarone
• cytotoxic agents: busulphan, bleomycin
• anti-rheumatoid drugs: methotrexate, sulfasalazine, gold
• nitrofurantoin
• ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)

Front 698

What are the differential diagnosis of haemoptysis?

Back 698

1. Lung cancer (History of smoking, Symptoms of malignancy: weight loss, anorexia)
2. Pulmonary oedema( Dyspnoea, Bibasal crackles and S3 are the most reliable signs)
3. Tuberculosis (Fever, night sweats, anorexia, weight loss)
4. Pulmonary embolism (Pleuritic chest pain,Tachycardia, tachypnoea)
5. Lower respiratory tract infection (Usually acute history of purulent cough)
6. Bronchiectasis (Usually long history of cough and daily purulent sputum production)
7. Mitral stenosis( Dyspnoea, Atrial fibrillation, Malar flush on cheeks, Mid-diastolic murmur)
8. Aspergilloma (Often past history of tuberculosis, Haemoptysis may be severe, Chest x-ray shows rounded opacity )
9. Wegener's granulomatosis (Upper respiratory tract: epistaxis, sinusitis, nasal crusting, Lower respiratory tract: dyspnoea, haemoptysis, Glomerulonephritis,
Saddle-shape nose deformity )
10. Goodpasture's syndrome (Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis)

Front 699

Explain influenza vaccination.

Back 699

Seasonal influenza still accounts for a significant morbidity and mortality in the UK each winter, with the influenza season typically starting in the middle of November. This may vary year from year so it is recommended that vaccination occurs between September and early November. There are three types of influenza virus; A, B and C. Types A and B account for the majority of clinical disease. Current vaccines are trivalent and consist of two subtypes of influenza A and one subtype of influenza B.


• it is an inactivated vaccine, so cannot cause influenza. A minority of patients however develop fever and malaise which may last 1-2 days
• should be stored between +2 and +8�C and shielded from light
• contraindications include hypersensitivity to egg protein.
• in adults the vaccination is around 75% effective, although this figure decreases in the elderly
• it takes around 10-14 days after immunisation before antibody levels are at protective levels

Front 700

Who should have annual influenza vaccination?

Back 700

The Department of Health recommends annual influenza vaccination for people older than 65 years and those older than 6 months if they have:
• chronic respiratory disease (including asthmatics who use inhaled steroids)
• chronic heart disease (heart failure, ischaemic heart disease, including hypertension if associated with cardiac complications)
• chronic kidney disease
• chronic liver disease: cirrhosis, biliary atresia, chronic hepatitis
• chronic neurological disease: (e.g. Stroke/TIAs)
• diabetes mellitus (including diet controlled)
• immunosuppression due to disease or treatment (e.g. HIV)
• asplenia or splenic dysfunction
• pregnant women

Other at risk individuals include:
• health and social care staff directly involved in patient care (e.g. NHS staff)
• those living in long-stay residential care homes
• carers of the elderly or disabled person whose welfare may be at risk if the carer becomes ill (at the GP's discretion)

Children in at risk groups should be vaccinated. Only children aged less than 9 years who have not received influenza vaccine before should receive a second dose of vaccine at least 4 weeks later.

Front 701

Who should be considered for immediate referral for patients with suspected cancer?

Back 701

Consider immediate referral for patients with:
• signs of superior vena caval obstruction (swelling of the face/neck with fixed elevation of jugular venous pressure)
• stridor

Front 702

Who should be considered for urgent referral for patients with suspected cancer?

Back 702

• persistent haemoptysis (in smokers or ex-smokers aged 40 years and older)
• a chest X-ray suggestive of lung cancer (including pleural effusion and slowly resolving consolidation)
• a normal chest X-ray where there is a high suspicion of lung cancer
• a history of asbestos exposure and recent onset of chest pain, shortness of breath or unexplained systemic symptoms

Front 703

who should be receive urgent CXR?

Back 703

• haemoptysis
• unexplained or persistent (longer than 3 weeks): chest and/or shoulder pain, dyspnoea, weight loss, chest signs, hoarseness, finger clubbing, cervical or supraclavicular lymphadenopathy, cough, features suggestive of metastasis from a
lung cancer (for example, secondaries in the brain, bone, liver, skin)
• underlying chronic respiratory problems with unexplained changes in existing symptoms

Front 704

What are the risk factors of lung cancer?

Back 704

Smoking
• increases risk of lung ca by a factor of 10

Other factors
• asbestos - increases risk of lung ca by a factor of 5
• arsenic
• radon
• nickel
• chromate
• aromatic hydrocarbon
• cryptogenic fibrosing alveolitis

Factors that are NOT related
• coal dust

Smoking and asbestos are synergistic, i.e. a smoker with asbestos exposure has a 10 * 5 = 50 times increased risk

Front 705

Define mycoplasma pneumoniae.

Back 705

Mycoplasma pneumoniae is a cause of atypical pneumonia which often affects younger patients. It is associated with a number of characteristic complications such as erythema multiforme and cold autoimmune haemolytic anaemia. Epidemics of Mycoplasma pneumoniae classically occur every 4 years. It is important to recognise atypical pneumonias as they may not respond to penicillins or cephalosporins

Front 706

What are the clinical features and complications of mycoplasma pneumoniae?

