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GP Flashcards

1
Q

What causes acne vulgaris?

A

It is caused by chronic inflammation with or without infection

  • It results from increased production of Sebum that traps keratin and blocks the pilosebaceous unit.
  • Androgenic hormones increase the production of sebum
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2
Q

What bacteria causes acne?

A

Propionibacterium acnes. Excessive growth of this bacteria can exacerbate acne

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3
Q

What are the different lesions that can occur in acne?

A
  • Macules are flat marks on the skin
  • Papules are small lumps on the skin
  • Pustules are small lumps containing yellow pus
  • Come domes are skin coloured papules representing blocked pilosebaceous units
  • Blackheads are open comedones with black pigmentation in the centre
  • Ice pick scars are small indentations in the skin that remain after acne lesions heal
  • Hypertrophic scars are small lumps in the skin that remain after acne lesions heal
  • Rolling scars are irregular wave-like irregularities of the skin that remain after acne lesions heal
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4
Q

What are the topical treatments for acne?

A
  • Benzoyl peroxide reduces inflammation
  • Topical retinoids (vitamin A) which slows the reduction of sebum
  • Topical antibiotics : clindamycin
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5
Q

What are the oral treatments for acne?

A
  • Lymecycline
  • Oral contraceptive pill
  • Oral retinoids: Isotretinoin
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6
Q

What is the most effective oral contraceptive pill for acne?

A

Co-cyprindiol (dianette): carries a high risk of thromboembolism

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7
Q

What are the side effects of Isotretinoin (Roaccutane)?

A
  • Strongly teratogenic
  • Dry skin and lips
  • Photosensitivity
  • Depression
  • Stevens-Johnson syndrome (toxic epidermal necrolysis)
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8
Q

What is eczema?

A

A chronic atopic condition caused by defects of continuity of the skin barrier leading to inflammation in the skin.

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9
Q

What areas is eczema often found?

A
  • Flexor surfaces
  • Face and neck
  • Flare periods
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10
Q

Describe the pathophysiology of eczem?

A

Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response

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11
Q

What is the management of eczema?

A
  • Use of emollients which create a barrier
  • Soap substitutes
  • Avoid using hot water and soaps which remove natural oils
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12
Q

What environmental factors effect eczema?

A
  • Cold temperature
  • Dietary products
  • Washing and cleaning products
  • Stress
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13
Q

How would you treat an eczema flare?

A

-Use of thicker emollients
- Wet wraps
- Steroid creams

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14
Q
A
  • ## zinc impregnated bandages,topical tacrolimus,
  • phototherapy
  • systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine.
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15
Q

Steroid ladder for eczema?

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

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16
Q

What is the most common bacterial infection in eczema and how would you treat it?

A

S.aureus and treat with flucloxacillin

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17
Q

What is eczema herpeticum?

A

Eczema herpeticum is a viral skin infection in patients with eczema caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV).

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18
Q

How does eczema herpeticum present?

A

Someone with eczema that has a widespread painful, vesicular rash with systemic symptoms such as fever and lethargy

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19
Q

What is the treatment of eczema herpeticum?

A

Acyclovir

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20
Q

What is atrophic vaginitis?

A
  • It refers to dryness and atrophy of the vaginal mucosa related to a lack of oestrogen .
  • It occurs in women entering the menopause
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21
Q

What happens to the epithelial lining in atrophic vaginitis?

A
  • The mucosa become thinner and less elastic
  • This makes it more prone to inflammation and infection as there is a change in vaginal pH
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22
Q

What are the symptoms of AV?

A
  • Itching
  • Dryness
  • Pain during sex
  • Bleeding due to localised inflammation
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23
Q

What are the treatments for AV?

A
  • Vaginal lubricants
  • Topical oestrogen ( think estriol)
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24
Q

What are some presentations of AV in older patients?

A
  • Recurrent UTIs
  • Stress incontinence
  • Pelvic organ prolapse
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25
Q

What will an examination of the vagina show in AV?

A

Pale mucosa
Thin skin
Reduced skin folds
Erythema and inflammation
Dryness
Sparse pubic hair

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26
Q

What are the contraindications of topical oestrogen?

A
  • Systemic HRT
  • Breast cancer
  • Angina
  • Venous thromboembolism

Can also cause endometrial hyperplasia and cancer

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27
Q

What is bacterial vaginosis?

A
  • It refers to an overgrowth of bacteria in the vagina specifically anaerobic bacteria
  • It is not Sexually transmitted
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28
Q

What causes BV?

A

Loss of lactobacilli which produce lactic acid and keep the vaginal pH low

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29
Q

What bacteria can cause BV?

A

Gardnerella vaginalis (most common)
Mycoplasma hominis
Prevotella species

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30
Q

What are the risk factors for BV?

A
  • Multiple sexual partners
  • Excessive vaginal cleaning
  • Recent antibiotics
  • Smoking
  • Copper coil
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31
Q

What is the presentation of BV?

A

Fishy-smelling watery grey or white vaginal discharge. Half of women with BV are asymptomatic.

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32
Q

What are the investigations for BV?

A
  • ## Test vaginal pH anything above 4.5 is badcharcoal vaginal swab can be taken for microscopy. This can be a high vaginal swab taken during a speculum examination or a self-taken low vaginal swab.
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33
Q

What cells are shown with BV?

A

Clue cells

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34
Q

What is treatment for BV?

A

Metronidazole

Or clindamycin but is less effective

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35
Q

What can’t you take with metronidazole?

A

Alcohol

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36
Q

What are the complications of BV?

A

It increases risk of STI

  • Also can cause problems in pregnancy
    Miscarriage
    Preterm delivery
    Premature rupture of membranes
    Chorioamnionitis
    Low birth weight
    Postpartum endometritis
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37
Q

What is Bell’s palsy?

A

An idiopathic conditions which causes unilateral lower motor neuron facial nerve palsy

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38
Q

What is the treatment if a patient presents within 72 hours?

A

Prednisolone
50mg for 10 days
60mg for 5 days followed by a 5-day reducing regime of 10mg a day

They will also require lubricating eye drops to prevent it from drying out

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39
Q

What are the two types of breast abscesses?

A

Lactational abscess (associated with breastfeeding)
Non-lactational abscess (unrelated to breastfeeding)

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40
Q

What does mastitis refer to?

A

Inflammation of breast tissue often related to breastfeeding but can be caused by an infection

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41
Q

What is a key risk factor for infective mastitis?

A
  • Smoking
  • Damage to the nipple
  • Underlying breast disease affecting the drainage of the breast
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42
Q

What are the causes of mastitis?

A

Staphylococcus aureus (the most common)
Streptococcal species
Enterococcal species
Anaerobic bacteria (such as Bacteroides species and anaerobic streptococci)

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43
Q

What are the symptoms of mastitis?

A
  • Nipple changes
  • Purulent nipple discharge (pus from the nipple)
  • Localised pain
  • Tenderness
  • Warmth
  • Erythema (redness)
  • Hardening of the skin or breast tissue
    Swelling
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44
Q

What is the key feature of a breast abscess?

A
  • Swollen fluctuant (can move around on palpation) tender lump within the breast
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45
Q

What is the management of non-lactational mastitis?

A
  • Analgesia
  • Antibiotics - need to be broad spectrum
  • Treatment for underlying cause
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46
Q

What are the antibiotics used to treat non-lactational mastitis?

A

Co-amoxiclav
Erythromycin/clarithromycin (macrolides) plus metronidazole (to cover anaerobes)

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47
Q

What is the treatment for Lactational mastitis?

A

Managed conservatively, with continued breastfeeding, expressing milk and breast massage.

Heat packs, warm showers and simple analgesia can help symptoms.

Antibiotics (flucloxacillin or erythromycin/clarithromycin where there is penicillin allergy) are required where infection is suspected or symptoms do not improve

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48
Q

What is Candidiasis?

A

Commonly referred to as thrush. It refers to a yeast infection most commonly candida albicans

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49
Q

What are the risk factors for thrush?

A
  • Increased oestrogen: pregnancy
  • Poorly controlled diabetes
  • Immunosuppression
  • Broad spectrum antibiotics
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50
Q

What are the symptoms of thrush?

A
  • Thick, white discharge that does not typically smell
  • Vulva and vaginal itching, irritation or discomfort
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51
Q

What can a severe thrush infection lead to?

A

Erythema
Fissures
Oedema
Pain during sex (dyspareunia)
Dysuria
Excoriation

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52
Q

What are the investigations for thrush?

A
  • Testing vaginal pH often it is below 4.5 in thrush but will be higher with vaginosis
  • Charcoal swab is gold standard
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53
Q

What is the treatment for thrush?

A
  • A single dose of intravaginal clotrimazole cream
  • A single clotrimazole pessary
  • A single dose of fluconazole
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54
Q

What is conjunctivitis?

A
  • Inflammation of the conjunctiva which is the tissue that covers the inside of the eyelids and the sclera
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55
Q

What are the 3 causes of Conjunctivitis?

A
  • Bacterial
  • Allergic
  • Viral
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56
Q

What are the symptoms of Conjunctivitis?

A
  • Red, bloodshot eye
  • Itchy or gritty sensation
  • Discharge

It does not cause pain, photophobia or reduced visual activity

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57
Q

What are the differences between viral and bacterial Conjunctivitis?

A
  • Bacterial often presents with a purulent discharge and worse in the morning also it is highly contagious
  • Viral conjunctivitis is common and usually presents with a clear discharge. It is often associated with other symptoms of a viral infection, such as a dry cough, sore throat and blocked nose
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58
Q

What are the causes of a painful red eye?

A

Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Corneal abrasions or ulceration
Keratitis
Foreign body
Traumatic or chemical injury

These tend to be more serious and require urgent intervention

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59
Q

How do you treat Conjunctivitis ?

A
  • It usually resolves in 1-2 weeks with no need for treatment
  • Chloramphenicol or fusidic acid eye drops are options for bacterial conjunctivitis if necessary.
  • Neonates under one month with conjunctivitis need urgent ophthalmology assessment. Neonatal conjunctivitis may be caused by gonococcal infection
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60
Q

What is Allergic Conjunctivitis?

A

It causes swelling of the conjunctival sac and eyelid with itching and a watery discharge.

Antihistamines (oral or topical) can help symptoms.

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61
Q

What is croup?

