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Phase 3A > GP 2 > Flashcards

GP 2 Flashcards

1
Q

What is otitis externa?

A

inflammation of the skin in the external ear canal

also known as swimmer’s ear

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2
Q

What are some potential causes of otitis externa?

A

bacterial infection
fungal infection (aspergillus or candida)
eczema
seborrhoeic dermatitis
contact dermatitis

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3
Q

What are the 2 most common bacterial causes of otitis externa?

A

pseudomonas aeruginosa
staphylococcus aureus

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4
Q

What are the typical symptoms of otitis externa?

A

ear pain
discharge
itchiness
conductive hearing loss

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5
Q

What signs of otitis externa can be seen on examination of the ear>

A

erythema and swelling of the ear canal
tenderness of the ear canal
pus or discharge in the ear canal
lymphadenopathy in the neck or around the ear

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6
Q

What is the management for otitis externa? mild/moderate

A

mild - acetic acid (can also be used prophylactically before and after swimming)

moderate - topical antibiotic and steroid e.g. neomycin, dexamethasone and acetic acid

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7
Q

What is malignant otitis externa?

A

severe and potentially life-threatening form of otitis externa where the infection spreads to the bones surrounding the ear and progresses to osteomyelitis of the temporal bone

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8
Q

What is psoriasis?

A

a chronic autoimmune condition which causes recurrent symptoms of psoriatic skin lesions with a large variety in severity of presentation

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9
Q

Briefly describe what patches of psoriasis look like

A

dry, flaky, scaly and faintly erythematous skin lesions which appear in raised and rough plaques

commonly occur over the extensor surfaces of the elbows and knees and on the scalp

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10
Q

What are the 4 types of psoriasis?

A

plaque psoriasis - MC form in adults, features thickened erythematous plaques with silver scales

guttate psoriasis - commonly occurs in children, small raised papules across the trunk and limbs which can turn into plaques, often triggered by a strep throat

pustular psoriasis - rare, severe form of psoriasis where pustules form under areas of erythematous skin, pus is non-infectious, MEDICAL EMERGENCY

erythrodermic psoriasis - rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin, MEDICAL EMERGENCY

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11
Q

WHat are 3 specific signs which suggest psoriasis?

A

auspitz sign - small points of bleeding when plaques are scraped off

koebner phenomenon - development of psoriatic lesions to areas of skin affected by trauma

residual pigmentation of the skin after the lesions resolve

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12
Q

What is the management 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

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13
Q

What is pelvic inflammatory disease/

A

inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix

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14
Q

what is salpingitis?

A

inflammation of the fallopian tubes

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15
Q

What are the causes of PID?

A

PID is usually associated an STI
neisseria gonorrhoea
chlamydia trachomatis
mycoplasma genitalium

less-commonly:
gardenerella vaginalis
haemophilus influenzae
E. coli

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16
Q

What are some risk factors for PID? x6

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)

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17
Q

How does PID usually present? x6

A

Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria

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18
Q

What are some possible findings on examination in PID? x4

A

Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge

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19
Q

What is the management for PID?

A

antibiotics depending on local and national guidelines

ceftriaxone (gonorrhoea)
doxycycline (chlamydia and mycoplasma)
metronidazole (gardnerella)

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20
Q

What is Fitx-hugh-curtis syndrome?

A

a complication of PID caused by inflammation and infection of the liver capsule (Glisson’s capsule) leading to adhesions between the liver and peritoneum

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21
Q

What is the definition of hypertension?

A

Blood pressure ≥140/90mmHg

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22
Q

What are the initiating factors for hypertension? (8)

A

DRIED ICE
- Disturbance of autoregulation
- Renal sodium retention
- Insulin resistance/hyperinsulinaemia
- Excess sodium intake
- Dysregulation of RAAS with elevated plasma renin activity
- Increased sympathetic drive
- Cell membrane transporter changes
- Endothelial dysfunction

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23
Q

Which medications increase blood pressure?

A
  • NSAIDs
  • SNRIs (serotonin and norepinephrine reuptake inhibitors)
  • Corticosteroids
  • Oral contraceptives (oestrogen containing)
  • Stimulants
  • Anti-anxiety drugs
  • Anti-TNFs
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24
Q

What are the risk factors for hypertension?

A
  • age >65yrs
  • moderate/high alcohol intake
  • sedentary lifestyle
  • FH of hypertension of CAD
  • obesity
  • metabolic syndrome
  • diabetes mellitus
  • black ancestry
  • hyperuricemia
  • obstructive sleep apnoea

** Smoking is NOT a risk factor

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25
Q

What is the equation for BP?

A

BP = CO x TPR

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26
Q

What factors affect blood pressure?

A
  • Preload
  • Contractility
  • Vessel hypertrophy
  • Peripheral constriction
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27
Q

What are the common symptoms of hypertension?

A

Most often symptomless.
- headache
- visual changes
- dyspnoea
- chest pain
- sensory of motor deficit

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28
Q

What is the gold standard screening for hypertension?

A

ECG

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29
Q

What is the management for hypertension?

A
  • Lifestyle modification and monitoring (increase exercise, reduce sodium intake, lose weight)

Medical treatment thresholds: low CDV risk = 160/100mmHg, high CDV risk = 140/90mmHg
- calcium channel blockers, ACEis, ARBs, diuretics, B-blockers

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30
Q

What is peripheral vascular disease?

A

A range of symptoms caused by atherosclerotic obstruction of the lower extremity arteries.

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31
Q

What is the most common cause of PVD?

A

Atherosclerosis

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32
Q

What are the risk factors for PVD?

A
  • Smoking
  • diabetes mellitus
  • hypertension
  • hyperlipidaemia
  • age >40yrs
  • history of CAD, CVD, sedentary lifestyle, CKD, T2DM
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33
Q

What are the key presentations of PVD?

A

Most often asymptomatic, intermittent claudication, diminished/absent pulse

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34
Q

What is the 1st line investigation for PVD?

A

Ankle-brachial index </= 0.90

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35
Q

What is the management for PVD?

A

Intermittent claudication: RF management

Chronic limb ischaemia: revascularization surgery (PCI if small, bypass if larger)

Acute limb threatening ischaemia: surgical emergency - revascularization within 4-6 hours other very high amputation risk

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36
Q

What are the 3 presentations of PVD?

A

Intermittent claudication (least severe)
Chronic critical limb ischaemia
Acute limb ischaemia

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37
Q

What are the 6 Ps that indicate limb-threatening ischaemia?

A

Pulselessness, Pallor, Pain, Persisting cold, Paralysis, Paraesthesia (the more that are present, the more limb threatening)

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38
Q

What are the causes of secondary hypertension?