Back 706

Features
• the disease typically has a prolonged and gradual onset
• flu-like symptoms classically precede a dry cough
• bilateral consolidation on x-ray
• complications may occur as below

Complications
• cold agglutins (IgM) may cause an haemolytic anaemia, thrombocytopenia
• erythema multiforme, erythema nodosum
• meningoencephalitis, Guillain-Barre syndrome
• bullous myringitis: painful vesicles on the tympanic membrane
• pericarditis/myocarditis
• gastrointestinal: hepatitis, pancreatitis
• renal: acute glomerulonephritis

Front 707

What is the investigation of mycoplasma pneumoniae?

Back 707

• diagnosis is generally by Mycoplasma serology
• positive cold agglutination test

Front 708

What is the management of mycoplasma pneumoniae?

Back 708

• erythromycin/clarithromycin
• tetracyclines such as doxycycline are an alternative

Front 709

What organisms cause community acquired pneumonia?

Back 709

• Streptococcus pneumoniae (accounts for around 80% of cases)
• Haemophilus influenzae
• Staphylococcus aureus: commonly after the 'flu
• atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
• viruses

Klebsiella pneumoniae is classically in alcoholics

Front 710

What are the clinical features of community acquired pneumonia?

Back 710

Characteristic features of pneumococcal pneumonia
• rapid onset
• high fever
• pleuritic chest pain
• herpes labialis

Front 711

What is the management of community acquired pneumonia?

Back 711

The British Thoracic Society published guidelines in 2009:
• low or moderate severity CAP: oral amoxicillin. A macrolide should be added for patients admitted to hospital
• high severity CAP: intravenous co-amoxiclav + clarithromycin OR cefuroxime + clarithromycin OR cefotaxime + clarithromycin

Front 712

What is the management of pulmonary embolism?

Back 712

Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a PE is diagnosed. An exception to this is for patients with a massive PE where thrombolysis is being considered. In such a situation unfractionated heparin should be used.
• a vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis
• the LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range
• warfarin should be continued for at least 3 months. At 3 months, NICE advise that clinicians should 'assess the risks and benefits of extending treatment'
• NICE advise extending warfarin beyond 3 months for patients with unprovoked PE. This essentially means that if there was no obvious cause or provoking factor (surgery, trauma, significant immobility) it may imply the patient has a tendency to thrombosis and should be given treatment longer than the norm of 3 months
• for patients with active cancer NICE recommend using LMWH for 6 months

Thrombolysis
• thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension). Other invasive approaches should be considered where appropriate facilities exist

Front 713

Define obstructive lung disease and give examples of condition.

Back 713

FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

Front 714

Define restrictive lung disease and give examples of condition.

Back 714

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis
Neuromuscular disorders

Front 715

respiratory syncytial virus causes...

Back 715

bronchiolitis

Front 716

parainfluenza virus causes...

Back 716

croup

Front 717

rhinovirus causes...

Back 717

common cold

Front 718

influenza virus causes...

Back 718

flu

Front 719

Streptococcus pneumoniae causes...

Back 719

The most common cause of community-acquired pneumonia

Front 720

Haemophilus influenzae causes...

Back 720

Community-acquired pneumonia
Most common cause of bronchiectasis exacerbations
Acute epiglottitis

Front 721

Staphylococcus aureus causes...

Back 721

Pneumonia, particularly following influenza

Front 722

Mycoplasma pneumoniae causes...

Back 722

Atypical pneumonia

Flu-like symptoms classically precede a dry cough. Complications include haemolytic anaemia and erythema multiform

Front 723

Legionella pneumophilia causes...

Back 723

Atypical pneumonia

Classically spread by air-conditioning systems, causes dry cough. Lymphopenia, deranged liver function tests and hyponatraemia may be seen

Front 724

Pneumocystis jiroveci causes...

Back 724

Common cause of pneumonia in HIV patients. Typically patients have few chest signs and develop exertional dyspnoea

Front 725

Mycobacterium tuberculosis causes...

Back 725

Causes tuberculosis. A wide range of presentations from asymptomatic to disseminated disease are possible. Cough, night sweats and weight loss may be seen

Front 726

What are the respiratory problems of rheumatoid arthritis?

Back 726

A variety of respiratory problems may be seen in patients with rheumatoid arthritis:
• pulmonary fibrosis
• pleural effusion
• pulmonary nodules
• bronchiolitis obliterans
• complications of drug therapy e.g. methotrexate pneumonitis
• pleurisy
• Caplan's syndrome - massive fibrotic nodules with occupational coal dust exposure
• infection (possibly atypical) secondary to immunosuppression

Front 727

What conditions cause chronic SOB?