A
  • An acute infective respiratory disease affecting young children
  • It typically affects children aged 6months to 2 years
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62
Q

What is dangerous about croup?

A

It causes oedema in the larynx

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63
Q

What is the most common cause of croup?

A

Parainfluenza

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64
Q

What are some other causes of croup?

A

Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

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65
Q

What used to cause croup?

A

It used to be caused by diphtheria. It leads to epiglottitis and has a high mortality.

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66
Q

What are the symptoms of croup?

A
  • Increased work of breathing
  • “Barking” cough, occurring in clusters of coughing episodes
  • Hoarse voice
  • Stridor
  • Low grade fever
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67
Q

What is the treatment of croup?

A

Mainly can be conservative but dexamethasone is effective if needed

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68
Q

What is the stepwise management of croup?

A

Oral dexamethasone
Oxygen
Nebulised budesonide
Nebulised adrenalin
Intubation and ventilation

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69
Q

What is impetigio?

A

A superficial bacterial skin infection usually caused by S.aureus

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70
Q

What is the characteristic feature of a S.aureus skin infection?

A

A golden crust

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71
Q

What else can cause impetigio?

A

S.pyogenes

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72
Q

What are the two types of impetigo?

A
  • Bullous
  • Non-bullous
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73
Q

What is non bullous impetigo?

A

occurs around the nose or mouth. The exudate from the lesions dries to form a “golden crust”. They are often unsightly but do not usually cause systemic symptom

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74
Q

What is the treatment for non-bullous impetigo?

A
  • Topical fusidic acid can be used to treat localised non-bullous impetigo
  • antiseptic cream (hydrogen peroxide 1% cream) first line rather than antibiotics for localised non-bullous impetigo.
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75
Q

What is bullous impetigo?

A
  • Always caused by S.aureus
  • They produce epidermolysis toxins that break down proteins that hold skin cells together
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76
Q

Which group does bullous impetigo typically affect?

A

Neonates and children under 2

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77
Q

What can happen if the lesions are widespread and severe in bullous impetgio?

A

Can cause severe infection called staphylococcus scalded skin syndrome

  • Treat with flucloxacillin
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78
Q

What are the complications of impetigo?

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

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79
Q

What is infectious mononucleosis (glandular fever)?

A
  • A condition caused by infection with the EBV.
  • Commonly known as the kissing disease or Mono
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80
Q

How can glandular fever spread?

A
  • It is found in the saliva of infected individuals and is spread by kissing, or sharing cups and toothbrushes
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81
Q

When does an infection with EBV become classified as infectious mononucleosis?

A
  • When symptoms present
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82
Q

What are the symptoms of infectious mononucleosis?

A
  • Fever
  • Sore throat
  • Fatigue
  • Lymphadenopathy
  • Tonsillar enlargement
  • Splenomegaly (can cause splenic rupture)
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83
Q

What happens if you treat a patient with infectious mononucleosis using amoxicillin?

A
  • A intensely itchy maculopapular rash will appear
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84
Q

What antibodies can be tested for to see if a patient has had infectious mononucleosis?

A

Heterophile antibodies

  • Monospot test: this introduces the patient’s blood to red blood cells from horses. Heterophile antibodies (if present) will react to the horse red blood cells and give a positive result.
  • Paul-Bunnell test: this is similar to the monospot test but uses red blood cells from sheep.
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85
Q

What is the management for infectious mononucleosis?

A
  • Is usually self-limiting and lasts 2-3 weeks but can cause fatigue for several months
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86
Q

What is the advice given to patients with infectious mononucleosis?

A
  • Avoid alcohol as EBV impacts the livers ability to process it
  • Avoid contact sports due to risk of splenic rupture
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87
Q

What are the complications of infectious mononucleosis?

A

Splenic rupture
Glomerulonephritis
Haemolytic anaemia
Thrombocytopenia
Chronic fatigue

EBV infection is associated with certain cancers, notable Burkitt’s lymphoma.

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88
Q

What bacteria causes Lyme disease?

A

B burgdorferi

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89
Q

What are the symptoms of Lyme disease?

A
  • Tick bite with rash called erythema migrans
  • Fever
  • Headache
  • Myalgias
  • Stiff neck
  • Facial palsy
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90
Q

What is the treatment for Lyme disease?

A

Doxycycline, unless there is just a rash that can’t be distinguished from cellulitis then use amoxicillin

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91
Q

What are the complications of Lyme disease?

A
  • Acute neurological complications
  • Cardiac complications such as AV block and myocarditis
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92
Q

What is menopause?

A
  • A retrospective diagnosis made after a woman has had no periods for 12 months
  • It is defined as a permanent end to menstruation
  • Menopause is the point at which menstruation stops
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93
Q

What is perimenopause, postmenopausal and premature menopause?

A
  • Perimenopause refers to the time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods.
  • Postmenopausal describes the period from 12 months after the final menstrual period onwards.
  • Premature menopause is menopause before the age of 40 years. It is the result of premature ovarian insufficiency.
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94
Q

What causes menopause?

A
  • It is caused by a lack of ovarian follicular function, resulting in changes in the sex hormones associated with the menstrual cycle
  • Oestrogen and progesterone levels are low
  • LH and FSH levels are high in response to an absence of negative feedback from oestrogen
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95
Q

Describe how oestrogen is released during the menstrual cycle ?

A
  • In the ovaries the process of primordial follicles maturing is into primary and secondary follicles is always occurring
  • At the start of the menstrual cycle FSH stimulates the further development of secondary follicles
  • As the follicles grow the granulosa cells that surround them secrete increasing amounts of oestrogen
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96
Q

How does the menopause begin?

A
  • The menopause begins with a decline in the development of ovarian follicles
  • Without the growth and development of the follicles there is reduced production of oestrogen
  • This results in increasing levels of LH and FSH as oestrogen has a negative feedback on these hormones in the pituitary gland
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97
Q

How is the menstrual cycle affected in the menopause?

A
  • Falling follicular development means ovulation does not occur (anovulation)
  • Without oestrogen the endometrium does not develop leading to a lack of menstruation (Amenorrhoea)
  • The low levels of oestrogen lead to the perimenopausal symptoms
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98
Q

What are the perimenopausal symptoms?

A
  • Hot flushes
  • Emotional lability or low mood
  • Premenstrual syndrome
  • Irregular periods
  • Joint pains
  • Heavier or lighter periods
  • Vaginal dryness and atrophy
  • Reduced libido
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99
Q

What does a lack of oestrogen increase the risks of?

A
  • CVD
  • Osteoporosis
  • Pelvic organ collapse
  • Urinary incontinence
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100
Q

How can menopause be diagnosed?

A
  • Symptoms without blood test
  • Use FSH blood test in women under 40 or aged 40-45 with menopausal symptoms
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101
Q

How long do women need to use contraception for after the menopause?

A
  • Two years after the last menstrual period in women under 50
  • One year after the last menstrual period in women over 50
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102
Q

What is the management of perimenopausal symptoms?

A

Hormone replacement therapy (HRT)

Tibolone, a synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)

Clonidine, which act as agonists of alpha-adrenergic and imidazoline receptors

Testosterone can be used to treat reduced libido (usually as a gel or cream)

Vaginal oestrogen cream or tablets, to help with vaginal dryness and atrophy (can be used alongside systemic HRT)

Vaginal moisturisers, such as Sylk, Replens and YES

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103
Q
A
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104
Q

What is anaemia?

A

When there is a decrease in haemoglobin.

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105
Q

What two things cause low haemoglobin levels?

A

Reduction in cell mass
Increased plasma volume

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106
Q

What element is key for making Hb?

A

Iron

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107
Q

What is the normal mean cell volume?

A

80-100 femtolitres

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108
Q

What are the 3 main subtypes of anaemia?

A

Microcytic- low MCV indicating small sized RBC
Normocytic- normal MCV indicating normal sized RBC
Macrocytic- high MCV indicating large sized RBC

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109
Q

What are the 5 causes of microcytic anaemia?

A

T- Thalassaemia
A- Anaemia of chronic disease
I- Iron deficiency
L- Lead poisoning
S- Sideroblastic anaemia

TAILS

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110
Q

What are 5 causes of normocytic anaemia?

A

A- anaemia of chronic disease
A- Acute blood loss
A- Aplastic
H- haemolytic
H- Hypothyroidism

3 As and 2 Hs

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111
Q

What are the two subtypes of macrocytic anaemia?

A

Megaloblastic
Normoblastic

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112
Q

What is megaloblastic anaemia and what causes it?

A

Problem in DNA synthesis caused by vitamin deficiency

Folate
B12

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113
Q

What causes normoblastic anaemia?

A

Alcohol
Hypothyroidism
Liver disease
Drugs such as azathioprine

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114
Q

What are the generic signs of anaemia?

A

Pale skin
Conjunctivital pallor
Tachycardia
Raised respiratory rate

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115
Q

How common is iron deficiency anaemia?

A

Most common cause in the world

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116
Q

What can cause iron deficiency anaemia?

A

Vegetarian diet
H. pylori infection
Pregnancy and breastfeeding
IBS
Coeliac
PPI’s
Increased iron loss through bleeding (this is the principal cause if Fe deficiency)

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117
Q

Why does iron loss cause microcytic anaemia?

A

Iron is needed for the formation of haemoglobin and when there is a lack of iron not enough haemoglobin is made to make normal sized RBC’s.

Therefore smaller RBC’s are produced by the bone marrow which can’t carry enough oxygen to meet the bodies demand hence hypoxia

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118
Q

Where is Iron mainly absorbed in the body?

A

Duodenum and jejunum

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119
Q

Why are women more prone than men to iron deficiency?

A

Women lose about 2mg daily when menstruating where as men will only on average lose 1mg a day

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120
Q

How can pregnancy cause anaemia?

A

Pregnancy results in net loss of 580mg of iron, due to expansion of RBC mass and growth of the foetus and placenta. Most occurs in the third trimester

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121
Q

Why does H.Pylori cause iron deficiency?

A

It traps Fe itself in the stomach preventing it from reaching the duodenum

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122
Q

How do PPI’s cause iron deficiency?

A

Iron requires acid from the stomach to stay in it’s soluble form fe2+ where as without acid it becomes insoluble Fe3+. Therefore PPI’s as they reduce amount of stomach acid can lead to Fe deficiency

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123
Q

Why can hair and nails be affected by Iron deficiency?