A

Renal disease (MC cause)
Obesity
Pregnancy or pre-eclampsia
Endocrine (T2DM, Conn’s, Cushing’s diseases)
Drugs (alcohol, steroids, NSAIDs, oestrogen)

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39
Q

What is trichomoniasis

A

an STI with the parasite trichomonas vaginalis which lives in the urethra of men and women and the vagina

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40
Q

What conditions does trichomonas infection increase the risk of?

A

HIV
Bacterial vaginosis
Cervical cancer
Pelvic inflammatory disease
Pregnancy-related complications

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41
Q

What are the symptoms of trichomoniasis?

A

up to 50% of cases are asymptomatic

non-specific symptoms;
Vaginal discharge (frothy and yellow-green)
Itching
Dysuria (painful urination)
Dyspareunia (painful sex)
Balanitis (inflammation to the glans penis)

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42
Q

What is the characteristic appearance of the cervix in trichomonas vaginalis?

A

strawberry cervix where there are tiny haemorrhages across the surface of the cervix, giving the appearance of a strawberry

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43
Q

What investigations are used to diagnosis trichomoniasis?

A

charcoal swab with microscopy
vaginal pH (>4.5)
urethral swab in men

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44
Q

What is the treatment for trichomoniasis?

A

metronidazole

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45
Q

What is tonsillitis?

A

inflammation of the tonsils (typically the palatine tonsils) which can occur due to viral or bacterial infection

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46
Q

What are the most common bacterial causes of tonsillitis?

A

group A streptococcus (MC)
streptococcus pneumoniae
haemophilus influenzae
moraxella catarrhalis
staphylococcus aureus

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47
Q

What are the symptoms of tonsillitis? x3

A

sore throat
fever >38
pain on swallowing

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48
Q

What is seen on examination of patients with tonsillitis>

A

red, inflamed and enlarged tonsils
+/- exudates
anterior cervical lymphadenopathy (swollen, tender lymph nodes in the anterior triangle of the neck)

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49
Q

What are the centor criteria for bacterial tonsillitis?

A

Fever >38
tonsillar exudates
absence of cough
tendor anterior cervical lymph nodes

3+ score = 40-60 % probability of bacterial tonsillitis and its appropriate to offer antibiotics

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50
Q

What is the treatment for tonsillitis?

A

viral is self-resolving
bacterial - 10 day course of penicillin V with relatively narrow spectrum of activity, effective against strep myogenes

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51
Q

What are some potential complications of tonsillitis? x6

A

peritonsillar abscess (quinsy)
otitis media
scarlet fever
rheumatic fever
post-strep glomerulonephritis
post-strep reactive arthritis

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52
Q

What is lyme disease?

A

a disease caused by infection with borrelia burgdorferi and the body’s immune response to this infection

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53
Q

How is lyme disease transmitted?

A

The b.burgdorferi spirochaete bacteria which causes lyme disease is carried by deer ticks which can attach to humans resulting in lyme disease

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54
Q

What are the stages of Lyme disease infection?

A
  1. Early/localised Lyme disease
    - circular, target-like rash which radiates from the site of the tick bite, known as erythema migrans
    - usually appears within 3-36 days
  2. Disseminated Lyme disease
    - flu-like illness which can include symptoms like joint and muscle pains, headache, fever, tiredness, nausea or vomiting
    - neurological disorders e.g. meningism, facial nerve palsies, mild encephalitis
    - occurs days to months later
  3. Late manifestations of Lyme disease
    - arthritis
    - acrodermatitis chronica atrophicans
    - late neurological disorders e.g. polyneuropathy, chronic encephalomyelitis, vertigo and psychosis
    - chronic Lyme disease and ‘post-Lyme syndrome’ (similar to CFS or fibromyalgia)
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55
Q

What are the investigations for Lyme disease?

A

It is difficult to make a diagnosis clinically

Patients with erythema migrans should be diagnosed and treated for Lyme disease based on clinical assessment without lab testing (at this point there is a high chance that the antibody test will be negative due to the time that it takes for the antibody response to develop)

If Lyme disease is suspected in people without erythema migrans, offer an enzyme-linked immunosorbent assay (ELISA) test for Lyme disease

IF the ELISA test is positive or equivocal, perform an immunoblot test for Lyme disease

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56
Q

What is the management for Lyme disease?

A

Treat with oral antibiotic for 2-3 weeks:
Doxycycline or amoxicillin

to treat later complications:
High dose IV benzylpenicillin, ceftriaxone

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57
Q

What is the definition of menopause? what is the average age at which it occurs?

A

a permanent end to menstruation which is confirmed after a woman has has no periods for 12 months

usually occurs around the age of 51

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58
Q

What is the perimenopausal period

A

the time around the menopause where the woman may be experiencing vasomotor symptoms and irregular periods

this includes the time leading up to the last menstrual period and the 12 months afterwards

typically in women older than 45 yrs

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59
Q

What is the definition of premature menopause and what causes it?

A

menopause before the age of 40 years which results from premature ovarian insufficiency

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60
Q

Briefly describe the physiology of menopause

A

menopause is caused by a decline in the development of the ovarian follicles which results in reduced oestrogen production

oestrogen has a negative feedback effect on the pituitary gland, suppressing the quantity of LH and FSH produced

as the level of oestrogen falls in the perimenopausal period, there is an absence of negative feedback on the pituitary gland, and increasing levels of LH and FSH

the failing follicular development means that ovulation does not occur, resulting in irregular menstrual cycles
without oestrogen, the endometrium does not develop, leading to a lack of menstruation

lower levels of oestrogen also cause the perimenopausal symptoms

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61
Q

What are the perimenopausal symptoms x8

A

hot flushes
emotional lability or low mood
premenstrual syndrome
irregular periods
joint pains
heavier or lighter periods
vaginal dryness and atrophy
reduce libido

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62
Q

Which conditions do women have an increased risk of following menopause due to lack of oestrogen ?

A

cardiovascular disease and stroke
osteoporosis
pelvic organ prolapse
urinary incontinence

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63
Q

How long do women need to use effective contraception for following their last menstrual period?

A

2 years after in women under 50
1 year after in women over 50

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64
Q

What are the management options for perimenopausal symptoms?

A

vasomotor symptoms are likely to resolve after 2-5 years without any treatment

options:
- no treatment
- HRT (most effective in treating hot flushes/night sweats, mood swings and vaginal/bladder symptoms)
- Tibolone (synthetic steroid hormone which acts as continuous combined HRT)
- Clonidine
- CBT
- SSRI antidepressants
- Testosterone to treat reduced libido
- Vaginal oestrogen cream or tablets to treat dryness and atrophy
- Vaginal moisturisers (Sylk, replens, YES)

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65
Q

What is mumps?