Back 727

1. Chronic obstructive pulmonary disease ( Seen invariably in smokers, Chronic productive cough is typical, Features of right heart failure may be seen)
2. Heart failure (A history of ischaemic heart disease or hypertension may be present, Orthopnoea and paroxysmal nocturnal dyspnoea are characteristic,
Bibasal crackles and a third heart sound (S3) are the most reliable features of left-sided failure,
Right heart failure causes peripheral oedema and a raised JVP)
3. Asthma ( Cough, wheeze and shortness of breath are typical, Symptoms are often worse at night and may be precipitated by cold weather or exercise, Associated with hay fever and eczema)
4. Aortic stenosis (Chest pain, SOB and syncope seen in symptomatic patients, An ejection systolic murmur radiating to the neck and narrow pulse pressure are found on examination)
5.Recurrent pulmonary emboli (There may be a history of predisposing factors e.g. Malignancy, Pleuritic chest pain and haemoptysis may be seen but symptoms are often vague, Tachycardia and tachypnoea are common in the acute situation, Symptoms of right heart failure may develop in severe cases)
6. Lung cancer ( Normally seen in smokers,Haemoptysis, chronic cough or unresolving infection are common presentations, Systemic symptoms e.g. Weight loss and anorexia)
7. Pulmonary fibrosis (Progressive shortness of breath may be the only symptom, Fine bibasal crackles are typical Spirometry shows a restrictive pattern)

8. Bronchiectasis ( Affected patients may produce large amounts of purulent sputum, Patients may have a history of previous infections (e.g. Tuberculosis, measles), bronchial obstruction or ciliary dyskinetic syndromes e.g. Kartagener's syndrome)
9. Anaemia (There may be a history of gastrointestinal symptoms, Pallor may be seen on examination)
10. Obesity ( Obese patients tend to be more SOB due to the increased work of activity)

Front 728

Define antiphospholipid syndrome

Back 728

Antiphospholipid syndrome is an acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia. It may occur as a primary disorder or secondary to other conditions, most commonly systemic lupus erythematosus (SLE)

Front 729

What are the clinical features of antiphospholipid syndrome.

Back 729

Features
• venous/arterial thrombosis
• recurrent fetal loss
• livedo reticularis
• thrombocytopenia
• prolonged APTT
• other features: pre-eclampsia, pulmonary hypertension

Front 730

What conditions are associated with SLE?

Back 730

Associations other than SLE
• other autoimmune disorders
• lymphoproliferative disorders
• phenothiazines (rare)

Front 731

What is the management of antiphospholipid syndrome?

Back 731

Management - based on BCSH guidelines
• initial venous thromboembolic events: evidence currently supports use of warfarin with a target INR of 2-3 for 6 months
• recurrent venous thromboembolic events: lifelong warfarin; if occurred whilst taking warfarin then increase target INR to 3-4
• arterial thrombosis should be treated with lifelong warfarin with target INR 2-3

Front 732

What are the complications of antiphophopid syndrome during pregnancy

Back 732

In pregnancy the following complications may occur:
• recurrent miscarriage
• IUGR
• pre-eclampsia
• placental abruption
• pre-term delivery
• venous thromboembolism

Front 733

What is the management of pregnant women with antiphopholipid syndrome?

Back 733

• low-dose aspirin should be commenced once the pregnancy is confirmed on urine testing
• low molecular weight heparin once a fetal heart is seen on ultrasound. This is usually discontinued at 34 weeks gestation
• these interventions increase the live birth rate seven-fold

Front 734

Define chronic lymphocytic leukaemia.

Back 734

Chronic lymphocytic leukaemia (CLL) is caused by a monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells (99%)

Front 735

What are the clinical features and complication of chronic lymphocytic leukaemia?

Back 735

Features
• often none
• constitutional: anorexia, weight loss
• bleeding, infections
• lymphadenopathy more marked than CML

Complications
• hypogammaglobulinaemia leading to recurrent infections
• warm autoimmune haemolytic anaemia in 10-15% of patients
• transformation to high-grade lymphoma (Richter's transformation)

Front 736

What are the investigations for suspected chronic lymphocytic leukaemia?

Back 736

Investigations
• blood film: smudge cells
• immunophenotyping

Front 737

Which score should be done on patients with suspected DVT?

Back 737

2 level DVT wells score

Front 738

What is the 2 level DVT wells score?

Back 738







Active cancer (treatment ongoing, within 6 months, or palliative) -1
Paralysis, paresis or recent plaster immobilisation of the lower extremities -1

Recently bedridden for 3 days or more or major surgery within 12 weeks requiring general or regional anaesthesia -1
Localised tenderness along the distribution of the deep
venous system - 1
Entire leg swollen -1

Calf swelling at least 3 cm larger than asymptomatic side
-1
Pitting oedema confined to the symptomatic leg- 1

Collateral superficial veins (non-varicose) -1
Previously documented DVT -1
An alternative diagnosis is at least as likely as DVT − minus 2

Clinical probability simplified score
• DVT likely: 2 points or more
• DVT unlikely: 1 point or less



Front 739

What the management of DVT wells score greater than 2 points?

Back 739

If a DVT is 'likely' (2 points or more)
• a proximal leg vein ultrasound scan should be carried out within 4 hours and, if the result is negative, a D-dimer test
• if a proximal leg vein ultrasound scan cannot be carried out within 4 hours a D-dimer test should be performed and low-molecular weight heparin administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)

Front 740

What is the management of DVT wells score less than or equal to 1?

Back 740

If a DVT is 'unlikely' (1 point or less)
• perform a D-dimer test and if it is positive arrange:
• a proximal leg vein ultrasound scan within 4 hours
• if a proximal leg vein ultrasound scan cannot be carried out within 4 hours low-molecular weight heparin should be administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)

Front 741

What is the management of confirmed DVT?