A

As iron is required for enzymes in the mitochondria, and as hair and nails are fast growing they are most affected by this deficit

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124
Q

What are the signs of Iron deficiency?

A
  • Conjunctivital pallor
  • Koilonychia (spoon shaped nails)
  • Angular stomatitis (redness around mouth)
  • Glossitis
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125
Q

What are the symptoms of iron deficiency?

A
  • Fatigue
    -Dyspnoea on exertion
  • Dizziness
  • Headache
  • Nausea
  • bowel disturbance
  • Hair loss
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126
Q

What investigations would you perform for a patient with suspected iron deficiency?

A

FBC- would have low Hb, low MCV
- Iron studies would measure the: serum iron, serum ferritin and total iron binding capacity

If ferritin in the blood is low it is highly suggestive of iron deficiency. If ferritin is high then this is difficult to interpret and is likely to be related to inflammation rather than iron overload. A patient with a normal ferritin can still have iron deficiency anaemia, particularly if they have reasons to have a raised ferritin such as infection.

transferrin levels increase in iron deficiency and decrease in iron overload.

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127
Q

How would you treat iron deficiency?

A
  • Treat underlying cause
  • Oral iron supplements ferrous sulphate/fumarate
  • Iron infusion e.g., cosmofer
  • Blood transfusion in severe cases
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128
Q

What are the complications associated with iron deficiency?

A
  • Cognitive impairment
  • Impaired muscular performance
  • Preterm delivery
  • High output heart failure
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129
Q

What are the investigations for anaemia?

A
  • New born screening with heel prick happens at day 5
  • FBC:normocytic anaemia with reticulocytotic
  • Blood film:sickled RBCs, target cells, Howell-Jolly bodies (RBC nuclear remnants seen later in the disease due to hyposplenism)
  • Hb electrophoresis and solubility: diagnosticinvestigation, demonstrating**increased HbS (2 alpha chains and 2 abnormal beta chains) and reduced/absent HbA (α2β2)
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130
Q

What is aplastic anaemia?

A

A stem cell disorder. It is characterised by anaemia, leukopenia and thrombocytopenia

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131
Q

What causes aplastic anaemia?

A
  • Idiopathic
  • radiation and toxins
  • Drugs
  • Infections HIV
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132
Q

What is B12 deficiency anaemia?

A

Anaemia caused by B12 deficiency it is a macrocytic megaloblastic anaemia

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133
Q

What causes B12 deficiency?

A
  • Inadequate intake (vegans and vegetarians as it is found in animal products)
  • Inadequate secretion of intrinsic factor
  • Malabsorption (crohn’s, patients who have had a gastric bypass)
  • Inadequate release of B12 from food (alcohol abuse and gastritis)
  • Can also be caused by pernicious anaemia which is where there is autoimmune destruction of the gastric epithelium
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134
Q

What are the signs of B12 deficiency?

A
  • Pallor
  • Signs of neurological defect
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135
Q

What are the symptoms of B12 deficiency?

A
  • SOB
  • Palpitations
  • Headaches
  • Fatigue
  • Glossitis
  • CNS involvement - Personality change
  • Depression
  • Memory loss
  • Visual disturbances
  • Numbness, weakness and paraesthesia affecting the lower extremities
  • Ataxia
  • Loss of vibration sense or proprioception
  • Autonomic dysfunction (e.g. bladder/bowel dysfunction)
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136
Q

How long does folate deficiency take to occur compared to B12?

A

folate= a few months
B12= A few years

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137
Q

What can cause folate deficiency?

A
  • Inadequate intake
  • Malabsorption
  • Increased requirement (malignancy and pregnancy)
  • Increased loss (chronic liver disease)
  • Alcohol abuse
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138
Q

What are the symptoms if folate deficiency?

A
  • Fatigue
  • Dyspnoea
  • Palpitations
  • Headache
  • Glossitis
  • Features of pancytopenia e.g. excessive bleeding and bruising due to thrombocytopenia, recurrent infections due to leukopenia
  • Symptoms of underlying cause e.g.
    • Coeliac disease: diarrhoea, bloating, dyspepsia and abdominal discomfort.
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139
Q

What is Anaemia of chronic disease?

A
  • A chronic disease due to chronic inflammation process from underlying infection, malignancy or systemic disease
  • Normally normocytic but can be microcytic
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140
Q

What two processes are the main cause of ACD?

A
  • Decreased lifespan as a result direct cellular destruction via toxins from cancers, viruses and bacteria
  • Decreased production of RBC- inflammation inhibits iron metabolism and cytokines inhibit erythropoietin production in the kidney
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141
Q

What is the treatment for ACD?

A
  • Treatment of underlying cause
  • EPO injections
  • Parenteral iron
  • Transfusions
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142
Q
A
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143
Q

What is an atrial flutter?

A

is a macro re-entrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm.

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144
Q

What can cause an atrial flutter?

A

Results from either structural or conduction abnormalities.

Structural= atrial dilation, incisional scars and fibrosis of the atrium.
Can also occur as a result of taking drugs for atrial fibrillation

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145
Q

What are the key presentations of an atrial flutter?

A

Presence of the risk factors and worsening heart failure or pulmonary symptoms. Leads to a atrial HR of 300.

2:1 (most common)= 150 heart rate in ventricles

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146
Q

What will an ECG show of a patient with an atrial flutter?

A

Sawtooth P waves with fast heart rate

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147
Q

What are symptoms of an atrial flutter?

A

Palpitations and fatigue, racing pulse

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148
Q

How would you manage an atrial flutter?

A

If haemodynamically unstable then cardiovert either electrically or chemically
Use beta-blockers and CCB’s if not. Treat underlying cause

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149
Q

What are complications associated with atrial flutter?

A

Acute stroke, myocardial ischaemia, then lots of medication related.

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150
Q

What is AF?

A

Atrial fibrillation (AF) is a common tachycardia. It can be caused by many other underlying illness, especially in the acutely unwell patient (such as sepsis, pneumonia, hyperthyroidism or other illness). It may be reversible by treating the underlying cause.
Is also very common idiopathic

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151
Q

What are the different types of AF?

A

Paroxysmal: episodes last >30 seconds but <7 days and are self-terminating but recurrent
* Persistent: episodes last less than or more than seven days but require electrical or chemical cardioversion
* Permanent: episodes fail to terminate with cardioversion OR a terminated episode that relapses within 24 hours OR long-standing AF (usually >1 year) in which cardioversion has not been indicated or attempted

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152
Q

What are the key presentations of AF?

A

Irregularly irregular pulse
Palpitations
Chest pain
Dyspnoea
Dizziness / syncope (particularly in paroxysmal)
ECG

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153
Q

What would an AF ECG look like?

A

No p wave
Fluttering baseline

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154
Q

What are the two principles for managing AF?

A

Two principles for treating AF:
Rate or rhythm control
Anticoagulation to prevent stroke

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155
Q

What are some rate control medications for AF?

A

Beta blocker bisoprolol , CCB amlodipine

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156
Q

How would you do rhythm control of AF?

A

Rhythm control can be achieved by either electrical or chemical cardioversion
Chemical cardioversion=
Flecainide
Amiodarone

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157
Q

What would be the long term treatment for AF?

A

Left atrial ablation

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158
Q

How would you determine anti-coagulant control?

A

Use CHAD-VASc score to determine anti-coagulant.

Used to be more warfarin now DOAC more commonly used e.g., apixaban/rivaroxaban

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159
Q

Complications of AF?

A

Acute stroke (most common) due to blood pooling and coagulating in the atrium
MI
Congestive heart failure
Amiodarone related pulmonary toxicity/thyroid dysfunction
Hypotension

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160
Q

What are the 2 shockable rhythms for a cardiac arrest?

A

Ventricular tachycardia
Ventricular fibrillation

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161
Q

What are the two non-shockable rhythms?

A

Asystole- when there is no electrical activity
Pulseless electrical activity

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162
Q

What are the different types of supraventricular tachycardia?

A

A sinus tachycardia

Focal atrial tachycardia

Atrioventricular re-entry tachycardia

AV nodal re-entry tachycardia

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163
Q

What is focal atria tachycardia?

A

A group of cells in the atria act as the pacemaker going quicker than the SAN node often seen in patients with chronic lung disease. Normal P wave

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164
Q

What is atrioventricular re-entry tachycardia (AVRT)?

A

Atrioventricular re-entry tachycardia- when there is an accessory pathway

ANTEGRADE (atria to ventricles) which is shown as pre-excitation on the resting ECG (the mythical DELTA wave) Wolf-Parkinson-White syndrome
RETROGRADE (ventricle to atria) which is not seen on a resting ECG

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165
Q

What is a AV nodal re-entry tachycardia (AVNRT)?

A

This is where re-entry circuits form within the AV node, or anatomically adjacent similar tissue.

Most common type and more common in women. Can be caused by drugs and lifestyle. Usually sudden onset and can cause shortness of breath.

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166
Q

How would you manage a haemodynamically unstable patient with a supraventricular tachycardia?

A

Cardiovert them either chemically or electrically

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167
Q

How would you manage a haemodynamically stable patient with a supraventricular tachycardia?

A

use vagal manoeuvres if that doesn’t work then can use adenosine which interrupts the AV node

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168
Q

Do supraventricular tachycardias have wide or narrow QRS complexes?

A

Narrow unless present with bundle branch block

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169
Q

What are the wide-complex QRS tachycardias?

A

Ventricular tachycardia,
Ventricular fibrillation
Torsades de pointes

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170
Q

What is ventricular tachycardia?

A

Usually observed in the setting of ischaemic heart disease. IHD and CAD are the most common. Things such as Chagas disease can also cause.

Other forms of structural heart disease, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and anomalous coronary arteries are also associated with ventricular arrhythmias.

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171
Q

What causes ventricular tachycardia?

A

Areas previously scarred are the substrate for re-entry causing rapid ventricular depolarisation

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172
Q

What are the symptoms of VF?

A

Hypotension and syncope. Along with racing pulse and dyspnoea

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173
Q

How would you treat a patient with VF?

A

Treatment if they are haemodynamically unstable with a pulse- do a cardioversion and look for underlying cause try and solve.

