Quesmed wrong answers Flashcards
What is the definition of COPD?
Chronic obstructive pulmonary disease (COPD) is characterised by irreversible, usually progressive obstruction of the airways. It is an encompassing term for two types of chronic lung diseases: chronic bronchitis and emphysema.
It comprises both:
1. Chronic bronchitis – involves hypertrophy and hyperplasia of the mucus glands in the bronchi
2. Emphysema – involves enlargement of the air spaces and destruction of alveolar walls
There are different phenotypes of COPD dependent on which of these pathologies is more prominent.
What are the risk factors and poor prognostic factors in COPD?
- Tobacco smoking (active or passive)
- Occupational exposure to dust
- Alpha-1 antitrypsin deficiency
Prognosis is worsened by:
-Advancing age
-Ongoing smoking
-Reduced body weight
-Low FEV1
What is the pathophysiology of chronic bronchitis?
- Chronic exposure to noxious particles such as smoking or air pollutants causes hypersecretion of mucus in the large and small bronchi.
- Airway inflammation and fibrotic changes result in narrowing of the airways and subsequently chronic airway obstruction.
- Cigarette smoke interferes with the action of cilia in removing noxious particles.
- Cigarette smoke also dampens the ability of leukocytes in eliminating the bacteria in the airways.
What is the pathophysiology of emphysema?
- Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls.
- This reduces the alveolar surface area thus impeding efficient gaseous exchange.
- Cigarette smoke stimulates accumulation of neutrophils and macrophages which produce neutrophil elastase that destroys alveolar walls.
- In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase. However, in emphysema, the normal balance of proteases and antiproteases is lost. The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin.
- This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping.
Where in the respiratory tract do 1. cigarette smoke, 2. Alpha-1-antitrypsin deficiency and 3. Fibrosis/atelectasis affect?
- The proximal part of the airways such as the respiratory bronchioles, mainly the upper lobes.
- The entire acini from respiratory bronchioles to alveolar duct and alveoli, mainly the lower lobes.
- The distal part of the airways, mainly the paraseptal region
What are the signs and symptoms of COPD?
Symptoms:
- Productive cough
- Recurrent respiratory infections
- Wheeze
- Dyspnoea
- Reduced exercise tolerance
- Weight loss
Signs
- Accessory muscle use for respiration
- Prolonged expiratory phase
- Pursed lip breathing
- Tachypnoea
- Hyperinflation – reduction of the cricosternal distance
- Reduced chest expansion
- Hyper-resonant percussion
- Decreased/quiet breath sounds
- Wheeze
- Cyanosis
- Cor pulmonale (signs of right heart failure)
How is COPD investigated?
- Bloods
- FBC – polycythaemia due to chronic hypoxia
- ABG – reduced paO2 +/– raised paCO2 (may be acute or compensated type 2 respiratory failure) - ECG
- P-pulmonale (right atrial hypertrophy)
- Right ventricular hypertrophy, if there is cor pulmonale - Chest X-ray
- Hyperinflated chest (>6 anterior ribs)
- Bullae
- Decreased peripheral vascular markings
- Flattened hemidiaphragms - Spirometry – can be performed at diagnosis or to monitor progression
- FEV1/FVC ratio <0.7
- Increased TLC
- Low TLCO – seen in patients who have significant emphysema without a significant chronic bronchitis element
- Reversibility testing is not required unless history/examination fails to differentiate between asthma and COPD
Severity is dependent on the value of FEV1 according to the GOLD criteria.
Other tests:
- Sputum culture – to identify exacerbating organisms
- Brain natriuretic peptide (BNP) + echocardiogram – to assess for heart failure
- Serum alpha-1 antitrypsin – to assess for genetic cause in young patients
- Consider high-resolution CT (HRCT) scan if the diagnosis remains ambiguous
What are the possible differentials for COPD?
The differential diagnosis for COPD includes:
1. Asthma: Characterised by reversible airway obstruction, episodic symptoms and response to bronchodilators.
2. Bronchiectasis: Persistent productive cough, recurrent respiratory infections and abnormal bronchial dilatation on CT chest.
3. Heart Failure: Shortness of breath, orthopnea, paroxysmal nocturnal dyspnoea, and signs of fluid overload such as peripheral oedema and elevated jugular venous pressure.