A

a viral infection which is spread by respiratory droplets and usually resolves without treatment after around a week

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66
Q

What are the symptoms and signs of mumps?

A

initial period of flu-like symptoms followed by painful parotid swelling which is associated with:
fever
muscle aches
lethargy
reduced appetite
headache
dry mouth

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67
Q

What are some potential complications of mumps and their symptoms x4

A

pancreatitis
orchitis
meningitis or encephalitis
sensorineural hearing loss

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68
Q

What are the investigations/management options for mumps

A

diagnosis can be confirmed using PCR saliva testing
antibody testing of blood or saliva can also be used to confirm diagnosis

NOTIFIABLE DISEASE

self-limiting condition so management is supportive with rest, fluids and analgesia

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69
Q

What is influenza and what are the types?

A

an RNA virus which has 3 variants: A, B and C which affect humans

Type A has different H and N subtypes and examples of the strains are H1N1 which caused the spanish flu pandemic

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70
Q

What are the typical presenting features of influenza? x8

A

fever
lethargy and fatigue
anorexia
muscle and joint aches
headache
dry cough
sore throat
coryzal symptoms

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71
Q

What are 3 things which help distinguish flu from the common cold?

A

flu tends to have an abrupt onset, whereas common cold is more gradual

fever is a typical feature of the flu but rare with a common cold

people with flu are wiped out with muscle aches and lethargy which is uncommon with a cold

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72
Q

WHat tests can be used to confirm influenza infection?

A

POC swab tests which detect viral antigens

Viral nasal or throat swabs for PCR testing

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73
Q

What is the management for influenza

A

usually self-resolving with supportive care measures (rest and fluid intake)

for people at risk of complications:
oral oseltamivir
inhaled zanamivir

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74
Q

What are some potential complications of influenza? x6

A

Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening chronic health conditions, such as COPD and heart failure
Febrile convulsions (young children)
Encephalitis

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75
Q

What is infectious mononucleosis/glandular fever?

A

a condition caused by infection with Epstein Barr virus (EBV)

commonly known as the kissing disease or mono

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76
Q

What are the key symptoms of glandular fever?

A

fever
sore throat
fatigue
lymphadenopathy
tonsillar enlargement
splenomegaly and in rare cases splenic rupture

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77
Q

What tests are used to diagnose glandular fever

A

Test for heterophile antibodies (multipurpose antibodies produced in response to but not specific to EBV antigens), almost 100% specific for IM but only 70-80% sensitive
- Monospot test - introduces pt’s blood to horse’s RBCs
- Paul-Bunnell test - like the monospot but uses sheep RBCs

Can also test for specific EBV antibodies which target viral capsid antigen:
- IgM antibody rises early and suggests acute infection
- IgG persists after the condition and suggests immunity

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78
Q

What is the management for glandular fever

A

usually self-limiting and lasts around 2-3 months
fatigue can last for several months once infection is cleared

avoid alcohol and sports (risk of splenic rupture)

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79
Q

WHat are the potential complications of glandular fever? x5

A

splenic rupture
glomerulonephritis
haemolytic anaemia
thrombocytopenia
chronic fatigue

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80
Q

What are the key symptoms of UTIs?

A

dysuria
suprapubic pain or discomfort
frequency
urgency
incontinence
haematuria
cloudy or foul-smelling urine
confusion (in old/frail patients)

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81
Q

What is the additional triad symptoms seen in pyelonephritis?

A

fever
loin or back pain
nausea or vomiting

may also have:
systemic illness
loss of appetite
haematuria
renal angle tenderness on examination

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82
Q

What are the bacteria which commonly cause UTIs?

A

Escherichia coli (gram-negative, anaerobic, rod-shaped bacteria)

Klebsiella pneumoniae (gram-negative, anaerobic, rod-shaped)

enterococcus
pseudomonas aeruginosa
staph saprophyticus

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83
Q

What are the important factors on MSU and what do they indicate?

A

Nitrites - suggestive of bacteria in the urine as they break down nitrates to nitrites

Leukocytes - significant rise can indicate infection or other cause of inflammation

Nitrites are a better indication of infection than leukocuytes
If both are present or nitrites are present the patient should be treated as a UTI but not if only leukocytes are present

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84
Q

What are some signs which indicate an atypical UTI?

A
  • seriously ill or septicaemia
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • failure to respond to suitable antibiotics within 48
    hours
  • infection with atypical (non-E. coli) organisms.
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85
Q

Which antibiotics are used to treat UTIs?

A

nitrofurantoin
trimethoprim

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86
Q

How is pyelonephritis managed?

A

referral to hospital is required if there are features of sepsis

cefalexin, co-amox, trimethoprim or ciprofloxacin antibiotics

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87
Q

What are the antibiotic options for treating UTIs in pregnant women?

A

nitrofurantoin (avoid in the 3rd trimester due to risk of neonatal haemolysis)

amoxicillin (only after sensitivities are known)

cefalexin (typical choice)

trimethoprim should be avoided due to folate antagonistic properties

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88
Q

what is urticaria? what causes it and what is it associated with?

A

Urticaria is hives i.e. small itchy lumps that appear on the skin.

They may be associated with angioedema (swelling of the deeper layers of the skin, caused by a build-up of fluid.) and flushing of the skin

Urticaria are caused by the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.

Most common form is spontaneous urticaria which can be acute (<6 weeks) or chronic (>6 weeks)

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89
Q

What are varicose veins?

A

distended superficial veins which measure >3mm in diameter usually affecting the legs

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90
Q

How do varicose veins develop?

A

when the valves in veins become incompetent they can’t carry out their function of preventing blood being drawn downwards by gravity and pooling in the veins

the deep and superficial veins are connected by vessels called the perforating veins which allow blood to flow from the superficial veins to the deep veins

when the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them

this leads to dilatation and engorgement of the superficial veins, forming varicose veins

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91
Q

What happens in chronic venous insufficiency?

A

blood pools in the distal veins and pressure builds up causing the veins to leak small amounts of blood into the tissues nearby

the haemoglobin in this leaked blood breaks down to haemosiderin which is deposited around the shins in the legs giving them a brown discolouration

pooling of blood in the distal tissues results in inflammation and the skin becoming dry and inflamed –> venous eczema

the skin and soft tissues become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipdermatosclerosis

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92
Q

What are the risk factors for varicose veins? x7

A

increasing age
family history
female
pregnancy
obesity
prolonged standing
deep vein thrombosis

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93
Q

What are some symptoms of varicose veins? x7

A

heavy or dragging sensation in the legs
aching
itching
burning
oedema
muscle cramps
restless legs

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94
Q

What are the special tests for varicose veins?