Consider using antiarrhythmic medication amiodarone

If stable then use adenosine/amiodarone then cardiovert if not successful

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174
Q

What is Torsades de pointes?

A

Looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline.

The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

175
Q

What causes Torsades de Pointes?

A

A prolonged QT interval means that there is a longer peroid before ventriuclar repolarisation

176
Q

What causes prolonged QT?

A

Long QT syndrome (inherited)
Medications (antipsychotics, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte disturbances- hypokalaemia, hypomagnesaemia, hypocalcaemia)

177
Q

How would you treat Torsades de Pointes?

A

Correct the disturbance
Magnesium sulphate
cardioversion if the problem does not resolve

178
Q

What is asthma?

A
  • A chronic inflammatory airway disease characterised by intermittent airway obstruction and hyperreactivity
179
Q

What are some risk factors for developing asthma?

A
  • History of atopy (allergies)
  • Viral URTI
  • Occupational exposure
180
Q

What are the signs and symptoms of asthma?

A
  • Episodic
  • Diurnal variability- worse at night and in the morning
  • Dry cough with wheeze and shortness of breath
  • Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
  • Family history of other ectopic disease such as eczema and hayfever
181
Q

What are the primary investigations for asthma?

A
  • Fractional exhaled nitric oxide a value of >40 ppb is positive
  • Spirometry will show a FVC/FEV1 ratio of less than 70% but will improve by 12% and increase by >200ml when using a bronchodilator
182
Q

What tests would you perform if you were unsure of a diagnosis of asthma?

A
  • PEFR: measured multiple times a day over a 2-4 week period. Variability of >20% throughout the day is diagnostic
  • Airway hyperreactivity testing: a histamine or methacholine direct bronchial challenge
183
Q

What are Short acting beta 2 adrenergic receptor agonists?

A

They work quickly but the effect only lasts for an hour or 2. Nor Adrenalin acts on smooth muscle of airways to cause relaxation.

Reliver or rescue medication salbutamol

184
Q

What are Long-acting beta 2 agonists (LABA)?

A

Same as short acting but last for longer salmeterol

185
Q

What are Long-acting muscarinic antagonists (LAMA)?

A

They block acetylcholine receptors =stimulated by the parasympathetic nervous system which cause bronchoconstriction.

tiotropium is an example

186
Q

What are Inhaled corticosteroids (ICS)?

A

They reduce inflammation and reactivity of the airways. They are used for maintenance and prevention.

Beclomethasone

187
Q

What are Leukotriene receptor antagonists?

A

Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion.

Montelukast

188
Q

What is the BTS/SIGN stepwise ladder for treatment of asthma?

A
  1. SABA as required for wheezy episodes
  2. Regular low dose ICS inhaler
  3. Add LABA e.g. salmeterol
  4. Consider LTRA e.g. Montelukast or oral beta 2 agonist, oral theophylline or an inhaled LAMA (i.e. tiotropium).
  5. Titrate up ICS
  6. Add oral steroids at lowest possible dose
189
Q

What is the NICE Guidelines (adapted from 2017 guidelines) for asthma

A
  1. SABA as required or wheezy episodes
  2. Regular lose dose ICS inhaler
  3. Add LTRA e.g. Montelukast
  4. Add LABA
  5. Consider MART
  6. Increase steroid dose
190
Q

What are the triggers for an asthma attack?

A
  • Allergy exposure
  • Viral infection
  • Smoking exposure
  • Pollution
  • Exercise
191
Q

What is investigated in an asthma attack?

A
  • PEFR
  • ABG: patients will initially have respiratory alkalosis. Abnormal or high PCO2 is concerning as it implies the patient is tiring
192
Q

What would be considered an moderate asthma attack?

A
  • PEFR 50-75% of predicted
193
Q

What would be considered a severe asthma attack?

A
  • PEFR 33-50%
  • Resp rate >25
  • Heart rate above 110
  • unable to complete sentences
194
Q

What would be considered a life threatening asthma attack?

A
  • PEFR <33%
  • Sats <92%
  • Becoming tired
  • No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
  • Haemodynamic instability (i.e. shock)
195
Q

What is the treatment for a moderate asthma attack?

A
  • Nebulised salbutamol
  • Nebulised ipratropium bromide
  • Steroids oral continue for 5 days after
196
Q

What is the treatment for a severe asthma attack?

A
  • Oxygen is required to maintain stats
  • Aminophylline infusion
  • Consider IV salbutamol
197
Q

What is the treatment for a life threatening asthma attack?

A
  • IV magnesium sulphate
  • Admission to ICU
  • Intubation in worst cases
198
Q

What is benign prostate hyperplasia?

A

Increase in the size of the prostate without malignancy. This causes bladder outlet obstruction and lower urinary tract symptoms.

199
Q

What are the risk factors for BPH?

A
  • Increasing age
  • Family history
  • Ethnicity more common in black people
  • Diabetes
  • Obesity due to increasing circulation of oestrogen
200
Q

What causes BPH?

A
  • Basal and luminal cells rely on stimulation from androgens for survival. Such as testosterone (produced by testicles) and dihydrotestosterone (produced by prostate). DHT is produced by 5α-reductase which converts testosterone into the more potent dihydrotestosterone.
  • As age increases levels of testosterone drop but levels of DHT increase as there is an increase in 5a-reductase activity
  • This will form hyperplastic nodules to form
201
Q

What are the signs of BPH?

A
  • Digital rectal exam will find smooth, enlarged and non-tender prostate
  • Lower abdominal tenderness and palpable bladder:
    Indicates acute urinary retention
    Perform bladder scan
    Requires urgent catheterisation
202
Q

What are the symptoms of BPH?

A
  • Voiding: weak stream and incomplete emptying
  • Storage: urgency and incontinence
  • Oliguria: if complete obstruction
  • Lower abdominal pain and inability to urinate
    Indicates acute urinary retention
203
Q

What are the investigations for BPH?

A
  • Prostate-specific antigen (PSA): predicts prostate volume, may suggest cancer if significantly raised but BPH can also raise it
  • International Prostate Symptom Score (I-PSS):a 7-symptom questionnaire with an additionalbother scoreto predict progression and outcome
204
Q

What are the non-surgical treatments for BPH that has bothersome symptoms?

A
  • α-1 antagonists: Tamsulosin it is considered first-line. It inhibits the action of noradrenaline and relaxes the smooth muscle. Can cause Postural hypotension, dizziness, dry mouth and depression
  • 5-α reductase inhibitors e.g. finasteride. This will work to reduce the prostate size but can take up to 6 months to work. Can cause: reduced libido, erectile dysfunction, adn gynaecomastia
205
Q

What are the the surgical options for BPH and when would they be used?

A

Prostate<30g
- Transurethral incision of the prostate (TUIP): one or two cuts in the small grooves of the bladder neck to open the urinary channel and allow urine to pass through more easily.

Prostate 30-80g
Transurethral resection of the prostate (TURP): accessing the prostate through the urethra and “shaving” off prostate tissue from inside using diathermy (heat)

Prostate >80g
Transurethral electrovaporisation of the prostate (TUVP): prostate tissue is removed using a laser
Open prostatectomy via abdominal or perineal incision

206
Q

What is TURP syndrome?

A

life-threatening triad of fluid overload, dilutional hyponatraemia and neurotoxicity due to systemic absorption of irrigation fluids during TURP procedure

207
Q

What are the most common causes of CKD?

A
  • Hypertension (second most common)
  • Diabetes (most common)
208
Q

What are the signs of CKD?

A
  • Hypertension
  • Fluid overload
  • Uraemic sallow: yellow or pale brown colour of skin
  • Uraemic frost: urea crystals can deposit in the skin
  • Pallor
  • Evidence of underlying cause
209
Q

What are the symptoms of CKD?

A
  • Pruritis
  • Loss of appetite
  • Nausea
  • Oedema
  • Muscle cramps
210
Q

What are the investigations for CKD?

A
  • Estimated GFR: can be checked using U&E blood test. Two tests required 3 months apart
  • Proteinuria: can be checked using a urine albumin:creatinine ratio. A result of greater than 3mg/mmol is significant
  • Haematuria: can be checked using a urine dipstick
  • Renal ultrasound
211
Q

What can be used to stage CKD?

A

G score and A score

212
Q

What is the G score?

A

G score is based of eGFR

G1: eGFR>90
G2: eGFR: 60-89
G3a: eGFR: 45-59
G3b: eGFR: 30-44
G4: eGFR: 15-29
G5: eGFR<15 known as end-stage renal failure

213
Q

What is the A score?

A

Based off the albumin:creatinine ratio:

A1: <3
A2: 3-30
A3: >30

214
Q

What score would indicate a paitient does not have CKD?

A

A1 combined with G1 or G2

215
Q

What is the management for CKD?

A

Slowing the progression of the disease

Optimise diabetic control
Optimise hypertensive control
Treat glomerulonephritis

Reducing the risk of complications
Exercise, maintain a healthy weight and stop smoking
Special dietary advice about phosphate, sodium, potassium and water intake
Offer atorvastatin 20mg for primary prevention of cardiovascular disease

216
Q

What are the complications of CKD?

A
  • Renal bone disease
  • Anaemia
  • Cardiovascular- hypertension, hypercholesterolemia , heart failure due to fluid overload and anaemia
217
Q

What is COPD?

A

Describes progressive and irreversible obstructive airway disease. It is a combination of emphysema and chronic bronchitis

218
Q

What are the risk factors for developing COPD?

A
  • Tobacco smoking (biggest risk factor)
  • Air pollution
  • A1AD
  • Occupational exposure such as dust, coal, cotton, cement and grain
219
Q

What are the two things that make up COPD?

A

Emphysema and bronchitis

220
Q

What are some signs of emphysema?

A
  • Barrel shaped chest due to air trapping and hyperinflation
  • Downward displacement of liver due to hyperexpansion of the lungs
221
Q

What is bronchitis?

A

Inflammation of the bronchial tubes of the lungs. It is said to be chronic when it causes a productive cough for at least 3 months every year for 2 or more years

222
Q

What are the signs of COPD?

A
  • Tachypnoea
  • Barrel chest
  • Cyanosis
  • Quiet breath sounds and wheeze
223
Q

What are the symptoms of COPD

A
  • Dyspnoea
  • Productive cough
  • Wheeze
  • Chest tightness
  • Weight loss
224
Q

What are signs of CO2 retention?