Back 741

Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a DVT is diagnosed.
• a vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis
• the LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range
• warfarin should be continued for at least 3 months. At 3 months, NICE advise that clinicians should 'assess the risks and benefits of extending treatment'
• NICE add 'consider extending warfarin beyond 3 months for patients with unprovoked proximal DVT if their risk of VTE recurrence is high and there is no additional risk of major bleeding'. This essentially means that if there was no obvious cause or provoking factor (surgery, trauma, significant immobility) it may imply the patient has a tendency to thrombosis and should be given treatment longer than the norm of 3 months
• for patients with active cancer NICE recommend using LMWH for 6 months

Front 742

Define G6PD deficiency.

Back 742

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the commonest red blood cell enzyme defect. It is more common in people from the Mediterranean and Africa and is inherited in a X-linked recessive fashion.

Front 743

What are the clinical features of G6PD deficiency?

Back 743

Features
• neonatal jaundice is often seen
• intravascular haemolysis- anaeia
• gallstones are common
• splenomegaly may be present
• Heinz bodies on blood films

Front 744

How is G6PD deficiency diagnosed?

Back 744

Diagnosis is made by using a G6PD enzyme assay

Front 745

What exacerbate a crisis of G6PD deficiency?

Back 745

Many drugs can precipitate a crisis as well as infections and broad (fava) beans.


Some drugs causing haemolysis
• anti-malarials: primaquine
• ciprofloxacin
• sulphonamides

Front 746

What medications were taught to be safe in G6PD deficiency?

Back 746

Some drugs thought to be safe
• penicillins
• cephalosporins
• macrolides
• tetracyclines
• trimethoprim

Front 747

Define hereditary spherocytosis.

Back 747

Basics
• most common hereditary haemolytic anaemia in people of northern European descent
• autosomal dominant defect of red blood cell cytoskeleton
• the normal biconcave disc shape is replaced by a sphere-shaped red blood cell
• red blood cell survival reduced as destroyed by the spleen

Front 748

Clinical features of hereditary spherocytosis.

Back 748

• failure to thrive
• jaundice, gallstones
• splenomegaly
• aplastic crisis precipitated by parvovirus infection
• degree of haemolysis variable

Front 749

Investigation of hereditary spherocytosis.

Back 749

• osmotic fragility test

Front 750

What is the management of hereditary spherocytosis?

Back 750

Management
• folate replacement
• splenectomy

Front 751

Define ITP.

Back 751

Idiopathic thrombocytopenic purpura (ITP) is an immune mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.

Front 752

How can ITP be divided?

Back 752

ITP can be divided into acute and chronic forms:

Acute ITP
• more commonly seen in children
• equal sex incidence
• may follow an infection or vaccination
• usually runs a self-limiting course over 1-2 weeks

Chronic ITP
• more common in young/middle-aged women
• tends to run a relapsing-remitting course

Front 753

Define evan's syndrome.

Back 753

Evan's syndrome
• ITP in association with autoimmune haemolytic anaemia (AIHA)

Front 754

Causes of generalised lymphadenopathy.

Back 754

There are many causes of generalised lymphadenopathy

Infective
• infectious mononucleosis
• HIV, including seroconversion illness
• eczema with secondary infection
• rubella
• toxoplasmosis
• CMV
• tuberculosis
• roseola infantum

Neoplastic
• leukaemia
• lymphoma

Others
• autoimmune conditions: SLE, rheumatoid arthritis
• graft versus host disease
• sarcoidosis
• drugs: phenytoin and to a lesser extent allopurinol, isoniazid

Front 755

How can macrocytic anaemia be divided?

Back 755

Macrocytic anaemia can be divided into causes associated with a megaloblastic bone marrow and those with a normoblastic bone marrow

Front 756

What are the causes of megaloblastic macrocytic anaemia?

Back 756

• vitamin B12 deficiency
• folate deficiency

Front 757

What are the causes of normoblastic macrocytic anaemia?

Back 757

• alcohol
• liver disease
• hypothyroidism
• pregnancy
• reticulocytosis e.g. haemolysis
• myelodysplasia
• drugs: cytotoxics

Front 758

Define polycythaemia. How can polycythaemia be divided?

Back 758

Polycythaemia may be relative, primary (polycythaemia rubra vera) or secondary

Relative causes
• dehydration
• stress: Gaisbock syndrome

Primary
• polycythaemia rubra vera

Secondary causes
• COPD
• altitude
• obstructive sleep apnoea
• excessive erythropoietin: cerebellar haemangioma, hypernephroma, hepatoma, uterine fibroids*

To differentiate between true (primary or secondary) polycythaemia and relative polycythaemia red cell mass studies are sometimes used. In true polycythaemia the total red cell mass in males > 35 ml/kg and in women > 32 ml/kg

*uterine fibroids may cause menorrhagia which in turn leads to blood loss - polycythaemia is rarely a clinical problem

Front 759

What are the risk factors of venous thromboembolism?