4. Pulmonary Fibrosis: Progressive dyspnoea, non-productive cough, and inspiratory crackles on auscultation.
What is the non-pharmacological management for COPD?
- Smoking cessation
- Nutritional support
- Flu and pneumococcal vaccinations
- Pulmonary rehabilitation
What are the 4 steps in the pharmacological management of COPD?
- Step 1: short-acting β2 agonist/short-acting muscarinic antagonist – these are continued as the patient goes up the management steps
- Step 2
- For patients with persistent exacerbations but no asthmatic features or evidence of steroid responsiveness:
add a long-acting β2 agonist AND a long-acting muscarinic antagonist
- For patients with persistent exacerbations with asthmatic features or evidence of steroid responsiveness:
increase management to a combination of long-acting β2 agonist and ICS - Step 3
- For patients on a long-acting β2 agonist + long-acting muscarinic antagonist combination who are still getting daily symptoms that affect their activities of daily living:
consider a 3-month trial of long-acting muscarinic antagonist + long-acting β2 agonist + ICS (triple therapy)
*if this does not work, revert back to long-acting β2 agonist + long-acting muscarinic antagonist
- For any patient on step 2 who is getting more than one severe or two moderate exacerbations in a year:
start long-acting muscarinic antagonist + long-acting β2 agonist + ICS - Step 4: if patients are still symptomatic, consider specialist referral
*Other adjuncts: oral theophylline, mucolytic agents, antidepressants.
*Corticosteroids should only be used in acute exacerbations, maintenance doses are not usually recommended.
*Consider LTOT for eligible patients
What are the indications for surgery in COPD?
Patients with severe COPD who remain breathless despite maximal medical therapy should be considered for lung volume reduction surgery if:
- they have upper lobe-predominant emphysema
- FEV1 >20% predicted
- paCO2 <7.3 kPa
- TLCO >20% predicted
Other surgical options include single bullectomy and single- or double-lung transplantation.
How is an acute exacerbation of COPD managed?
- Ensure a patent airway
- Ensure oxygen saturations of 88–92% (if there is a history of CO2 retention)
- Nebulisers – salbutamol, ipratropium
- Steroids – oral prednisolone or IV hydrocortisone (if severe)
- Antibiotics if any evidence of infection (eg. fever or raised inflammatory markers)
Monitor closely for signs of type 2 respiratory failure: drowsiness, asterixis, agitation as this may indicate the need for noninvasive ventilation (BiPaP).
Treatment escalation plans should be closely considered for these patients.
What is T2DM?
Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.
What is the aetiology of type 2 DM?
T2DM results from a combination of genetic and environmental factors. Known contributors include:
- Poor dietary habits
- Lack of physical activity
- Obesity
What are the signs and symptoms of type 2 DM?
Individuals with T2DM may initially be asymptomatic, but over time, they may develop:
- Polyuria
- Polydipsia
- Unexplained weight loss
- Blurry vision
- Fatigue
What are the possible differentials for type 2 DM?
The primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:
- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.
- MODY: Early onset (typically before 25 years), non-insulin dependent, and often has a strong family history.
- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).
How is type 2 DM investigated?
If symptomatic, one of the following results is sufficient for diagnosis:
- Random blood glucose ≥ 11.1mmol/l
- Fasting plasma glucose ≥ 7mmol/l
- 2-hour glucose tolerance ≥ 11.1mmol/l
- HbA1C ≥ 48mmol/mol (6.5%)
If the patient is asymptomatic, two results are required from different days.
How is type 2 diabetes managed?
- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation
- Pharmacological interventions:
- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.
- Following initial management, consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).
- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary. - Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.
DPP-4 inhibitors: Mechanism, names, contraindications
These inhibit the enzyme DPP-4 which normally destroys the hormone incretin (GLP-1).
Incretin stimulates insulin secretion from the beta cells and inhibits glucagon release by the alpha cells.
Therefore, inhibition of the breakdown of incretin leads to higher incretin levels and therefore insulin levels (as well as lower glucagon levels).
‘Gliptins’ eg alogliptin, linagliptin, saxagliptin, sitagliptin
CI in ketoacidosis, reduce in renal impairment (not linagliptin), and hepatic impairment (not linagliptin or sitagliptin)
Thiazolidinediones (glitazones): Mechanism, names, contraindications
Promotes insulin sensitivity and improves uptake of glucose through agonism at the peroxisome-proliferator-activated receptor gamma (PPARG).