A

tap test (apply pressure at the SFJ and tap the distal varicose vein –> thrill?)

cough test (apply pressure to the SFJ while patient coughs –> thrill?)

trendelenburg’s test - lift affected leg to drain the veins then apply a tourniquet to thigh and get the patient to stand - the tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve, reassess at different levels to identify the location of the incompetent valves

perthes test

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95
Q

What is the management for varicose veins?

A

weight loss
staying physically active
keeping the leg elevated when possible to help drainage
compression stockings

surgical options:
endothermal ablation (catheter insertion and radiofrequency ablation)
sclerotherapy (irritant foam injection to close the vein)
stripping (veins are ligated and pulled out of the leg)

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96
Q

What happens in a vasovagal episode?

A

the vagus nerve receives a strong stimulus e.g. an emotional event, painful sensation or change in temperature and stimulates the parasympathetic nervous system

parasympathetic activation counteracts the sympathetic nervous system which keeps the smooth muscle in blood vessels constricted

as the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of the brain tissue

this causes the patient to lose consciousness and ‘faint’

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97
Q

What are venous ulcers?

A

wounds or breaks in the skin which occur due to the pooling of blood and waste products in the kin secondary to venous insufficiency

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98
Q

What are the typical features of venous ulcers which differentiate them from arterial ulcers?

A

occur in the gaiter area (between the top of the foot and bottom of the calf muscle)
are associated with chronic venous changes, e.g. hyperpigmentation, venous eczema and lipodermatosclerosis
occur after a minor injury to the leg
are larger and more superficial than arterial ulcers
have irregular, gently sloping borders
high chance of bleeding
pain relieved by elevation and worse on lowering the leg

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99
Q

How are venous ulcers managed?

A

wound care (cleaning, debridement, dressing)
compression therapy
antibiotics for infection
analgesia for pain

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100
Q

What is peripheral arterial disease?

A

the narrowing of arteries supplying the limbs and peripheries, reducing blood flow to these areas

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101
Q

What is intermittent claudication?

A

a symptom of ischaemia in a limb, occurring during exertion and relieved by rest

typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity

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102
Q

What are the features of acute limb ischaemia? 6P’s

A

Pain
Pallor
Pulseless
Paralysis
Paraesthesia
Perishing cold

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103
Q

What is Leriche syndrome?

A

occlusion in the distal aorta or proximal common iliac artery which presents with a clinical triad of:
- thigh/buttock claudication
- absent femoral pulses
- male impotence

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104
Q

What are some signs of arterial disease seen on inspection?

A

skin pallor
cyanosis
dependent rubor (deep red colour when the limb is lower than the rest of the body)
muscle wasting
hair loss
ulcers
poor wound healing
gangrene

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105
Q

What is Buerger’s test?

A

with patient lying supine, lift their legs to 45 degree angle and hold them for 1-2 mins, looking for pallor

then gt the patient to sit up with their legs hanging over the edge of the bed
in PAD the legs, rather than turning pink, will go initially blue and then dark red (rubor)

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106
Q

What are the investigations for peripheral arterial disease?

A

Ankle-brachial pressure index (ABPI)
Duplex USS
Angiography

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107
Q

What is the ankle-brachial pressure index?

A

the ratio of systolic blood pressure in the ankle compared with the systolic blood pressure in the arm

0.9-1.3 is normal
0.6 – 0.9 indicates mild peripheral arterial disease
0.3 – 0.6 indicates moderate to severe peripheral arterial disease
Less than 0.3 indicates severe disease to critical ischaemic

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108
Q

How is intermittent claudication managed?

A

lifestyle changes

exercise training (programme of regularly walking to the point of near-maximal claudication and pain, then resting and repeating)

atorvastatin, clopidogrel, naftidrofuryl oxalate (peripheral vasodilator)

endovascular angioplasty and stenting, endarterectomy, bypass surgery

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109
Q

What is critical limb ischaemia and how is it managed?

A

the end-stage of PAD, where there is an inadequate supply of blood to a limb to allow it to function normally at rest

medical emergency requiring urgent referral to the vascular team

urgent revascularisation is needed via:
Endovascular angioplasty and stenting
Endarterectomy
Bypass surgery

Amputation of the limb if it is not possible to restore the blood supply

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110
Q

What is acute limb ischaemia and how is it managed?

A

refers to a rapid onset of ischaemia in a limb, typically due to a thrombus

management options:
Endovascular thrombolysis or thrombectomy
surgical thrombectomy
endarterectomy
bypass surgery
amputation of the limb if impossible to restore the blood supply

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111
Q

What are the risk factors for atherosclerosis/PAD?

A

Non-modifiable
- older age
- family history
- male

Modifiable
- smoking
- alcohol consumption
- poor diet
- low exercise/sedentary lifestyle
- obesity
- poor sleep
- stress

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112
Q

What is rhinosinusitis

A

inflammation of the paranasal sinuses in the face (sinusitis) combined with inflammation of the nasal cavity (rhinitis)

can be acute (<12 wks) or chronic (>12 wks)

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113
Q

What are some potential causes of rhinosinusitis? x4

A

infection
allergies
obstruction of drainage e.g. foreign body, trauma or polyps
smoking

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114
Q

What are the symptoms associated with rhinosinusitis? x6

A

nasal congestion
nasal discharge
facial pain or headache
facial pressure
facial swelling over the affected areas
loss of smell

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115
Q

What is the management for rhinosinusitis>

A

Patients with systemic infection or sepsis require admission to hospital for emergency management.

NICE recommend not offering antibiotics to patients with symptoms for up to 10 days. Most cases are caused by a viral infection and resolve within 2-3 weeks.

NICE 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)

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116
Q

What are viral exanthema?

A

eruptive widespread rashes

originally there were 6 viral exanthema which have now been renamed:

First disease: Measles
Second disease: Scarlet Fever
Third disease: Rubella (AKA German Measles)
Fourth disease: Dukes’ Disease
Fifth disease: Parvovirus B19
Sixth disease: Roseola Infantum

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117
Q

What are warts>

A

non-cancerous viral skin growths which affect the squamous epithelium and usually occur on the hands and feet but can also affect the genitals or face

they are caused by the human papillomavirus

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118
Q

What is the treatment for warts?