Back 759

Common predisposing factors include malignancy, pregnancy and the period following an operation. The comprehensive list below is partly based on the 2010 SIGN venous thromboembolism (VTE) guidelines:

General
• increased risk with advancing age
• obesity
• family history of VTE
• pregnancy (especially puerperium)
• immobility
• hospitalisation
• anaesthesia
• central venous catheter: femoral >> subclavian

Underlying conditions
• malignancy
• thrombophilia: e.g. Activated protein C resistance, protein C and S deficiency
• heart failure
• antiphospholipid syndrome
• Behcet's
• polycythaemia
• nephrotic syndrome
• sickle cell disease
• paroxysmal nocturnal haemoglobinuria
• hyperviscosity syndrome
• homocystinuria

Medication
• combined oral contraceptive pill: 3rd generation more than 2nd generation
• hormone replacement therapy
• raloxifene and tamoxifen
• antipsychotics (especially olanzapine) have recently been shown to be a risk factor

SIGN also state that the following are risk factors for recurrent VTE:
• previous unprovoked VTE
• male sex
• obesity
• thrombophilias

Front 760

What is warfarin?

Back 760

Warfarin is an oral anticoagulant which inhibits the reduction of vitamin K to its active hydroquinone form, which in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

Front 761

What are the indications of warfarin?

Back 761

• venous thromboembolism: target INR = 2.5, if recurrent 3.5
• atrial fibrillation, target INR = 2.5
• mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.

Front 762

What factor may potentiate warfarin?

Back 762

Factors that may potentiate warfarin
• liver disease
• P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
• cranberry juice
• drugs which displace warfarin from plasma albumin, e.g. NSAIDs
• inhibit platelet function: NSAIDs

Front 763

What are the side effects of warfarin?

Back 763

• haemorrhage
• teratogenic, although can be used in breast-feeding mothers
• skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis
• purple toes

Front 764

What is the management of INR > 8 with minor bleeding and > 8 without bleeding?

Back 764

1. INR > 8.0 Minor bleeding

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0



2. INR > 8.0 No bleeding

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

Front 765

What is the management of INR > 5 with minor bleeding and > 5 without bleeding?

Back 765

1.INR 5.0-8.0 Minor bleeding
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

2. INR 5.0-8.0 No bleeding

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

Front 766

What is the management of major INR related bleeding?

Back 766

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

*as FFP can take time to defrost prothrombin complex concentrate should be considered in cases of intracranial haemorrhage

Front 767

What tumours cause bone metastases?

Back 767

Most common tumour causing bone metastases (in descending order)
• prostate
• breast
• lung

Most common site (in descending order)
• spine
• pelvis
• ribs
• skull
• long bones

Front 768

What is the NICE guideline regarding referral for suspected breast cancer?

Back 768

Urgent referrals (i.e. within 2 weeks)
• any breast lump with features suggestive of cancer (hard, tethered etc)
• any breast lump in a post-menopausal woman, regardless of features suggestive of cancer
• any breast lump in a women more than 30 years old without features suggestive of cancer but which persists after her next period
• if there is past history of breast cancer any breast lump should warrant urgent referral
• spontaneous unilateral bloody nipple discharge
• unilateral eczematous skin or nipple change that does not respond to topical treatment, or with nipple distortion of recent onset

Non-urgent referrals
• women < 30 years old who present with a breast lump with no features suggestive of cancer, no relevant family history and no change in the size of the lump

Front 769

What is the top ten causes of cancer in the UK ? ( commonest -> least)

Back 769

• 1. Breast
• 2. Lung
• 3. Colorectal
• 4. Prostate
• 5. Bladder
• 6. Non-Hodgkin's lymphoma
• 7. Melanoma
• 8. Stomach
• 9. Oesophagus
• 10. Pancreas

*excludes non-melanoma skin cancer

Front 770

What is the top ten causes of death in the UK? ( commonest-> least)

Back 770

The most common causes of death from cancer in the UK are as follows:
• 1. Lung
• 2. Colorectal
• 3. Breast
• 4. Prostate
• 5. Pancreas
• 6. Oesophagus
• 7. Stomach
• 8. Bladder
• 9. Non-Hodgkin's lymphoma
• 10. Ovarian

Front 771

Explain cervical cancer and its clinical features.

Back 771

The incidence of cervical cancer peaks around the 6th decade. It may be divided into
• squamous cell cancer (80%)
• adenocarcinoma (20%)


Features
• may be detected during routine cervical cancer screening
• abnormal vaginal bleeding: postcoital, intermenstrual or postmenopausal bleeding
• vaginal discharge

Risk factors
• human papilloma virus 16,18 & 33
• smoking
• human immunodeficiency virus
• early first intercourse, many sexual partners
• high parity
• lower socioeconomic status
• combined oral contraceptive pill*

*the strength of this association is sometimes debated but a large study published in the Lancet (2007 Nov 10;370(9599):1609-21) confirmed the link

Front 772

Explain chemotherapy side effects: nausea and vomiting.

Back 772

Nausea and vomiting are common side-effects of chemotherapy. Risk factors for the development of symptoms include:
• anxiety
• age less than 50 years old
• concurrent use of opioids
• the type of chemotherapy used

For patients at low-risk of symptoms then drugs such as metoclopramide may be used first-line. For high-risk patients then 5HT3 receptor antagonists such as ondansetron are often effective, especially if combined with dexamethasone

Front 773

Explain chronic lymphocytic leukaemia and its clinical features/complications/ investigation.