Pioglitazone
CI in ketoacidosis, hx of HF, previous/active bladder cancer, haematuria, hepatic impairment. Fallen out of favour in recent years due to the presence of multiple adverse effects and warnings regarding their use (e.g. congestive heart failure, bladder cancer) and the availability of safer and more effective alternatives for patients with type 2 diabetes mellitus.
SGLT2-inhibitors: Mechanism, names, contraindications
Bind to SGLT2 in the luminal membrane in the early segments of the nephron where they block glucose resorption.
‘Flozins’ - Canaglifozin, Dapagliflozin, Empagliflozin, Ertuglifozin
CI in ketoacidosis. Caution or avoid with renal or hepatic impairment.
Sulphonylureas: Mechanism, names, contraindications
Stimulate insulin production from beta cell (by closing ATP-sensitive K-channels in the beta cell membrane that result in insulin release
Gliclazide, Glimepiride, Glipizide, Tolbutamide
CI in ketoacidosis, has a moderate/high risk of hypoglycaemia, particularly in older people. Caution or avoid in hepatic or renal impairment.
Which insulin therapy might be used in Type 2 DM?
NICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.
Long acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).
Mixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.
What are the possible complications of diabetes mellitus?
- Gastrointestinal Complications: Gastroparesis - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.
- Neurological Complications: Autonomic Neuropathy - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.
- Vascular Complications: Peripheral Arterial Disease (PAD) - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).
- Foot Complications: Diabetic Foot Infections - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.
- Sexual Dysfunction - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.
- Cardiac Complications - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.
What is eczema?
Eczema is a chronic inflammatory disorder of the skin characterised by dermal inflammation (dermatitis) with resultant spongiotic change in the epidermis histologically, with chronic features including epidermal acanthosis, hyperkeratosis, and parakeratosis.
What is the pathophysiology of atopic dermatitis?
Dermatitis triggers the disease process. The normal dermis has a small amount of lymphocytes and other immune cells but in skin with eczema there is a vast infiltrate visible.
Keratinocytes in the epidermis start detaching from one another, becoming rounder and the intercellular spaces widening between them. If the eczema has come on acutely, this separation may be so severe that vesicles form. Under the microscope, this makes the epidermis look like a sponge, hence ‘spongiotic’ change.
With chronic inflammation, histology shows:
- Epidermal acanthosis: thickening of the epidermis due to hyperplasia.
- Hyperkeratosis: thickening specifically of the stratum corneum.
- Parakeratosis: retained nuclei in the stratum corneum indicating problems with the usual differentiation process.
In many cases, atopic dermatitis is associated with an IgE-mediated allergic response to environmental allergens. Sensitisation to allergens such as house dust mites, pet dander, pollen, and certain foods can lead to the production of specific IgE antibodies. Upon re-exposure to these allergens, IgE-mediated immune responses are triggered, resulting in skin inflammation and pruritus. This plays a significant role in exacerbations of atopic dermatitis.
Often, the terms eczema and dermatitis are used interchangeably as the two are so closely linked. However, there are other instances where there is dermal inflammation without eczematous changes. Therefore, the two terms are not entirely the same.
What are the types of atopic dermatitis?
- Atopic eczema
- Allergic contact dermatitis
- Irritant contact dermatitis
- Seborrheic dermatitis
- Venous eczema (stasis dermatitis)
- Asteatotic dermatitis (eczema craquele)
- Erythrodermic eczema
- Pompholyx eczema
What are the clinical features of atopic eczema?
Childhood predominance: symptoms tend to become less severe with age.
Associated with atopic phenotype: asthma, hayfever, raised eosinophils.
In infants, the face is a common site. In older children/adults, the antecubital fossa and posterior knee (flexor surfaces) are affected.
The skin is itchy, erythematous, and oozing. There may be vesicles, which may have crusted over.
Eventually, the skin becomes dry and flaky. Repeated scratching causes lichenification (thick, leathery skin, also called lichen simplex et chronicus.)
What are the clinical features of erythrodermic eczema?
This is a dermatological emergency and may complicate atopic eczema.
It is syndrome characterised by widespread redness (>90%)
There is often skin exfoliation too, which leads to exfoliative dermatitis.