A

salicyclic acid, or cryotherapy

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119
Q

What are dermatophytosis infections? how are they classified

A

also known as ringworm/tinea infections, they are fungal infections caused by dermatophytes - a group of fungi which invade and grow in dead keratin

they tend to grow outwards on skin, producing a ring-like pattern which gave them the name ringworm

classified according to site:
scalp - tinea capitis
feet - tinea pedis
nail - onychomycosis
groin - tinea cruris
body - tinea corporis

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120
Q

How does ringworm/dermatophysis present?

A

itchy rash which is erythematous, scaly and well-demarcated

tinea capitis - hair loss in a demarcated region plus itching dryness and scalp erythema

tinea pedis (athlete’s foot) - white or red, flaky, cracked, itchy patches between the toes

onychomycosis - thickened, discoloured and deformed nails

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121
Q

What is the management for ringworm/dermatophysis>

A

usually clinical supported by good response to antifungal meds

antifungal creams e.g. clotrimazole and miconazole

antifungal shampoo eg. ketoconazole

antifungal oral meds e.g. fluconazole, griseofulvin and itraconazole

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122
Q

What is contact dermatitis?

A

an inflammatory process of the skin that occurs in response to contact with exogenous substances and involves pruritic and erythematous patches

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123
Q

What are the 2 types of contact dermatitis/

A

Allergic contact dermatitis - a type IV delayed hypersensitivity reaction. It occurs after sensitisation and subsequent re-exposure to an allergen.

Irritant contact dermatitis - an inflammatory response that occurs after damage to the skin, usually by chemicals. This is not an allergy and can occur in any individual significantly exposed to an irritant. This may be acute or chronic/cumulative.

124
Q

What are the signs/symptoms of contact dermatitis?

A

skin redness
vesicles or papules over the affected area
crusting and scaling of skin
itching of an affected area
fissures
hyperpigmentation
pain or burning sensation from an affected area

125
Q

What is the treatment for contact dermatitis?

A

identify and avoid the irritant

protect skin with protective equipment and creams

more severe or chronic forms can benefit from topical corticosteroid cream

126
Q

What is herpes simplex virus?

A

a virus causing cold sores and genital herpes which can become latent after initial infection in the associated sensory nerve ganglia

2 main strains, HSV-1 (most associated with cold sores) and HSV-2 (typically causes genital herpes)

it is spread through direct contact with affected mucous membranes or viral shedding in mucous secretions

127
Q

What is the usual disease pathway of HSV-1?

A

often contracted initially in childhood (before 5 years) and remains dormant in the trigeminal nerve ganglion and reactivates as cold sores, particularly in times of stress

genital herpes caused by HSV-1 is usually contracted through oro-genital sex, where the virus spreads from a person with an oral infection to the person that develops a genital infection `

128
Q

What are the signs and symptoms of genital herpes?

A

can be asymptomatic

ulcers or blistering lesions
neuropathic type pain
flu-like symptoms
dysuria
inguinal lymphadenopathy

129
Q

What is the management for genital herpes?

A

aciclovir + supportive measures e.g. analgesia, fluids, loose clothing

130
Q

What is folliculitis?

A

inflammation of the hair follicles of the skin which can occur for a variety of reasons

can be acute or chronic

131
Q

What are the specific types of folliculitis?

A

sycosis barbae - chronic folliculitis in the beard area of the face where the skin is painful and crusted with burning and itching on shaving, numerous pustules develop in the hair follicles

hot tub folliculitis - caused by pseudomonas aeruginosa

gram-negative folliculitis - can occur after acne has been treated with long-term antibiotics

pseudo-folliculitis - razor bumps caused by inflammation from shaving and ingrown hairs

132
Q

what are the most common causes of CKD?

A

diabetes (mc)
hypertension

133
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

134
Q

What are the symptoms of CKD?

A

pruritis
loss of appetite
nausea
oedema
muscle cramps

135
Q

What are the investigations for CKD?

A
  • estimated GFR - can be checked with U+E bloods, 2 tests required 3 months apart
  • proteinuria, checked using a urine albumin:creatinine ration
  • haematuria - checked using a urine dipstick
  • renal USS
136
Q

What is the G score in CKD staging?

A

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

137
Q

What is the A score in CKD staging?

A

Based off the albumin:creatinine ratio:

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

138
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

139
Q

What are some potential complications of CKD?

A

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

140
Q

Define what a Supraventricular Tachycardia is. What are the 4 types? What is the most common?

A

Any tachycardia which arises from the atrium or AV junction

Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia (AVNRT) (MC)
AV reciprocating tachycardia (AVRT)

141
Q

Supraventricular Tachycardias - What is atrial flutter? What things characterise it?

A

It is irregular ORGANSIED atrial firing, around 250 - 300BPM (conduction pathway typically from around opening of tricuspid valve)

Often associated with AF
Atrial HR = 300 BPM
Ventricular rate = 150/100/75 BPM (due to AV node conducting every 2nd/3rd/4th beat “flutter beat” , so see at least 2 P waves for every QRS complex - but QRS complexes will be regular

ECG - see flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1

142
Q

Supraventricular Tachycardias - Name some causes of atrial flutter

A
  • Idiopathic (30%)
  • Coronary heart disease
  • Thyrotoxicosis
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
143
Q

Supraventricular Tachycardias - Outline the pathophysiology behind atrial flutter.

A

It is caused by the electrical signal re-entering/ re-circulating back into the atrium, due to an extra electrical pathway

It goes round and round, without interruption, so Atrial contraction is at 300bpm

The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.

Can be sudden and brief in episodes, or on going

144
Q

Supraventricular Tachycardias - what would you see on an ECG that would indicate Atrial flutter?

A

ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave

145
Q

Supraventricular Tachycardias - what is the management of atrial flutter?

A
  • Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
  • Rate/rhythm controlwith beta blockers or cardioversion (use of electric shock to put heart back into rhythm)
  • Radiofrequency ablationof the re-entrant rhythm (Uses heat generated by radio waves to destroy tissue)
  • Anticoagulationbased on CHA2DS2VASc score
146
Q

Supraventricular Tachycardias - What characterises AV nodal re-entry tachycardia (AVNRT)?

A

Most common type of SVT - AV nodal re-entry tachycardia (AVNRT)
Twice as common in women than men

The electrical conduction of the atrium re enters back through the AV node, Due to the presence of a “ring” of conducting pathways in the AV node, of which the “limbs” have different conduction times and refractory periods
This allows a re-entry circuit and an impulse to produce a circus movement tachycardia

147
Q

Supraventricular Tachycardias - what is the are the key presentations of someone with AV nodal re-entry tachycardia/AV reciprocating Tachycardia?