A
  • Drowsy
  • Asterixis (flapping tremor of hands)
  • Confusion
225
Q

What is the usual drive for respiration and how does this change in how does this change in COPD?

A

The usual drive for respiration is CO2 however body becomes desensitised to high CO2.
- Hypoxaemia becomes the new drive for respiration.

226
Q

What is the MRC dyspnoea scale?

A

5 point scale for assessing impact of breathlessness.

Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

227
Q

How would you make a diagnosis of COPD?

A
  • Clinical presentation plus spirometry
228
Q

What would spirometry show for COPD?

A

FEV1/FVC ratio less than 0.7

Important to note that it does not show a dramatic response to reversibility testing with salbutamol (beta-2 agonist). If it does then consider asthma as a differential

229
Q

What is used to classify the severity of airway obstruction?

A

GOLD classification
Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

230
Q

What is the initial management for COPD?

A

STOP SMOKING

  • Annual flu vaccine and the pneumococcal vaccine (this is a one off vaccine)
231
Q

What are the different bronchodilators used to treat COPD?

A
  • SABA:short-acting beta-agonist (e.g. salbutamol)
  • SAMA: short-acting muscarinic antagonist (ipratropium)
  • LABA: long-acting beta-agonist (e.g. salmeterol)
  • LAMA: long-acting muscarinic antagonist (e.g. tiotropium)
232
Q

What causes an exacerbation of COPD?

A
  • Usually triggered by viral or bacterial infection
  • Can be heart failure, pulmonary embolism or medications
233
Q

Why do you have to be careful giving oxygen to someone with COPD and how would you manage this?

A
  • Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive.
  • Venturi masks are designed to deliver specific percentage concentrations of oxygen
  • If retaining CO2 aim for oxygen saturations of 88-92% titrated by Venturi mask
  • If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%
234
Q

Define type 1 diabetes

A

Type 1 diabetes mellitus is a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency.

235
Q

What happens as a result of low insulin levels?

A

Due to insulin deficiency glucose can’t be utilised from muscle and adipose.

Stimulates secretion of glucagon (adrenaline, cortisol, and growth hormone)

So increased Lipolysis, = weight loss

More glucose in urine - Polyuria and Polydipsia

236
Q

What are the most common key presentations of type 1 diabetes?

A
  • Hyperglycaemia (above 11.1).
  • Polyuria (passing urine frequently).
  • Polydipsia (drinking water frequently)
  • Tiredness
237
Q

What are some other common key presentations of type 1 diabetes?

A

young age, weight loss, blurred vision, nausea, and vomiting, Abdo pain,

238
Q

What are the first line investigations for children in type 1 diabetes?

A
  • Random plasma glucose (above 11)
  • Fasting plasma glucose (above 7)
239
Q

What is the gold standard test for diagnosing type 1 diabetes in children?

A

Glycohemoglobin test (HbA1c)

Reflects the degree of hyperglycaemia over the preceding 3 months greater than 6.5% (48 mmol/mol) indicates diabetes

240
Q

What is the management of type 1 diabetes?

A

o Basal-bolus insulin (insulin glargine s/c)
o Pre-meal insulin correction dose
o Amylin analogue (pramlintide)
2nd line: fixed insulin dose

241
Q

What would you monitor for patients with diabetes?

A

Measure HbA1c levels every 3 months in children and every 3-6 months in adults
Make sure level is under 6.5% (48 mmol/mol)

Also monitor BP and kidney function

242
Q

What are the long-term complications associated with type 1 diabetes?

A
  • Microvascular: retinopathy, peripheral or autonomic neuropathy
  • Cardiovascular disease, diabetic kidney disease.
  • Potential for depression and eating disorder#
  • Foot amputations
  • Blindness
243
Q

What are some risk factors for type 2 diabetes?

A

Ageing
high BMI
gestational diabetes
non-white ancestry
polycystic ovary syndrome
hypertension

244
Q

What are the key presentations for type 2 diabetes?

A

Hyperglycaemia with presence of risk factors

E.g., Overweight, certain ethnic groups, age

245
Q

What are symptoms of type 2 diabetes?

A

Polydipsia
Polyuria
candidal infections,
skin infection,
UTIs,
fatigue,
blurred vison
uncommon symptoms

246
Q

What are first line investigations for type 2 diabetes?

A

Fasting glucose, 2-hour post load glucose (75g orally) random plasma glucose

247
Q

What is the gold standard test for type 2 diabetes?

A

HbA1c

248
Q

What are some macrovascular complications of diabetes?

A

Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

249
Q

What are some microvascular complications of diabetes?

A

Peripheral neuropathy- nerves in the body’s extremities, such as the hands, feet and arms, are damaged
Retinopathy- damage to vessels in the eye
Kidney disease, particularly glomerulosclerosis

250
Q

When should a second anti-diabetic drug be added to the use of metformin?

A

When HBA1c rises above 58mmol/mol despite maximum dose of metformin

251
Q

How does metformin work?

A
  • Metformin which increases the rate of gluconeogenesis in the liver??????? tom i think this is the exact opposite of what it does
  • Increases cell sensitivity to insulin
  • Helps with weight issues
  • reduces CVS risk in diabetes
252
Q

What are some other anti-diabetic drugs?

A
  • Sulfonylureas (gliclazide) they promote insulin secretion but only work in people with functional B-cells. Risk of hypoglycaemia and weight gain. Increased risk of CVD when used as a monotherapy
  • Dipeptidyl peptidase-4 inhibitor (DPP-4i) (incretins): they are hormones produced in the GI tract which increase Increase insulin secretions, Inhibit glucagon production, Slow absorption by the GI tract
  • SGLT-2 inhibitors “-gliflozin”, such as empagliflozin, canagliflozin and dapagliflozin- it inhibits glucose reabsorption from the the urine into the blood
253
Q

What is the definition of hypertension?

A

A blood pressure above 140/90

254
Q

Name some environmental factors that can lead to hypertension?

A
  • Obesity
  • Sleep apnoea
  • Alcohol intake
  • Sodium intake
  • Stress
  • Insulin intake
255
Q

What are some causes of secondary hypertension?

A
  • All renal disease
  • Endocrine diseases e.g., Cushing’s, Conn’s acromegaly
  • Congenital disease
  • Neurological diseases e.g., brainstem lesions and raised intercranial pressure
  • Pregnancy- pre-eclampsia
  • Drugs - Oral contraceptives
256
Q

What is benign and what is malignant hypertension?

A

Benign- is the stable elevation of BP over many years (is still dangerous)
Malignant- is the acute and severe elevation of BP. If undiagnosed then it can lead to death within 2 years

257
Q

What is classified as mild hypertension?

A

> 140 systolic or >90 diastolic

258
Q

What is classified as moderate hypertension?

A

> 160 systolic or >100 diastolic

259
Q

What is classified as severe hypertension?

A

> 180 systolic or >110 diastolic

260
Q

How would you diagnose hypertension?

A

Clinical BP of 140/90 and ABPM or HBPM of above 135/90

261
Q

What other tests might you perform on patients diagnosed with hypertension?

A
  • Bloods- HbA1c look for diabetes, creatinine and urea to asses renal function
  • ECG/echo to look for ventricular hypertrophy
262
Q

What would the first-line treatment be for a 50 year old white man diagnosed with hypertension?

A

ACE inhibitor (Ramipril and enalapril)

263
Q

What would the first-line treatment be for a 50 year old black man diagnosed with hypertension?

A

Calcium channel blocker (amlodipine) or thiazide diuretic if not CCB not tolerated

264
Q

What are some complications associated with hypertension?

A

Cardiovascular- Atherosclerosis, aortic aneurysm , cardiac failure, AF, stroke
Renal- renal failure
Eye effects- visual disturbances
Systemic hypertensive heart disease- changes that were initially adaptive to cope with the hypertension, lead to cardiac dilatation, congestive heart failure, and even sudden death

265
Q

What are the risk factors for migraines?

A
  • Family history
  • Female gender 3 times more common
  • Obesity
  • Triggers
266
Q

What are some triggers for migraines?

A

CH- Chocolate
OC- Oral contraceptive
OL- alcohOL
A- anxiety
T- travel
E- exercise
CHOCOLATE

Other triggers can be red wine, bright lights and menstruation

267
Q

What are the different types of migraine?

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (just the aura without the headache)
  • Hemiplegic migraine
268
Q

What are the headache symptoms of a migraine?

A

Last between 4-72 hours:
- Pounding or throbbing in nature
- Usually unilateral (can be bilateral more common in children)
- Photophobia
- Phonophobia (loud noises)
- Aura
- Nausea and vomiting

269
Q

What is a hemiplegic migraine?

A

They can mimic a stroke. Need to rule out if patient has symptoms:
- typical migraine
- Sudden onset
- Hemiplegia
- Ataxia
- Change in consciousness

270
Q

What are the 5 stages of a migraine?

A
  • Prodromal stage subtle symptoms such as yawning, fatigue or mood changes
  • Aura
  • headache
  • Resolution the headache can fade away and be relieved by vomiting or sleeping
  • Postdromal stage
271
Q

What is the diagnostic criteria for migraines with aura?

A

At least two headaches filling criteria shown in picture

272
Q

What is the diagnostic criteria for migraines without aura?

A

At least five headaches filling criteria shown in picture

273
Q

What is the management for migraines?

A
  • Analgesia (avoid opioids)
  • Oral triptan ( 500mg sumatriptan) as the headache starts
  • Antiemetics metoclopramide
274
Q

What are triptans?

A

They 5HT (serotonin) receptor agonists and they cause:
- smooth muscle contraction in arteries
- Peripheral pain receptors to inhibit activation of pain receptors
- Reduce neuronal activity in the central nervous system

275
Q

What are the medications used for migraine prophylaxis?

A
  • Propranolol
  • Topiramate (don’t use in pregnancy as it is teratogenic and can cause cleft lip)
  • Amitriptyline
276
Q

What are the non-pharmacological treatments for migraines?

A
  • Acupuncture: if both propranolol and topiramate are ineffective or unsuitable
  • Riboflavin (vitamin B2): **may be effective in some people, but avoid in pregnancy
277
Q

What should not be given to a female who experiences migraines with aura?

A

The combined pill it increases the risk of a stroke

278
Q

What is osteoporosis/osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones.