What are the clinical features of seborrhoeic dermatitis?
This common condition is thought to happen due to Malassezia Furfur, a commensal organism on the skin. A predisposed individual due to genetic and environmental factors may develop an inflammatory response to the organism.
The skin is flakey with a fine scale, oily, and erythematous. There is usually minimal pain or stinging or itch.
The scale may coalesce into thicker plaques.
It tends to affect the face (especially hairline, nasolabial fold, and brow area) in adults.
Risk factors for the development include:
- Family history
- Oily skin
- Immunosuppression (such as HIV)
- Neurological and psychiatric diseases (such as Parkinson’s Disease or Depression)
- Stress
Dandruff is the common term used to describe a mild, non-inflamed form of seborrheic dermatitis
Managed with anti-fungal agents, such as ketoconazole shampoo.
Infantile seborrheic dermatitis (cradle cap) is asymptomatic. It appears as a diffuse, yellow, greasy scale, coalescing into plaqaues on the scalp/groin/armpit. Emollients (such as olive oil) loosen the scales, which can then be brushed off. Antifungal shampoos may be used if the issue persists.
What are the clinical features of stasis dermatitis?
Also known as venous eczema.
This is eczema associated with chronic venous insufficiency (venous hypertension), usually affecting the gaiter area.
There may be associated skin changes therefore, including: venous ulcers, lipodermatosclerosis, and hemasiderosis.
What are the clinical features of pompholyx eczema?
This is a subtype of eczema associated with intensely itchy vesicles that erupt in the hands.
It is also referred to as dishydrotic eczema.
How is eczema investigated?
Eczema is a clinical diagnosis and investigations aren’t always needed. However, investigations may include:
- Tests prior to commencing systemic treatments with traditional DMARDs or biologics.
- Bloods:
*If concerns regarding superadded infection.
*Total IgE and raised eosinophils may confirm atopic phenotype.
*Patients with atopic eczema often have concerns about ‘allergies’ as triggers (i.e. Type 1 mediated immune reactions) The relationship between eczema and allergy is complicated, and it is not thought that eczema is a direct manifestation of a Type 1 allergic process. However, allergies are common amongst patients with eczema, especially atopic eczema. Therefore, it is often sensible to perform testing if it is a subject of genuine concern. This can be in the form of RAST IgE or skin-prick testing. These have a high sensitivity but low specificity, and as such if negative are useful, but if positive do not necessarily indicate allergy.
- Patch test: The allergen is applied to the skin under occlusion for 48 hours to confirm a delayed (type IV) allergic process implicated in allergic contact dermatitis.
- Swabs: bacterial and viral swabs if concerns regarding superadded infection.
- Skin biopsy: if the diagnosis is uncertain, especially with erythrodermic presentations.
How is the severity of eczema scaled?
Mild - areas of dry skin, and infrequent itching (with or without small areas of redness)
Moderate - areas of dry skin, frequent itching, and erythema (with or without excoriation and localized skin thickening)
Severe - widespread areas of dry skin, incessant itching, and erythema (with/without excoriation, extensive skin thickening, bleeding, oozing, cracking, and alteration of pigmentation)
Infected - if eczema is weeping, crusted, or there are pustules, with fever or malaise
How is eczema treated?
- Conservative:
- Avoid triggers: soaps, perfumes, biological detergents, or synthetic fabrics. Replace these where possible (soap substitutes, non biological detergents, natural fabrics e.g. cotton.)
- Avoid allergens.
- Keep the area cool and dry.
- Sedating antihistamine can reduce itching and aid sleep.
- Liberal emollients should be applied frequently.
- Psychological support may be needed. - Topical treatment for eczema:
- Mild eczema - liberal emollient usage + mild topical corticosteroid (such as hydrocortisone 1%) for areas of red skin.
- Moderate eczema - liberal emollient usage + moderate topical corticosteroid (such as clobetasone butyrate 0.5% - Eumovate) for 5 days. Hydrocortisone 1% should be used for the face and flexures. Consider prescribing maintenance topical corticosteroids to control areas of skin prone to frequent flares.
- Severe eczema - liberal emollient usage + potent topical corticosteroid (for example betamethasone valerate 0.1% - Betnovate) to be used on inflamed areas. For the face and flexures, use a moderate potency corticosteroid (such as Eumovate).