(What’s the slightly rogue one)

A

Presentation
Regular rapid palpitations – abrupt onset and sudden termination
Neck pulsation – JV pulsations

Polyuria – due to release of ANP in response to increased atrial pressure during tachycardia
Chest pain and SOB

Symptoms
Palpitations
Dizziness
Dyspnoea
Central chest pain
Syncope

148
Q

Supraventricular Tachycardias - What is AV reciprocating tachycardia? What is the best known type of this?

A

The eletrical signals goes back in the atria via an accessory pathway.

The best known type of this is Wolff-Parkinson-White Syndrome, there is an accessory pathway (bundle of kent) between atria and ventricles

149
Q

Supraventricular Tachycardias - What would you see on an ECG of someone with AV Nodal re-entry tachycardia?

A

P waves are either not visible, or are seen immediately before or after the QRS complex (short PR interval)
QRS complex is a normal shape because the ventricles are activated in the normal way (down bundle of His)

150
Q

Supraventricular Tachycardias - what would you see on an ECG for AV Nodal Reciprocating Tachycardia? (WPW syndrome)

A

The early depolarisation of part of the ventricle leads:

  • shortened PR interval
  • slurred start to the QRS (delta wave)
  • QRS is narrow
    Patients are also prone to atrial and occasionally ventricular fibrillation
151
Q

Supraventricular Tachycardias - What is the initial management of AV Nodal re-entry tachycardia and AV Reciprocating tachycardia?

A

Breath-holding
Carotid massage - massage the carotid on one side gently with two fingers.
Valsalva manoeuvre - Pt blows hard into resistance

152
Q

Supraventricular Tachycardias - if carotid massage and Valsalva manoeuvre are unsuccessful, what can you give to treat AVNRT and AVRT?

A

If manoeuvres unsuccessful, IV adenosine
Causes a complete heart block for a fraction of a second
Effective at terminating AVNRT and AVRT

153
Q

Supraventricular Tachycardias - What is Atrial fibrilation?

A

Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregular. This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.

This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles.

154
Q

What does atrial fibrillation lead to?

A
  • Irregularly irregularventricular contractions
  • Tachycardia
  • Heart failuredue topoor fillingof the ventricles duringdiastole
  • Risk ofstroke
155
Q

What are some common causes of atrial fibrillation?

A

PE/COPD
IHD, Heart failure
Rheumatic heart disease, Valve abnormalities
Alcohol intake
Thyroid issues - Hyperthyroidism
Sleep Apnoea
Electrolyte disturbances - Hyper/Hypo Kalaemia, Hypo magnesia

PIRATE

156
Q

What are some signs and symptoms of AF?

A
  • Irregular irregular pulse
  • Hypotension:red flag; suggest haemodynamic instability
  • Evidence of heart failure: red flag; such as pulmonary oedema
  • Palpitations
  • Dyspnoea
  • Chest pain: red flag
  • Syncope: red flag

Can also be asymptomatic!

157
Q

What investigations would you carry out for AF

A

ECG

Tests to look for causes of AF:
Serum Electrolytes
Thyroid Function Tests
Cardiac biomarker - eg Troponin
Chest x-ray look for heart failure
Transthorasic Echo - look for functional heart disease

158
Q

What is the management for someone who is haemodynamically unstable with AF? What signs could indicate that this is the case?

A

Emergency electrical synchronised DC cardioversion

  • Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
  • Syncope
  • Myocardial ischaemia
  • Heart failure:
159
Q

What is the first line management for someone who is haemodynamically stable with AF? What signs could indicate that this is the case? What Rate control would you do?

A

Start by controlling either rate of rhythm

Rate control:
- First line: beta-blocker (e.g. bisoprolol) or arate-limiting calcium-channel blocker (e.g. verapamil)
- Digoxin: may be considered first-line in patients with AF and heart failure

OF HAEMODYNAICALLY STABLE, DO RATE CONTROL BEFORE RHYTHM CONTROL

160
Q

What Further management might be necessary for persistent AF/ or AF that has not been treated with meds

A

Left atrial ablation - small burns/freezes to scar heart tissue to break up electrical signals that cause irregular heartbeats

Electrical DC cardioversion

Anticoagulants - DOACS - Apixaban to reduce risk of strokes, or Warafarin if DOACs are CI, (aka in Metal heart valves)

161
Q

Anticoagulants are often given to patient with AF to reduced their likelihood of developing clots that can cause strokes.
What scoring system is used to calculate stroke risk in AF? What types of factors are included on it?

A

CHADS2VASc score used to calculate stroke risk in AF

0 = no anticoagulation
1 = consider oral anticoagulation or aspirin
2 = Anticoagulants - DOACS - Apixaban to reduce risk of strokes

Congestive Heart failure = 1
Hypertension = 1
Age > 75 = 2
Age 65-74 = 1
Diabetes Mellitus = 1
Stroke or TIA = 2
Vascular disease = 1
Female sex = 1

162
Q

What would you see on an ECG for someone in AF?

A

Irregularly irregular
F (Fibrillatory) waves
No clear P waves
Rapid QRS complex
absence of [isoelectric]
baseline
variable ventricular rate

163
Q

What Rhythm control would you do in AF?

A

Rhythm control: - either pharmacological or electrical cardioversion
- Pharmacological: - anti-arrhythmics
- Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
- Amiodarone: if structural/ischaemic heart disease is present
- Electrical cardioversion:rapidly shock the heart back into sinus rhythm

IF HAEMODYNAICALLY UNSTABLE, DO RHYTHM CONTROL BEFORE RATE CONTROL (aka Cardioveresion)

164
Q

What is a Delta wave? Why does it occur?

A

“ A delta wave is slurring of the upstroke of the QRS complex.

Occurs because the action potential from the SA node is able to conduct to the ventricles very quickly through the accessory pathway

=> QRS occurs immediately after the P wave, making the delta wave.

165
Q

Define obesity

A

Abnormal or excessive fat accumulation which poses a risk to health.
BMI > 30.

166
Q

What are some potential consequences of obesity ?

A
  • Type II Diabetes
  • Hypertension
  • Coronary artery disease
  • Stroke
  • Osteoarthritis
  • Gout
  • Obstructive sleep apnoea
  • Carcinoma (breast, endometrium, colon, prostate)
167
Q

What are 5 risk factors for obesity

A
  • Hypothyroidism
  • Hypercortisolism
  • Corticosteroid therapy
  • Diet high in sugar and fats
  • High alcohol intake
168
Q

What is leptin and its action?

A

A hormone released by adipocytes which switches off appetite and stimulates the immune system. Leptin levels in the blood increase after eating and decrease after fasting.