Back 773

Chronic lymphocytic leukaemia (CLL) is caused by a monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells (99%)

Features
• often none
• constitutional: anorexia, weight loss
• bleeding, infections
• lymphadenopathy more marked than CML

Complications
• hypogammaglobulinaemia leading to recurrent infections
• warm autoimmune haemolytic anaemia in 10-15% of patients
• transformation to high-grade lymphoma (Richter's transformation)


Investigations
• blood film: smudge cells
• immunophenotyping

Front 774

Which patients should be referred urgently ( ie. < 2 weeks) rule to colorectal services for investigation?

Back 774

• patients > 40 years old, reporting rectal bleeding with a change of bowel habit towards looser stools and/or increased stool frequency persisting for 6 weeks or more
• patients > 60 years old, with rectal bleeding persisting for 6 weeks or more without a change in bowel habit and without anal symptoms
• patients > 60 years old, with a change in bowel habit to looser stools and/or more frequent stools persisting for 6 weeks or more without rectal bleeding
• any patient presenting with a right lower abdominal mass consistent with involvement of the large bowel
• any patient with a palpable rectal mass
• unexplained iron deficiency anaemia in men or non-menstruating women (Hb < 11 g/dl in men, < 10 g/dl in women)

Front 775

What is the colorectal cancer screening?

Back 775

Overview
• most cancers develop from adenomatous polyps. Screening for colorectal cancer has been shown to reduce mortality by 16%
• the NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 69 years. Patients aged over 70 years may request screening
• eligible patients are sent faecal occult blood (FOB) tests through the post
• patients with abnormal results are offered a colonoscopy

At colonoscopy, approximately:
• 5 out of 10 patients will have a normal exam
• 4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
• 1 out of 10 patients will be found to have cancer

Front 776

MOA, Adverse effects, class:Cyclophosphamide

Back 776

Alkylating agent - causes cross-linking in DNA

Side effect:
Haemorrhagic cystitis, myelosuppression, transitional cell carcinoma

Front 777

MOA, Adverse effects, class: Bleomycin

Back 777

Cytotoxic antibiotics
Degrades preformed DNA
S/E: Lung fibrosis

Front 778

MOA, Adverse effects, class: Doxorubicin

Back 778

Cytotoxic antibiotics
Stabilizes DNA-topoisomerase II complex inhibits DNA & RNA synthesis
S/E: Cardiomyopathy

Front 779

MOA, Adverse effects, class:Methotrexate

Back 779

Inhibits dihydrofolate reductase and thymidylate synthesis
S/E: Myelosuppression, mucositis, liver fibrosis, lung fibrosis

Front 780

MOA, Adverse effects, class:Fluorouracil (5-FU)

Back 780

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase (works during S phase)
S/E: Myelosuppression, mucositis, dermatitis

Front 781

MOA, Adverse effects, class: 6-mercaptopurine

Back 781

Purine analogue that is activated by HGPRTase, decreasing purine synthesis
S/E: Myelosuppression

Front 782

MOA, Adverse effects, class:Vincristine, vinblastine

Back 782

Acts on microtubules

Inhibits formation of microtubules
S/E: Vincristine: Peripheral neuropathy (reversible) , paralytic ileus
S/E: Vinblastine: myelosuppression

Front 783

MOA, Adverse effects, class: Docetaxel

Back 783

Acts on microtubules

Prevents microtubule depolymerisation & disassembly, decreasing free tubulin
S/E: Neutropaenia

Front 784

MOA, Adverse effects, class: Cisplatin

Back 784

Causes cross-linking in DNA

S/E: Ototoxicity, peripheral neuropathy, hypomagnesaemia

Front 785

MOA, Adverse effects, class: Hydroxyurea (hydroxycarbamide)

Back 785

Inhibits ribonucleotide reductase, decreasing DNA synthesis

S/E: Myelosuppression

Front 786

Explain endometrial cancer.

Back 786

Endometrial cancer is classically seen in post-menopausal women but around 25% of cases occur before the menopause. It usually carries a good prognosis due to early detection

Front 787

What are the risk factors of endometrial cancer?

Back 787

The risk factors for endometrial cancer are as follows*:
• obesity
• nulliparity
• late menopause
• unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
• diabetes mellitus
• tamoxifen
• polycystic ovarian syndrome

Front 788

What are the clinical features of endometrial cancer?

Back 788

• post-menopausal bleeding is the classic symptom
• pre-menopausal women may have a change intermenstrual bleeding
• pain and discharge are unusual features

Front 789

Investigation of endometrial cancer.

Back 789

• first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
• hysteroscopy with endometrial biopsy

Front 790

Management of endometrial cancer.

Back 790

• localised disease is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. Patients with high-risk disease may have post-operative radiotherapy
• progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery

Front 791

What is protective to endometrial cancer?

Back 791

COCP

Front 792

What is the epidemiology of gastric cancer?

Back 792

• 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

Front 793

What is gastric cancer associated with?

Back 793

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

Front 794

Investigation of gastric cancer

Back 794

• diagnosis: endoscopy with biopsy
• staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT

Front 795

Explain oesophageal cancer

Back 795

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.

Front 796

What are the risk factors of oesophageal cancer?

Back 796

Risk factors
• smoking
• alcohol
• GORD
• Barrett's oesophagus
• achalasia
• Plummer-Vinson syndrome
• rare: coeliac disease, scleroderma

Front 797

Explain ovarian cancer.