- If there is severe, extensive eczema causing psychological distress, consider prescribing a short course of an oral corticosteroid (refer children under 16 years of age).
- Topical calcineurin inhibitors (e.g. tacrolimus) - can be considered as a steroid sparing agent. These are second-line and should be prescribed by a specialist.
- Light therapy: aims to suppress dermal inflammation. The most common type used is narrow band UV-B. - Systemic therapies:
- Oral steroids: if widespread and severe, e.g. erythroderma.
- Systemic retinoids: such as alitretinoin may be used for hand eczema recalcitrant to topical therapies.
- Traditional DMARDs:
*Methotrexate: a dihydrofolate reductase inhibitor.
*Ciclosporin: a calcineurin inhibitor.
*Azathioprine: inibits purine synthesis.
- Biologics: as per the NICE guidelines, reserved for patients with moderate to severe eczema not responding to at least 1 traditional systemic therapy:
*Dupilumab: IL-4Rα inhibitor
*Baricitinib: JAK inhibitor
When should eczema be referred to dermatology?
- Eczema is severe and has not responded to optimum topical treatment after 1 week (urgent referral; within 2 weeks)
- The diagnosis is, or has become, uncertain.
- Current management has not controlled eczema satisfactorily (for example the person is having one to two flares per month), or the person is reacting adversely to many emollients.
- Facial eczema that is treatment-resistent.
- Contact allergic dermatitis is suspected
What are the possible complications of eczema?
- Scratching:
- Poor sleep - sedating antihistamines (e.g. chlorphenamine) can be prescribed to aid sleep
- Poor mood
- Skin breakdown: bacterial infection (take a swab - usually Staphylococcal or Streptococcal), scarring, and post inflammatory hyper/hypopigmentation. -Skin thickening (lichenification) with chronic scratching. - Psycho-social:
- Insecurities surrounding skin appearance, especially if there are scars/pigment changes/lichenified skin, or changes from long term steroid use.
- Normal daily activities may be disrupted due to skin condition e.g. avoiding swimming.
- Poor mood and poor sleep from itch. - Eczema herpeticum:
A dermatological emergency.
- This is a disseminated herpes simplex virus in a patient with eczema, usually atopic eczema, and normally occurs when the patient is first infected with HSV.
- Vesicles and punched out erosions where the vesicles have deroofed will appear, and may affect large areas of skin, including sites that are apparently not currently eczematous.
- There may be multi organ involvement, and the patient is unwell.
- Admission is required for intravenous antiviral therapy (aciclovir.) Often given concomitantly with antibiotics as concomitant bacterial infection is common and difficult to exclude clinically.
- Diagnosis can be confirmed with a swab & Tzanck test.
What is candidiasis?
Vulvovaginal candidiasis, often referred to as a yeast infection, is an inflammation of the vagina and the vulva due to an overgrowth of the yeast fungus, primarily Candida Albicans.
Recurrent vulvovaginal candidiasis is defined as four or more symptomatic episodes in one year, with at least two episodes confirmed by microscopy or culture when symptomatic.
Transmission is typically non-sexual.
What are the risk factors for candidiasis?
Key factors that increase the risk of developing a Candida infection include:
- Pregnancy
- Antibiotic use
- Immunosuppression
What are the clinical features of candidiasis in men and women?
- Women
- Symptoms: Itching, white curdy or lumpy discharge, sour milk odour, dysuria, superficial dyspareunia, pruritus, tenderness, and a burning sensation.
- Examination findings: Redness, fissuring, swelling, intertrigo, thick white discharge. - Men
- Symptoms: Soreness, pruritus, redness.
- Examination findings: Dry, dull, red glazed plaques and papules.
What are the possible differentials for candidiasis?
The following conditions can present similarly to vulvovaginal candidiasis and should be considered:
1. Bacterial vaginosis: Characterised by greyish-white discharge, fishy odour, and absence of significant inflammation.
2. Trichomoniasis: Presents with yellow-green, frothy discharge, dysuria, and itching.
3. Chlamydia or Gonorrhoea: These sexually transmitted infections can cause similar symptoms such as discharge, but often also present with pelvic pain or bleeding.
4. Genital herpes: Characterised by painful blisters or open sores in the genital area.
How is candidiasis investigated?