169
Q

What is ghrelin and its action?

A

A hormone released by endocrine cells of the stomach which stimulates growth hormone release and appetite. Blood levels are high when fasting and fall after eating.

170
Q

What is the action of insulin?

A
  • suppresses hepatic glucose output (decreases glycogenolysis and gluconeogenesis)
  • increases glucose uptake into muscle and fat
  • suppresses lipolysis and muscle breakdown
171
Q

What is the action of glucagon?

A
  • increases hepatic glucose output (increases glycogenolysis and gluconeogenesis)
  • reduce peripheral glucose uptake
  • stimulate peripheral release of gluconeogenic precursors (glycerol, AAs) - increases lipolysis and muscle breakdown
172
Q

What is Type I diabetes?

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction.

173
Q

What are the risk factors for T1 Diabetes?

A
  • HLA DR3 and DR4 and islet cell antibodies
  • Other autoimmune diseases
  • Environmental infections (e.g. viruses)
174
Q

What is diabetes mellitus?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia.

175
Q

How does DM cause morbidity and mortality?

A
  • Acute hyperglycaemia (leads to diabetic ketoacidosis and hyperosmolar hyperglycaemic state if untreated)
  • Chronic hyperglycaemia leading to tissue complications
  • Side effects of treatment - hypoglycaemia
176
Q

What random plasma glucose level with symptoms indicates diabetes mellitus?

A

> 11mmol/l

177
Q

What fasting plasma glucose value indicates diabetes mellitus?

A

> 7mmol/l

178
Q

What is GTT and what are the fasting and 2hr values that indicate diabetes mellitus?

A

GTT = Glucose tolerance test
GTT (75g glucose) fasting > 7mmol/l
or 2hr value >11mmol/l (repeated on 2 occasions)

179
Q

What is HbA1c and what value is associated with diabetes mellitus?

A

HbA1c = glycated haemoglobin, a form of haemoglobin used to measure the average haemoglobin-associated glucose in blood over the last three months, HbA1c >48mmol/mol (6.5%) is seen in patients with diabetes mellitus

180
Q

What is the cause of Type I diabetes?

A

Beta cells express HLA (human leukocyte antigen) which activates a chronic cell mediated immune process leading to chronic ‘insulitis’ and consequently insulin insufficiency

181
Q

What is the typical presentation/symptoms of Type I DM?

A

Young lean pt
- polydipsia
- nocturia/polyuria
- glycosuria
- polyphagia (excessive eating) + weight loss
- excessive tiredness

182
Q

What is the treatment for T1DM?

A

Basal Bolus Insulin
- basal = longer acting to maintain stable insulin levels throughout day
- bolus = faster acting, 30 mins preprandial to give “insulin spike”

183
Q

What are the risk factors for T2DM?

A

genetic link, smoking, obesity, sedentary lifestyle

184
Q

What is the pathophysiology of T2DM?

A

Peripheral insulin resistance (e.g. malfunctional insulin intracellular activation pathway) leads to decrease GLUT4 receptor expression + minor destruction of pancreatic islets.
This results in hyperglycaemia with increased insulin demand from depleted beta cell population.

185
Q

What is the typical presentation and symptoms of T2DM?

A

Obese, hypertensive, older patient
- persistant hyperglycaemia
- polydypsia
- nocturia + polyuria
- glycosuria
- blurred vision
- recurrent infections
- tiredness
- acanthosis nigiricans (dark pigmentation of skin folds) suggesting insulin resistance

186
Q

What are IGT and IFG?

A

IGT = Impaired Glucose Tolerance
IFG = Impaired Fasting Glycaemia
Conditions of slightly elevated blood glucose but not high enough to be classed as diabetic so are called prediabetic states

187
Q

What is the treatment for T2DM?

A
  • Lifestyle changes (weight loss, exercise, diet changes)
  • medications to control BP, blood glucose + lipids
  • Metformin (1st line)
  • DPP-IV inhibitors (vildagliptin, sitagliptin)
  • GLP analogues (exenatide, liraglutide)
  • SGLT-2 inhibitors (empagliflozin, canagliflozin)
  • Sulphonylureas (gliclazide, glibenclamide)
  • Thiazolidinediones (pioglitazone)
188
Q

What are the actions of sulphonylureas?

A
  • Stimulate insulin release by binding to beta-cell receptors
  • improve glycaemic control at the expense of significant weight gain
    *risk of hypoglycaemia
189
Q

What are the actions of thiazolinediones?

A
  • Bind to the nuclear receptor PPARy and activate genes concerned with glucose uptake and utilisation and lipid metabolism
  • improve insulin sensitivity
  • need insulin for therapeutic effect
190
Q

What is the action of metformin?

A

improves action of insulin in reducing blood glucose

191
Q

What is the action of GLP-1 analogues?

A

They extend the duration of GLP-1 which is a gut hormone that stimulates insulin release and reduces appetite. GLP-1 analogues extend the duration of GLP-1 action and so lower blood glucose and help to reduce weight and cardiovascular disease.

192
Q

What is the action of DPP-IV inhibitors?

A

DPP-IV is an enzyme which destroys incretin, a hormone which helps the body reduce blood glucose. DPP-IV inhibitors stop the destruction of incretin and so help lower blood glucose however the effect is not highly significant and has no effect on CVD or weight.

193
Q

What is the action of SGLT2 inhibitors?

A

They inhibit the sodium glucose transporters in the renal proximal tubules, blocking the reabsorption of glucose and so increasing glucose excretion and lowering blood glucose levels.

194
Q

Define hypothyroidism

A

Abnormally low thyroid hormone levels

195
Q

What is the physiological cause of primary hypothyroidism?

A

Absence/dysfunction of thyroid gland

196
Q

What condition is the cause of most cases of primary hypothyroidism?

A

Hashimoto’s thyroiditis

197
Q

What are the physiological causes of secondary and tertiary hypothyroidism?

A

Secondary - pituitary disfunction
Tertiary - hypothalamic dysfunction

198
Q

What are the causes of primary hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • ^(131)I therapy
  • Thyroidectomy
  • Postpartum thyroiditis
  • Thyroiditis
  • Drugs
  • Iodine deficiency
  • Thyroid hormone resistance
199
Q

Which drugs can cause hypothyroidism?

A
  • Iodine (inorganic or organic)
  • Iodide
  • Iodinated contrast agents
  • Amiodarone
  • Lithium
  • Thionamides
  • Interferon-a
200
Q

What are the causes of hypothyroidism in children/neonates?