Back 797

Ovarian cancer is the fifth most common malignancy in females. The peak age of incidence is 60 years and it generally carries a poor prognosis due to late diagnosis. Around 90% of ovarian cancers are epithelial in origin

Front 798

What are the risk factors of ovarian cancer?

Back 798

Risk factors
• family history: mutations of the BRCA1 or the BRCA2 gene
• many ovulations: early menarche, late menopause, nulliparity

It is traditionally taught that infertility treatment increases the risk of ovarian cancer, as it increases the number of ovulations. Recent evidence however suggests that there is not a significant link. The combined oral contraceptive pill reduces the risk (fewer ovulations) as does having many pregnancies.

Front 799

clinical features of ovarian cancer?

Back 799

Clinical features are notoriously vague
• abdominal distension and bloating
• abdominal and pelvic pain
• urinary symptoms e.g. Urgency
• early satiety
• diarrhoea

Diagnosis is difficult and usually involves diagnostic laparotomy

Front 800

Palliative care prescribing: agitation and confusion

Back 800

Underlying causes of confusion need to be looked for and treated as appropriate, for example hypercalcaemia, infection, urinary retention and medication. If specific treatments fail then the following may be tried:
• first choice: haloperidol
• other options: chlorpromazine, levomepromazine

In the terminal phase of the illness (for example a patient on the Care of the Dying pathway) then agitation or restlessness is best treated with midazolam

Front 801

Palliative care prescribing: hiccups

Back 801

Management of hiccups
• chlorpromazine is licensed for the treatment of intractable hiccups
• haloperidol, gabapentin and baclofen are also used

Front 802

What is the NICE guideline in use of opioids in palliative care patients?

Back 802

Starting treatment
• when starting treatment, offer patients with advanced and progressive disease regular oral modified-release (MR) or oral immediate-release morphine (depending on patient preference), with oral immediate-release morphine for breakthrough pain
• if no comorbidities use 20-30mg of MR a day with 5mg morphine for breakthrough pain. For example, 15mg modified-release morphine tablets twice a day with 5mg of oral morphine solution as required
• oral modified-release morphine should be used in preference to transdermal patches
• laxatives should be prescribed for all patients initiating strong opioids
• patients should be advised that nausea is often transient. If it persists then an antiemetic should be offered

Front 803

What is the SIGN guideline on the control of pain in adult with cancer?

Back 803

• the breakthrough dose of morphine is one-sixth the daily dose of morphine
• all patients who receive opioids should be prescribed a laxative
• opioids should be used with caution in patients with chronic kidney disease. Alfentanil, buprenorphine and fentanyl are preferred
• metastatic bone pain may respond to NSAIDs, bisphosphonates or radiotherapy

Front 804

How many percent should the next dose of opioids be increased by in palliative care patients?

Back 804

When increasing the dose of opioids the next dose should be increased by 30-50%.

Front 805

What are the side effects of opioid ?

Back 805

transient- nausea and drowsiness
persistent- constipation

Front 806

What is the conversion between oral codeine to oral morphine?

Back 806

divide by 10

Front 807

What is the conversion between oral tramadol to oral morphine?

Back 807

divide by 5

Front 808

What is the conversion between oral morphine to oral oxycodone?

Back 808

divide by 2

Front 809

What does 12 microgram transdermal fentayl patch equate to oral morphine daily?

Back 809

• a transdermal fentanyl 12 microgram patch equates to approximately 45 mg oral morphine daily

Front 810

what does 20 microgram patch transdermal buprenorphine equate to oral morphine daily?

Back 810

• a transdermal buprenorphine 20 microgram patch equates to approximately 30 mg oral morphine daily.

Front 811

What is the conversion factor between oral morphine to subcutaneous diamorphine?

Back 811

divide by 3

Front 812

What is the conversion factor between oral oxycodone to subcutaneous diamorphine?

Back 812

divide by 1.5

Front 813

What are the treatment options of localised prostate cancer (T1/T2)

Back 813

Treatment depends on life expectancy and patient choice. Options include:
• conservative: active monitoring & watchful waiting
• radical prostatectomy
• radiotherapy: external beam and brachytherapy

Front 814

What are the treatment option of localised advanced prostate cancer (T3/T4)?

Back 814

Options include:
• hormonal therapy: see below
• radical prostatectomy
• radiotherapy: external beam and brachytherapy



Synthetic GnRH agonist
• e.g. Goserelin (Zoladex)
• cover initially with anti-androgen to prevent rise in testosterone

Anti-androgen
• cyproterone acetate prevents DHT binding from intracytoplasmic protein complexes

Front 815

what are the treatment options of metastatic prostate cancer disease?

Back 815

1. Hormonal
Synthetic GnRH agonist
• e.g. Goserelin (Zoladex)
• cover initially with anti-androgen to prevent rise in testosterone

Anti-androgen
• cyproterone acetate prevents DHT binding from intracytoplasmic protein complexes


2. Orchidectomy

Front 816

What is the gleason score?

Back 816

The Gleason score is used to predict prognosis in patients with prostatic cancer. The grading system is based on the glandular architecture seen on histology following hollow needle biopsy

The most prevalent and the second most prevalent pattern seen are added to obtain a Gleason score. The Gleason grade ranges from 1 to 5 meaning the Gleason score ranges from 2 to 10 (i.e. two values added)

The higher the Gleason score the worse the prognosis

Front 817

Define spinal cord compression.