Routine investigations are not typically required for acute, uncomplicated vulvovaginal candidiasis cases. However, in instances where the clinical presentation is unclear or recurrent episodes occur, the following investigations may be necessary:
- Microscopy: Detection of blastospores, pseudohyphae and neutrophils suggests Candida infection.
- Culture: Recommended for recurrent vulvovaginal candidiasis cases to identify the Candida species.
How is candidiasis managed?
Vulvovaginal candidiasis is primarily managed with antifungal treatment:
- Oral (-azoles) e.g., fluconazole, itraconazole
- Intravaginal e.g., clotrimazole pessary
- Vulval e.g., topical clotrimazole cream
Common regimens include:
- Fluconazole oral capsule 150mg as a single dose.
- Clotrimazole intravaginal pessary 500mg as a single dose.
- Clotrimazole intravaginal cream (10%) 5g as a single dose.
- Clotrimazole intravaginal pessary 200mg at night for 3 consecutive nights.
Recurrent vulvovaginal candidiasis is managed with a induction and maintainence regimen:
- Induction with Fluconazole oral capsule 150mg every 72 hours for a total of three doses
- Maintainence with Fluconazole oral capsule 150mg once weekly for six months
- These regimens can be supplemented with topical -azole therapy if vulval symptoms persist.
Oral therapies should be avoided in pregnant women, women at risk of pregnancy, and breastfeeding women. Intravaginal and topical treatments may compromise the integrity of latex condoms and diaphragms.
What is the intrauterine device?
The intra-uterine device (IUD) is a long-term form of contraception that is inserted into the uterus. It operates by releasing copper, which is toxic to both the egg and sperm, thereby preventing fertilization and subsequent implantation.
What are the possible side effects of the IUD?
After IUD insertion, some women may experience spotting and period-like pains. It is important for women to regularly check the position of their device and report any changes to their healthcare provider.
What are the possible differentials for unexplained bleeding or pain following IUD insertion?
In cases of unexplained bleeding or pain following IUD insertion, differential diagnoses could include:
- Displacement or expulsion of the IUD
- Uterine perforation
- Pelvic inflammatory disease
- Pregnancy (including ectopic pregnancy)
What are the rules for use of the IUD?
It is crucial to conduct follow-up investigations 3-4 weeks post-insertion to confirm absence of pregnancy and discuss future contraception plans.
The device is not suitable for women with a current pelvic infection, a distorted uterus, a history of frequent sexually transmitted infections, unexplained bleeding or an abnormal cervix.
It can be inserted either 48 hours within giving birth or after four weeks postpartum
What are the DVLA guidelines for driving a car/motorbike or a bus/coach/lorry when someone has had a seizure?
- Car/motorbike licence
- one off seizure = reapply in 6 months
- more than one seizure = reapply in one year
- seizure following change in antiepileptic medications = reapply to drive if seizure was more than 6 months ago or you’ve been back on previous medication for 6 months - Bus/coach/lorry licence
- one off seizure - reapply in 5 years or if you haven’t taken anti epileptic medications for 5 years
- more than one seizure = reapply once you haven’t had a seizure for 10 years or you haven’t taken any anti-epileptic medication for 10 years
The guidelines apply for all categories of license and are more strict for those that are Taxi and HGV drivers.
Which conditions are associated with smoking?
- Malignancy: Lung, oesophagus, stomach, urinary tract, kidney and pancreas
- COPD and asthma
- Pneumonia
- Atheromatous disease: Stroke, ischaemic heart disease, peripheral vascular disease, mesenteric ischaemia
- Peptic ulcers
Passive smoking is also associated with increased risk of lung cancer and heart disease as well as asthma, chest infection and otitis media in children.
What are the medical management options for smoking cessation?
- Nicotine replacement therapy (NRT)
- Multiple formulations are available including patches and oral preparations and can be used for up to 8 weeks.
- Works by reducing cravings caused by nicotine withdrawal.
- Should be started on the quit day.
- Should not be used with varenicline or bupropion and is contra-indicated in severe cardiovascular disease.
- Common side-effects include nausea, dizziness, vivid dreams and palpitations. - Bupropion
- Originally developed as an anti-depressant it has been shown to be effective in helping smoking cessation. It inhibits reuptake of dopamine, noradrenaline and serotonin in the brain.