Osteopenia refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures.

279
Q

What can cause osteporosis?

A
  • Primary disease
  • Malignancy
  • Endocrine dysfunction
  • COPD
  • IBD
  • CLD
  • CKD
280
Q

What are the risk factors for developing osteoporosis?

A

S- Steroid use
H- Hyperthyroidism, hyperparathyroidism
A- Alcohol and tobacco use
T- Thin
T- Testosterone decrease
E- early menopause- oestrogen is protective
R- renal or liver failure
E- Erosive/inflammatory bone disease
D- dietary e.g., reduced Ca2+, malabsorption, diabetes

281
Q

Why does bone mass decrease as we get older?

A
  • Osteoclasts are responsible for the breakdown of bone and osteoblasts are responsible for the formation. As we age osteoclast activity is increased however this is not matched by osteoblast activity
  • The peak mass we reach as young adults is key a higher peak bone mass can be protective
282
Q

How can a fall in levels of oestrogen cause bone mass to decrease?

A
  • Oestrogen deficiency leads to an increased rate of bone loss. It is key yo the activity of bone cell receptors found on osteoblasts, osteocytes, and osteoclasts.
  • It is thought that osteoclasts survive longer in the absence of oestrogen and there is an arrest of osteoblastic synthetic architecture
283
Q

What is the FRAX tool?

A

It gives a prediction of the risk of a fragility fracture over the next 10 years

It involves the inputting of information such as age, BMI, co-morbidities, smoking, family history and if done you can enter a bone mineral score from a DEXA scan

284
Q

What do the different T-scores represent?

A

More than -1: Normal

-1 to -2.5: Osteopenia

Less than -2.5: Osteoporosis

Less than -2.5 plus a fracture: Severe Osteoporosis

285
Q

What is the management for someone who has had a FRAX score without a DEXA scan?

A

Low risk- reassure
Medium risk- offer DEXA scan and recalculate the risk with the results
High risk: offer treatment

286
Q

What is the treatment for someone at high risk of a fracture?

A

Bisphosphonates- they interfere with osteoclast activity reducing their activity. eg:

Alendronate 70mg once weekly
Riseronate 35mg once weekly
Zoledronic acid 5 mg once yearly (intravenous)

287
Q

What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?

A
  • Activty and exercise
  • Weight control
  • Reduce alcohol/stop smoking

NICE recommend calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium. An example of this would be Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).

Patients with an adequate calcium intake but lacking sun exposure should have vitamin D supplementation.

288
Q

What are the side effects of bisphosphonates?

A
  • Reflux and oesophageal erosions.
  • Osteonecrosis of the jaw and external auditory canal

They are taken on an empty stomach and person should sit upright for 30 minutes before taking

289
Q

What is diverticular disease?

A

Diverticular disease may be defined as any clinical state caused by symptoms pertaining to colonic diverticula and includes a wide-ranging spectrum from asymptomatic to severe and complicated disease

290
Q

What is diverticulosis?

A

The presence of diverticula (out-pouching) in an asymptomatic patient

291
Q

What is diverticulitis?

A

Diverticulitis refers to inflammation and infection of diverticula.

292
Q

What are the risk factors for developing diverticular disease?

A
  • Increasing age
  • Low fibre diets
  • Obesity
  • NSAIDs
  • Smoking
293
Q

What can cause diverticulitis?

A
  • When faecal matter becomes lodged in the diverticula or more often due to the erosion of the diverticular wall from high luminal pressure
  • This can cause inflammation and the rupture of vessels leading to bleeding
294
Q

What are the symptoms of diverticular disease?

A
  • Bowel habits changed
  • Bloating a flatulence
  • Left lower quadrant pain
  • Nausea and vomiting
295
Q

What is the management for mild diverticulitis?

A
  • Oral co-amoxiclav (at least 5 days)
  • Analgesia (avoiding NSAIDs and opiates, if possible)
  • Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
  • Follow-up within 2 days to review symptoms
296
Q

What is gout?

A

A type of crystal arthritis which is associated with chronically high levels of uric acid. Urate crystals are deposited in the joint causing it to become hot swollen and painful

297
Q

What are the overproduction causes of gout?

A
  • Increased cell turnover
  • Cytotoxic drugs e.g., chemotherapy
  • Purine rich diet, seafood and alcohol
  • Obesity
  • Severe psoriasis
298
Q

What are the decreased secretion of uric acid causes of gout?

A
  • CKD
  • Diuretics e.g., thiazide and loop
  • Pyrazinamide
  • Lead toxicity
  • High fructose intake

They are the more common cause they account for 90%

299
Q

What are risk factors for developing gout?

A
  • Elderly
  • Men
  • Post-menopausal women
  • Alcohol
  • Diabetes
  • IHD
  • High diet intake of purines
300
Q

What the signs of Gout and where is affected?

A
  • Gout tophi are deposits of uric acid
  • Ears
  • Base of big toe
  • Wrists
  • Base of thumb
301
Q

What are the symptoms of gout?

A
  • Red, tender, hot and swollen joints
  • Joint stiffness
  • Rapid onset of severe pain
302
Q

How would you diagnose gout?

A

Can be made on just clinical presentation but excluding septic arthritis is key

  • Joint aspiration will show no bacterial growth, needle shaped crystals, Negatively birefringent of polarised light, Monosodium urate crystals
  • Measure serum urate levels 4-6 weeks after attack as they can be low at time of attack
303
Q

What is the treatment of gout during an acute flare?

A
  • NSAIDs first line
  • Colchicine second line- severe diarrhoea is a side effect
  • Steroids as third line
304
Q

What is used to prevent gout?

A

Lifestyle management and a Xanthine oxidase inhibitor

  • First-line Allopurinol
  • Second-line Febuxostat
305
Q

What is pseudogout?

A

Is a form of inflammatory arthritis caused by the deposition of calcium pyrophosphate crystals in the synovium

306
Q

What are risk factors of pseudogout?

A
  • Hyperparathyroidism
  • Hemochromatosis
  • Hypomagnesaemia
  • Hypophosphatemia
  • Wilson’s disease
  • Acromegaly
307
Q

What is Parkinson’s disease (PD)?

A

A neurodegenerative disorder characterised by the loss of dopaminergic neurons within the substantia nigra pars compacta (SNPC) of the basal ganglia.

308
Q

What are the 3 key presentations of PD?

A
  • Bradykinesia
  • Tremor
  • Rigidity

PD symptoms usually start unilaterally and then become bilateral later in the disease course.

309
Q

What does the bradykinesia look like in PD?

A
  • Handwriting gets smaller
  • Only take small steps (shuffling gait)
  • Difficulty initiating movement
  • Difficulty turning around when standing
  • Reduced facial movements and expressions
310
Q

What does the tremor look like in PD?

A
  • A unilateral resting tremor. Described as pill rolling tremor looks like they are rolling pill between thumb and finger
  • The tremor is worse at resting and when they are distracted like using the other hand

Frequency of 4-6 times a second

311
Q

What are the differences between a PD tremor and a benign essential tremor?

A
  • PD= asymmetrical BET= symmetrical
  • PD= frequency= 4-6 BET= 5-8
  • PD= worse at rest BET= better at rest
  • PD= improves with intentional movement BET= worse
  • PD= no change with alcohol BET= better with alcohol
312
Q

What is used to diagnose PD?

A

PD is a clinical diagnosis and should be suspected in a patient with bradykinesia and at least one of the following:
- Tremor
- Rigidity
- Postural instability

313
Q

What is the management for PD?

A

Motor symptoms not affecting quality of life:
A choice of one of the following:

Dopamine agonist(non-ergot derived)
- Pramipexole, ropinirole
Monoamine oxidase B inhibitor (MOA-B)
- Selegiline, rasagiline
- Stop breakdown of circulating dopamine

Motor symptoms affecting the quality of life:

  • Synthetic dopamine levodopa given with a drug that stops it being broken down. These are peripheral decarboxylase inhibitors. Carbidopa and benserazide.

Co-benyldopa (levodopa and benserazide)
Co-careldopa (levodopa and carbidopa)

314
Q

What symptoms would not be present in the early stages of PD?

A
  • Incontinence
  • Dementia
  • Early falls
  • Symmetry

Can be a sign of normal pressure hydrocephalus

315
Q

What are the risk factors for developing prostate cancer?

A
  • Being tall
  • Obesity and high fat diet
  • Use of steroids
  • Cadmium exposure found in cigarettes, batteries and those in welding industry
  • BRCA1 and BRCA”
316
Q

Where does prostate cancer usually spread to if it becomes metastatic?

A

-Spreads to the bines of the vertebrae and pelvis resulting in hip and in back pain

317
Q

What are the signs of prostate cancer?

A
  • Asymmetrical, hard and nodular prostate with the loss of the median sulcus
  • Urinary retention
318
Q

What are the symptoms of prostate cancer?

A
  • Frequency
  • Dribbling
  • Haematuria or haematospermia
  • Dysuria
  • Bone pain (suggests metastatic disease)
319
Q

What is brachytherapy?

A

Involves the implanting of radioactive seeds into the the prostate delivering continuous targeted radiotherapy.

The radiation can cause inflammation in nearby organs, such as the bladder (cystitis) or rectum (proctitis). Other side effects include erectile dysfunction, incontinence and increased risk of bladder or rectal cancer.

320
Q

What is the hormone therapy used to treat prostate cancer?

A
  • it aims to reduce the levels of testosterone that can stimulate the tumour to grow

Drugs include
androgen-receptor blockers-bicalutamide
GnRH agonists- such as goserelin (Zoladex) or leuprorelin (Prostap)
Bilateral orchidectomy- removal of the testicles

321
Q

What are the risk factors for Acute pyelonephritis?

A
  • Sexual intercourse
  • Catheter
  • Diabetes
  • Pregnancy
  • Renal stones
322
Q

What can help to distinguish Acute pyelonephritis from a lower tract UTI?

A
  • Fever
  • Loin/back pain
  • Nausea/vomiting
  • Renal angle tenderness
323
Q

What is cystitis?

A

A lower UTI that involves the bladder

324
Q

Why are UTI’s more common in women?

A

The urethra is much shorter in women so it makes it easier for bacteria to reach the bladder and kidneys

325
Q

What are the symptoms of cystitis?