Back 817

Spinal cord compression is an oncological emergency and affects up to 5% of cancer patients. Extradural compression accounts for the majority of cases, usually due to vertebral body metastases. It is more common in patients with lung, breast and prostate cancer

Front 818

Clinical features of spinal cord compression

Back 818

Features
• back pain - the earliest and most common symptom - may be worse on lying down and coughing
• lower limb weakness
• sensory changes: sensory loss and numbness
• neurological signs depend on the level of the lesion. Lesions above L1 usually result in upper motor neuron signs in the legs and a sensory level. Lesions below L1 usually cause lower motor neuron signs in the legs and perianal numbness. Tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion

Front 819

Management of spinal cord compression

Back 819

• high-dose oral dexamethasone
• urgent oncological assessment for consideration of radiotherapy or surgery

Front 820

Define superior vena cava obstruction.

Back 820

Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer.

Front 821

Clinical features of superior vena cava obstruction

Back 821

• dyspnoea is the most common symptom
• swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
• headache
• visual disturbance
• pulseless jugular venous distension

Front 822

Causes of superior vena cava obstruction

Back 822

• common malignancies: small cell lung cancer, lymphoma
• other malignancies: metastatic seminoma, Kaposi's sarcoma, breast cancer
• aortic aneurysm
• mediastinal fibrosis
• goitre
• SVC thrombosis

Front 823

Management of superior vena cava obstruction

Back 823

• general: dexamethasone, balloon venoplasty, stenting
• small cell: chemotherapy + radiotherapy
• non-small cell: radiotherapy

Front 824

When is syringe driver used?

Back 824

A syringe driver should be considered in the palliative care setting when a patient is unable to take oral medication due to nausea, dysphagia, intestinal obstruction, weakness or coma.

Front 825

What are the two main types of syringe drivers in the UK?

Back 825

In the UK there are two main types of syringe driver:
• Graseby MS16A (blue): the delivery rate is given in mm per hour
• Graseby MS26 (green): the delivery rate is given in mm per 24 hours

Front 826

What medications used in syringe drivers are compatible and recommended with 0.9% sodium chloride?

Back 826

• granisetron
• ketamine
• ketorolac
• octreotide
• ondansetron

Front 827

What are the commonly used drugs in syringe drivers?

Back 827

• nausea and vomiting: cyclizine, levomepromazine, haloperidol, metoclopramide
• respiratory secretions: hyoscine hydrobromide
• bowel colic: hyoscine butylbromide
• agitation/restlessness: midazolam, haloperidol, levomepromazine
• pain: diamorphine is the preferred opioid

Front 828

In mixing a syringe driver, which drugs are compatible with diamorphine?

Back 828

• diamorphine (the most commonly used drug) is compatible with the majority of other drugs used including cyclizine*, dexamethasone, haloperidol, hyoscine butylbromide, hyoscine hydrobromide, levomepromazine, metoclopramide, midazolam

*precipitation may be seen at higher doses

Front 829

In mixing a syringe driver, which drugs are incompatible with cyclizine?

Back 829

• cyclizine is incompatible with a number of drugs including clonidine, dexamethasone, hyoscine butylbromide (occasional), ketamine, ketorolac, metoclopramide, midazolam, octreotide, sodium chloride 0.9%

Front 830

Define testicular cancer.

Back 830

Testicular cancer is the most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may essentially be divided into:
• seminomas
• teratomas

Other type of germ cell tumours include yolk sac tumours. Non-germ cell tumours include Leydig cell tumours and sarcomas.

The peak incidence for teratomas is 25 years and seminomas is 35 years

Front 831

What are the risk factors for testicular cancer?

Back 831

Risk factors include:
• cryptorchidism
• infertility
• family history
• Klinefelter's syndrome
• mumps orchitis

Front 832

What are the clinical features of testicular cancer?

Back 832

• a painless lump is the most common presenting symptom
• pain may also be present in a minority of men
• other possible features include hydrocele, gynaecomastia

Front 833

What is the first line investigation for testicular cancer?

Back 833

• ultrasound is first-line

Front 834

What is the management of testicular cancer?

Back 834

• orchidectomy
• chemotherapy and radiotherapy may be given depending on staging

Front 835

What is the prognosis of testicular cancer?

Back 835

Prognosis is generally excellent
• 5 year survival for seminomas is around 95% if Stage I
• 5 year survival for teratomas is around 85% if Stage I

Front 836

How are tumour markers divided?

Back 836

Tumour markers may be divided into:
• monoclonal antibodies against carbohydrate or glycoprotein tumour antigens ( CA 125, CA 19-9, CA 15-3)
• tumour antigens ( PSA, AFP, CEA)
• enzymes (alkaline phosphatase, neurone specific enolase)
• hormones (e.g. calcitonin, ADH)

Front 837

CA 125

Back 837

Ovarian cancer

Front 838

Ca 19-9

Back 838

Pancreatic cancer

Front 839

CA 15-3

Back 839

breast cancer

Front 840

Prostate specific antigen (PSA)

Back 840

Prostatic carcinoma

Front 841

alpha-feto protein ( AFP)

Back 841

Hepatocellular carcinoma, teratoma

Front 842

Carcinoembryonic antigen (CEA)

Back 842

Colorectal cancer