- Taken as an oral medication and started 7-14 days before the quit date.
- Contraindicated in: Epilepsy (decreases seizure threshold), Eating disorders and bipolar disorder, CNS tumours, Those experiencing current benzodiazepine or alcohol withdrawal, Pregnancy and breast-feeding
- Important side-effects include seizures and severe hypersensitivity though these are rare. - Varenicline (Champix)
- Works as a partial nicotinic acetylcholine receptor agonist.
- Taken as an oral medication and started 7-14 days before the quit date and is titrated in dose.
- Contraindicated in pregnancy.
- Important side-effects include increase in suicidal thoughts/behaviours, nausea and abnormal dreams.
Using e-cigarettes (vaping) is not currently advocated as a first-line smoking cessation technique and though those who are still vaping can still be referred to smoking cessation services they cannot be prescribed medications.
Vaping could be considered for those who have failed to quit using conventional techniques in the past.
What are the types of urinary incontinence?
Urinary incontinence can be categorised into:
1. Stress incontinence
2. Urge incontinence
3. Overflow incontinence
4. Functional incontinence
5. Mixed incontinence
How is urinary incontinence investigated?
- Physical examination
An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles. - Questionnaires
These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment - Bladder diary
These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms. - Urinalysis
This will help to rule out infection as an acute cause - Cystometry
This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear. - Cystogram
If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.
What is stress incontinence?
This involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.
What are the risk factors, triggers and causes of stress incontinence?
- Risk factors
- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.
- Hysterectomy
Triggers
Acts such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.
Causes
Any abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.
How can stress incontinence be managed?
- Conservative management
- General lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.
- Pelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. - Medical management
- Duloxetine can help with stress incontinence, but it’s only recommended if conservative measures fail and the patient is not a surgical candidate. - Surgical management
- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn’t recommended by NICE. It would be worth trying if there was a clinical prolapse.
- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn’t as efficacious as other methods
- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.
- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It’s minimally invasive and can be performed in the outpatient setting.
What is urge incontinence?
This involves the sudden and involuntary loss of urine associated with urgency.
What are the risk factors for urge incontinence?
Risk factors for urgency include:
- Recurrent urinary tract infections
- High BMI
- Advancing age
- Smoking
- Caffeine
How is urge incontinence managed?
- Conservative management
- General lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.
- Pelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful. - Medical/surgical management
- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.
Examples include: Oxybutynin, Tolterodine, Fesoterodine, Solifenacin. If one agent has limited impact, it can be combined with another.
*Anticholinergics are contraindicated in glaucoma and are best avoided in frail/elderly patients so mirabegron (B3 agonists) are the medication of choice.
- Bladder instillation: Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.
- Sacral neuromodulation: Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.
What is functional incontinence?
This involves an individual having the urge to pass urine, but for whatever reason they’re unable to access the necessary facilities and as a result are incontinent.
What are the possible causes of functional incontinence?
Functional incontinence associated with:
- Sedating medications
- Alcohol
- Dementias
What is overflow incontinence?
This occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.
What are the causes of overflow incontinence?
This occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.
What is tonsillitis?
Tonsillitis is a medical condition that is characterized by the inflammation of the tonsils, which are the masses of lymphoid tissue located at the back of the throat. This inflammation is primarily due to an infection.
What is the aetiology of tonsillitis?
The aetiology of tonsillitis is usually due to a viral or bacterial infection.
Common viruses include the Epstein-Barr virus, influenza virus, adenovirus, and rhinovirus.
Bacterial tonsillitis can be caused by Group A streptococcus, which is also responsible for strep throat.
What are the signs and symptoms of tonsillitis?
Patients with tonsillitis typically present with the following symptoms:
- Sore throat
- Headache
- Fever (pyrexia)
- Enlarged and tender lymph nodes (lymphadenopathy)
What are the possible differential diagnoses for tonsillitis?
When diagnosing tonsillitis, it’s important to differentiate it from other conditions with similar symptoms such as:
- Pharyngitis: Symptoms include sore throat, fever, and headache. Unlike tonsillitis, patients do not usually present with lymphadenopathy.
- Mononucleosis: Characterized by fatigue, sore throat, fever, and swollen lymph nodes. A key difference is the presence of severe fatigue and splenomegaly.