A
  • Dysuria
  • Frequency
  • Urgency
  • Nocturia
  • changes in appearance
  • Suprapubic discomfort
326
Q

What is the gold standard test for cystitis?

A
  • Mid-stream urine microscopy, culture and sensitivity (MC&S):
    • The most specific and sensitive test; bacteria, WBCs, +/- RBCs expected
327
Q

What are the treatments for non-pregnant women with cystitis/Lower UTI

A

Treatment may be delayed if symptoms are mild

  • First line would be 3 days of nitrofurantoin avoided in patients with CKD or trimethoprim
  • Second line Antibiotic course for 3 days -pivmacillinam or fosfomycin single-dose sachet
328
Q

What are the treatments for pregnant women/catheter related/men with cystitis/Lower UTI?

A
  • First line: Antibiotic course for 7 days - nitrofurantoin avoid in third trimester. Trimethoprim is avoided in first trimester as it increases the risk of neural tube defects
  • Second line: Antibiotic course for 7 days - amoxicillin or cefalexin
329
Q

What are the complications of UTIs in pFregnancy?

A
  • Pre-term delivery
  • Low-birthweight
330
Q

What is Urethritis?

A

Urethral inflammation due to infectious or non-infectious causes. It is primarily a sexually acquired disease!

331
Q

What are some non-infective causes of urethritis?

A
  • Trauma
  • Irritation
  • Urinary calculi (in english we call these kidney stones why use silly words)
332
Q

What are the common symptoms of urethritis?

A
  • Urethral discharge
  • Urethral irritation/itching
  • Dysuria
  • Penile discomfort
  • Skin lesions
333
Q

What are the investigations for urethritis?

A
  • Nucleic acid amplification test
  • Microscopy of gram-stained smears of genital secretions
  • Culture of urethral discharge
  • Urine dipstick to rule out UTI
334
Q

What are the signs of prostatitis?

A
  • Tender, hot swollen prostate (on digital rectal exam)
  • Palpable bladder
  • Tachycardia
  • Pyrexia
335
Q

What are the symptoms of prostatitis?

A
  • Dysuria
  • Frequency and retention
  • Straining
  • Back pain
  • Fever
  • Perineal, rectal or pelvic pain
336
Q

What are the investigations for prostatitis?

A
  • Digital rectal exam
  • Urine dipstick
  • MSU, semen and blood culture
337
Q

What is the treatment for prostatitis?

A

First line- Oral ciprofloxacinor ofloxacin
Second line- Oral levofloxacin or co-trimoxazole

338
Q

What is epididymo-Orchitis?

A

Inflammation of the epididymis (epididymitis) and inflammation of the testicle (orchitis)

339
Q

What are the signs of Epididymo-Orchitis?

A
  • Tenderness and palpable swelling
  • Prehn’s sign positive: pain is relieved with lifting the testicle, negative in testicular torsion
  • Cremasteric reflex preserved- unlike testicular torsion
340
Q

What are the symptoms of Epididymo-Orchitis?

A
  • Unilateral tender, red, and swollen testicle
    • Pain develops over a few days
  • Lower urinary tract symptoms e.g. dysuria
  • Urethral discharge: may and or may not be present
341
Q

What is the treatment for enteric organism causes of Epididymo-Orchitis?

A
  • Fluoroquinolone e.g., ofloxacin or ciprofloxacin
342
Q

What are the complications of Epididymo-Orchitis?

A
  • Musculoskeletal: reactive arthritis
  • Infective: disseminated infection secondary to gonorrhoea
343
Q

What are the risk factors for developing prostate cancer?

A
  • Being tall
  • Obesity and high fat diet
  • Use of steroids
  • Cadmium exposure found in cigarettes, batteries and those in welding industry
  • BRCA1 and BRCA”
344
Q

Where does prostate cancer usually spread to if it becomes metastatic?

A

-Spreads to the bines of the vertebrae and pelvis resulting in hip and in back pain

345
Q

What are the signs of prostate cancer?

A
  • Asymmetrical, hard and nodular prostate with the loss of the median sulcus
  • Urinary retention
346
Q

What are the symptoms of prostate cancer?

A
  • Frequency
  • Dribbling
  • Haematuria or haematospermia
  • Dysuria
  • Bone pain (suggests metastatic disease)
347
Q

What is brachytherapy?

A

Involves the implanting of radioactive seeds into the the prostate delivering continuous targeted radiotherapy.

The radiation can cause inflammation in nearby organs, such as the bladder (cystitis) or rectum (proctitis). Other side effects include erectile dysfunction, incontinence and increased risk of bladder or rectal cancer.

348
Q

What is the hormone therapy used to treat prostate cancer?

A
  • it aims to reduce the levels of testosterone that can stimulate the tumour to grow

Drugs include
androgen-receptor blockers-bicalutamide
GnRH agonists- such as goserelin (Zoladex) or leuprorelin (Prostap)
Bilateral orchidectomy- removal of the testicles

349
Q

What is Benign paroxysmal positional vertigo?

A
  • A common cause of recurrent episode of vertigo triggered by head movements
  • A common trigger is turning over in bed and symptoms last for around 60 seconds.
  • It does not cause hearing loss or tinnitus
350
Q

What causes Benign paroxysmal positional vertigo?

A
  • Calcium carbonate crystals called otoconia become displaced in the semi-circular canals and the disrupt the flow of the endolymph
351
Q

What is the manoeuvre used to test for Benign paroxysmal positional vertigo called?

A

Dix-Hallpike Manoeuvre

352
Q

What is used to treat Benign paroxysmal positional vertigo?

A

Epley Manoeuvre

353
Q

What are the symptoms of measels?

A

fever,
cough,
runny nose,
conjunctivitis,
marked malaise,
Koplik spots,
Maculopapular rash- it typically starts on the face

It is a notifiable disease

354
Q

What are the complications of measles?

A

Pneumonia
Diarrhoea
Dehydration
Encephalitis
Meningitis
Hearing loss
Vision loss
Death

occur in 30% of patients

355
Q

When is the MMR given?

A
  • 1 year
  • 3 years and 4 months
356
Q

What are the screening tools for dementia?

A

mini mental state examination (MMSE)/ Montreal cognitive assessment scale (MoCA

357
Q

What is otitis externa?

A
  • Inflammation of the skin in the external ear canal.
  • Often called swimmers ear as swimming can lead to inflammation in the ear#
  • Wax is protective and earbuds and earplugs are predisposing
358
Q

What are the causes of otitis externa?

A

Bacterial infection
Fungal infection (e.g., aspergillus or candida) if gets worse with antibiotics
Eczema
Seborrhoeic dermatitis
Contact dermatitis

359
Q

What are the main bacteria that cause otitis externa?

A

Pseudomonas aeruginosa
Staphylococcus aureus

360
Q

Presentation of otitis externa?

A

Ear pain
Discharge
Itchiness
Conductive hearing loss (if the ear becomes blocked)

Examination can show:

Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
Lymphadenopathy (swollen lymph nodes) in the neck or around the ear

361
Q

What is the treatment for mild otitis externa?

A

acetic acid 2%

362
Q

What is the treatment for moderate otitis externa?

A

Topical antibiotic and steroid.

Exclude perforated tympanic membrane before prescribing aminoglycoside

Severe might require oral antibiotics

363
Q

What is malignant otitis externa and what are the risk factors?

A

The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull.

Diabetes
Immunosuppressant medications (e.g., chemotherapy)
HIV

364
Q

What is otitis media?

A
  • Infection of the middle ear which is the space that sits between the tympanic membrane and the inner ear
  • This is where the nerves are found
365
Q

What causes otitis media?

A
  • Bacteria enter from the back of the thorat through the eustachian tube
  • A Viral URTI often precedes otitis media
366
Q

What is the most common cause of otitis media?

A

Strep pneumoniae

367
Q

What is the presentation of otitis media?

A
  • Ear pain
  • Reduced hearing
  • Feeling unwell
  • Signs of URTI
368
Q

Examination otitis media?

A
  • Otoscope tympanic membrane will look bulging red and perforation will show discharge and hole in tympanic membrane
369
Q

Management otitis media?

A

Most otitis media cases will resolve without antibiotics within around three days, sometimes up to a week. Antibiotics make little difference to symptoms or complications.

Amoxicillin for 5-7 days first-line
Clarithromycin (in pencillin allergy)
Erythromycin (in pregnant women allergic to penicillin)

370
Q

What is Pelvic inflammatory disease?

A
  • Is the inflammation and infection of the organs of the pelvis, caused by infection spreading through the cervix
  • It is a significant cause of tubular infertility and chronic pelvic pain
371
Q

What are the different types of PID?

A
  • Endometritis is inflammation of the endometrium
  • Salpingitis is inflammation of the fallopian tubes
  • Oophoritis is inflammation of the ovaries
  • Parametritis is inflammation of the parametrium, which is the connective tissue around the uterus
  • Peritonitis is inflammation of the peritoneal membrane
372
Q

What are the main causes of PID?

A

Tends to be caused by STIs

Neisseria gonorrhoeae tends to produce more severe PID

Chlamydia trachomatis

Mycoplasma genitalium

373
Q

What are the risk factor for PID?

A
  • Multiple sexual partners
  • Previous PID
  • Intrauterine device
  • Younger age
374
Q

What are the symptoms of PID?

A
  • Pelvic or lower abdominal pain
  • Abnormal vaginal discharge
  • Pain during sex
  • Fever
  • Dysuria
375
Q

What signs would be present on examination in PID?

A
  • Pelvic tenderness
    -Cervical motion tenderness (cervical excitation)
  • Inflamed cervix (cervicitis)
  • Purulent discharge
376
Q

What is the management for PID?

A
  • A single dose of intramuscular ceftriaxone for gonorrhoea
  • Doxycycline for chlamydia

-Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)

Ceftriaxone and doxycycline will cover many other bacteria, including H. influenzae and E. coli.

377
Q

What are the complications of PID?

A
  • Sepsis
  • Abscess
  • Infertility
  • Chronic pelvic pain
  • Ectopic pregnancy
378
Q

What is Fitz-Hugh-Curtis syndrome?

A
  • Caused by inflammation and infection of the liver, leading to adhesions between liver and the peritoneum
  • It results in right upper quadrant pain
379
Q

What is the presentation of sinusitits?

A

The typical presentation of acute sinusitis is someone with a recent viral upper respiratory tract infection presenting with:

Nasal congestion
Nasal discharge
Facial pain or headache
Facial pressure
Facial swelling over the affected areas
Loss of smell

380
Q

What is the treatment for sinusitis?

A

ICE recommend for patients with symptoms that are not improving after 10 days, the options of:

  • High dose steroid nasal spray for 14 days (e.g., mometasone 200 mcg twice daily)
  • A delayed antibiotic prescription, used if worsening or not improving within 7 days (phenoxymethylpenicillin first-line)
381
Q

What is peripheral vascular/arterial disease?

A

PAD includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries.

382
Q

What causes PAD?

A

Atherosclerosis

Can also be acute due to a thrombus

383
Q

What are the risk factors for PAD?

A

Smoking
Alcohol
High BMI
Age
Gender

384
Q

What are the four different classifications of PAAD?

A

Stage 1: asymptomatic
Stage 2: Mild claudication/severe
Stage 3: Ischaemia rest pain
Stage 4: Ulceration or gangrene

385
Q

What are the signs of PAD?

A
  • Weak pulse
  • Cold distal limbs
  • Postural colour change (Bureger’s test)
386
Q

What are the symptoms of PAD?

A
  • Cyanosis
  • Dependant redor
  • Muscle wasting
  • Hair loss
  • Ulcers
  • Poor wound healing
  • Gangrene
387
Q

What is the ankle-brachial index?

A

Used to determine extent of PAD.

Measures the difference between systolic blood pressure of arm to ankle. Done using a Doppler probe

388
Q

What do the different ratios on ABI indicate?

A

0.9-1.3 is normal
0.6-0.9 indicates mild
0.3-0.6 indicates moderate to severe
<0.3 indicates critical ischaemia

389
Q

What are some differential diagnosis of PAD?

A

Spinal stenosis
Arthritis
Venous claudication

390
Q

How would you monitor PAD?

A

Annual visits recommended for those with claudication ABI taken and Duplex ultrasound

391
Q

What is Buerger’s test?

A

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:

Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration

392
Q

What is polymyalgia rheumatica?

A

Polymyalgia rheumatica (PMR) is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck.

There is a strong association with giant cell arteritis, and the two conditions often occur together.

393
Q

How would you diagnose PMR?

A

Diagnosis is based on clinical presentation, response to steroids and excluding differentials.

394
Q

What is the treatment of PMR?

A

15mg prednisolone daily initially

Treatment with steroids typically lasts 1-2 years. NICE suggest the following reducing regime of prednisolone:

15mg until the symptoms are fully controlled, then
12.5mg for 3 weeks, then
10mg for 4-6 weeks, then
Reducing by 1mg every 4-8 weeks

395
Q

What is psoriasis?

A

Patches of psoriasis are dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, commonly over the extensor surfaces of the elbows and knees and on the scalp.

These skin changes are caused by the rapid generation of new skin cells, resulting in an abnormal buildup and thickening of the skin in those areas.

396
Q

What are the different types of psoriasis?

A

Plaque psoriasis: features the thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp

Guttate psoriasis: is the second most common form of psoriasis and commonly occurs in children. It presents with many small raised papules across the trunk and limbs.

Pustular psoriasis: is a rare severe form of psoriasis where pustules form under areas of erythematous skin.

Erythrodermic psoriasis: is a rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin.

397
Q

What are the treatments for psoriasis?

A

Topical steroids

Topical vitamin D analogues (calcipotriol)

Topical dithranol

Topical calcineurin inhibitors (tacrolimus) are usually only used in adults

Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis

398
Q

What is tonsillitis and what are the causes of it?

A
  • Inflammation of the tonsil most commonly caused by a viral infection
  • Most common cause of bacterial is strep pyogenes (strep A)
399
Q

What is the centor criteria?

A
  • Used to estimate the probability that the tonsillitis is due to a bacterial infection

Fever over 38
Tonsillar exudates
Absence of cough
Tender cervical lymph nodes

A score of 3 or more indicates a 40-60% likelihood it is bacterial

400
Q

What us the fever PAIN score?

A

A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis:

Fever during previous 24 hours
P – Purulence (pus on tonsils)
A – Attended within 3 days of the onset of symptoms
I – Inflamed tonsils (severely inflamed)
N – No cough or coryza

401
Q

What is the management of tonsillitis?

A
  • Safety net advice for viral and say come back in 3 days if not better
  • Penicillin V for a 10- day course is typically first-line
  • Clarithromycin if penicillin allergy
402
Q

What is trichomonas vaginalis ?

A

A type of parasite spread through sexual intercourse

403
Q

What is the presentation of trichomonas vaginalis ?

A

-Vaginal discharge (frothy green which may have a fishy smell
- Itching
- Dysuria
- Balanitis
- Painful sex

50% of cases are asymptomatic

404
Q

What is the sign of trichomonas vaginalis ?

A

Strawberry cervix” (also called colpitis macularis). A strawberry cervix is caused by inflammation (cervicitis) relating to the trichomonas infection

Also vaginal pH would be high like bacterial vaginosis

405
Q

What is the treatment for trichomonas vaginalis ?

A

Metronidazole

406
Q

What are the two types of urinary incontinence?

A

urge incontinence
stress incontinence.

407
Q

What causes urge incontinence?

A

Overactivity of the detrusor muscle

408
Q

What causes stress incontinence?

A

Weakness of the pelvic floor and sphincter muscles

409
Q

What are the ways of testing for urinary incontinence?

A
  • A bladder diary
  • Urodynamic tests
410
Q

What ate the managements for stress incontinence?

A
  • Avoid dirutetics
  • Weight loss
  • Pelvic floor exercises
  • Duloxetine
411
Q

What is the management for urge incontinence?

A
  • Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin

They have side effects which include dry mouth dry eyes, postural hypotension and can lead to cognitive decline

412
Q

What is an alternative treatment for urge incontinence?

A

Mirabegron but is a beta-3 agonist so raises BP

413
Q

What is Urticaria?

A

Urticaria are also known as hives. They are small itchy lumps that appear on the skin.

They may be associated with a patchy erythematous rash.

This can be localised to a specific area or widespread. They may be associated with angioedema and flushing of the skin.

414
Q

What is the main treatment of Urticaria?

A

Fexofenadine cream

415
Q

What virus causes chickenpox?

A

Varicella zoster

416
Q

What are the complications of chickenpox?

A

Bacterial superinfection
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presenting as ataxia)

417
Q

What is the treatment for anaphylaxis?

A

Adrenaline (IM*) 1:1000 (repeat after 5 minutes if no better)
500 micrograms (0.5 mL)

(give 300 micrograms IM [0.3 mL] in a child who is small or prepubertal)

300 micrograms (0.3 mL) 150 micrograms (0.15 mL) 100-150 micrograms (0.1 to 0.15 mL)

can also give steroids and anti-histamines

418
Q

WH

A
419
Q

What are the causes of primary syncope?

A
  • Dehydration
  • Missed meals
  • Extended standing in warm environment
  • Vasovagal response to stiumli
420
Q

What are the causes of secondary syncope?

A
  • Hypoglycaemia
  • Anaemia
  • Hypovolaemia e.g. due to haemorrhage, GI bleeding, ruptured aortic aneurysm
  • Infection
  • Anaphylaxis
  • Arrhythmias
  • Valvular heart disease
  • Hypertrophic obstructive cardiomyopathy
  • Pulmonary embolism: causing hypoxia
421
Q

What is a vasovagal episode (neurocardiogenic) syncope?

A
  • Caused by problems with the autonomic nervous system regulating blood flow to the brain
  • When the vagus nerve receives strong stimulus it causes an increase in parasympathetic activation which causes vasodilation and reduction in BP and blood flow to brain leading to the loss of consciousness
422
Q

What is Carotid sinus hypersensitivity?

A

This occurs when mild external pressure on the carotid bodies in the neck is enough to induce this reflex response (vagal stimulation). Mild pressure could be due to shaving, neck turning, tight collar etc

423
Q

What is s orthostatic hypotension syncope?

A
  • A drop of blood pressure of more than 20mmHg or a reflex tachycardia of more than 20 beats. When a person goes from lying down to standing
  • It occurs when there’s a delay in constriction of the lower body veins, which is needed to maintain an adequate blood pressure when changing position to standing.

As a result, blood pools in the veins of the legs for longer and less is returned to the heart, leading to a reduced cardiac output.

424
Q

What are the primary investigations for syncope?

A

Clinical Hx and examination

Ix to rule out pathological causes:
Bloods - infection
FBC - anaemia
ECG- arrythmia
Glucose - Hypoglycaemia
B-hCG - ectopic pregnancy

425
Q

What are the 6 viral exanthemas?

A
  • First disease: measles
  • Second disease: scarlet fever
  • Third disease: Rubella
  • Fourth disease: Dukes’ disease
  • Fifth disease: Parvovirus b19- slapped cheek syndrome
  • Sixth disease: Roseola infantum- can lead to febrile convulsions
426
Q

What can rubella lead to in pregnancy?

A

can lead to congenital rubella syndrome, which is a triad of deafness, blindness and congenital heart disease.

427
Q

What is whooping cough?

A

URTI caused by Bordetella pertussis

428
Q

Who is affected by whooping cough?

A

Mainly children 90% are under 5

429
Q

What is the catarrhal stage of whooping cough?

A
  • Dry unproductive cough
  • Low grade fever
  • Conjunctivitis
  • Coryzal symptoms
430
Q

What is the paroxysmal of whooping cough?

A
  • Coughing fits: typically consist of a short expiratory burst followed by an inspiratory gasp, causing the ‘whoop’ sound
  • Post-tussive vomiting
431
Q

What is the characteristic symptom of whooping cough?

A

Whoop sound caused by sharp inhalation of breath after coughing bout

432
Q

What are the investigations for whooping cough?

A

Nasopharyngeal swab/aspirate: culture/PCR

Anti-pertussis toxin IgG

433
Q

What is the treatment of whooping cough?

A

Notify PHE

  • Antibiotics marcolids clarithromycin or azithromycin
  • Stay off school as highly contagious
434
Q

What are the complications of whooping cough?

A
  • Pneumonia
  • Encephalopathy
  • Otitis media
  • Injuries from coughing e.g., pneumothorax and seizures

3A (11 decks)

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