A
  • Thyroid agenesis
  • Thyroid ectopia
  • Thyroid dishormonogenesis
  • Resistance to thyroid hormone
  • Isolated TSH deficiency
201
Q

What are the clinical features of hypothyroidism?

A
  • Fatigue
  • Weight gain
  • cold intolerance
  • Constipation
  • Menstrual disturbance
  • muscle cramps
  • Slow cerebration (thinking)
  • Dry, rough skin
  • Periorbital oedema
  • Carotenaemia
  • Oedema
202
Q

What are the investigations for primary hypothyroidism?

A

Elevated TSH and usually low free T4 and T3

203
Q

What are the investigations for secondary/tertiary hypothyroidism?

A

TSH inappropriately low for reduced free T4/T3 levels

204
Q

What is the treatment of choice for hypothyroidism?

A

Synthetic Levothyroxine (T4)
- in primary dose is titrated until TSH normalises
- in secondary T4 is monitored as TSH will remain low

205
Q

What are the stages of hypertension?

A

1 - Clinic blood pressure from 140/90 to 159/99 mmHg or average HBPM from 135/85 to 149/95 mmHg

2 - Clinic BP ≥160/100 but <180/120 mmHg and HBPM average ≥150/95

3 - Clinic systolic BP ≥180 mmHg or clinic diastolic BP ≥120 mmHg

206
Q

What are some potential causes of otitis externa?

A

bacterial infection
fungal infection (aspergillus or candida)
eczema
seborrhoeic dermatitis
contact dermatitis

207
Q

What are the 2 most common bacterial causes of otitis externa?

A

pseudomonas aeruginosa
staphylococcus aureus

208
Q

What are the typical symptoms of otitis externa?

A

ear pain
discharge
itchiness
conductive hearing loss

209
Q

What signs of otitis externa can be seen on examination of the ear>

A

erythema and swelling of the ear canal
tenderness of the ear canal
pus or discharge in the ear canal
lymphadenopathy in the neck or around the ear

210
Q

What is the management for otitis externa? mild/moderate

A

mild - acetic acid (can also be used prophylactically before and after swimming)

moderate - topical antibiotic and steroid e.g. neomycin, dexamethasone and acetic acid

211
Q

What is malignant otitis externa?

A

severe and potentially life-threatening form of otitis externa where the infection spreads to the bones surrounding the ear and progresses to osteomyelitis of the temporal bone

212
Q

What is psoriasis?

A

a chronic autoimmune condition which causes recurrent symptoms of psoriatic skin lesions with a large variety in severity of presentation

213
Q

Briefly describe what patches of psoriasis look like

A

dry, flaky, scaly and faintly erythematous skin lesions which appear in raised and rough plaques

commonly occur over the extensor surfaces of the elbows and knees and on the scalp

214
Q

What are the 4 types of psoriasis?

A

plaque psoriasis - MC form in adults, features thickened erythematous plaques with silver scales

guttate psoriasis - commonly occurs in children, small raised papules across the trunk and limbs which can turn into plaques, often triggered by a strep throat

pustular psoriasis - rare, severe form of psoriasis where pustules form under areas of erythematous skin, pus is non-infectious, MEDICAL EMERGENCY

erythrodermic psoriasis - rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin, MEDICAL EMERGENCY

215
Q

WHat are 3 specific signs which suggest psoriasis?

A

auspitz sign - small points of bleeding when plaques are scraped off

koebner phenomenon - development of psoriatic lesions to areas of skin affected by trauma

residual pigmentation of the skin after the lesions resolve

216
Q

What is the management 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

217
Q

What is pelvic inflammatory disease/

A

inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix

218
Q

what is salpingitis?

A

inflammation of the fallopian tubes

219
Q

What are the causes of PID?

A

PID is usually associated an STI
neisseria gonorrhoea
chlamydia trachomatis
mycoplasma genitalium

less-commonly:
gardenerella vaginalis
haemophilus influenzae
E. coli

220
Q

What are some risk factors for PID? x6

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)

221
Q

How does PID usually present? x6

A

Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria

222
Q

What are some possible findings on examination in PID? x4

A

Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge

223
Q

What is the management for PID?

A

antibiotics depending on local and national guidelines

ceftriaxone (gonorrhoea)
doxycycline (chlamydia and mycoplasma)
metronidazole (gardnerella)

224
Q

What is Fitx-hugh-curtis syndrome?

A

a complication of PID caused by inflammation and infection of the liver capsule (Glisson’s capsule) leading to adhesions between the liver and peritoneum

225
Q

What is the definition of hypertension?

A

Blood pressure ≥140/90mmHg

226
Q

What are the initiating factors for hypertension? (8)

A

DRIED ICE
- Disturbance of autoregulation
- Renal sodium retention
- Insulin resistance/hyperinsulinaemia
- Excess sodium intake
- Dysregulation of RAAS with elevated plasma renin activity
- Increased sympathetic drive
- Cell membrane transporter changes
- Endothelial dysfunction

227
Q

Which medications increase blood pressure?

A
  • NSAIDs
  • SNRIs (serotonin and norepinephrine reuptake inhibitors)
  • Corticosteroids
  • Oral contraceptives (oestrogen containing)
  • Stimulants
  • Anti-anxiety drugs
  • Anti-TNFs
228
Q

What are the risk factors for hypertension?

A
  • age >65yrs
  • moderate/high alcohol intake
  • sedentary lifestyle
  • FH of hypertension of CAD
  • obesity
  • metabolic syndrome
  • diabetes mellitus
  • black ancestry
  • hyperuricemia
  • obstructive sleep apnoea

** Smoking is NOT a risk factor

229
Q

What is the equation for BP?

A

BP = CO x TPR

230
Q

What factors affect blood pressure?

A
  • Preload
  • Contractility
  • Vessel hypertrophy
  • Peripheral constriction
231
Q

What are the common symptoms of hypertension?

A

Most often symptomless.
- headache
- visual changes
- dyspnoea
- chest pain
- sensory of motor deficit

232
Q

What are the causes of secondary hypertension?

A

Renal disease (MC cause)
Obesity
Pregnancy or pre-eclampsia
Endocrine (T2DM, Conn’s, Cushing’s diseases)
Drugs (alcohol, steroids, NSAIDs, oestrogen)

233
Q

What is diabetic ketoacidosis?

A

Result of too much gluconeogenesis so that glucose is converted to ketone bodies which are acidic. Caused by poorly managed T1 DM or from infection/illness

234
Q

What are the signs of diabetic ketoacidosis?

A

T1DM symptoms +…
- Kussmaul breathing (deep laboured breaths to compensate for increased CO2)
- Pear drop breath (breath smells fruity due to ketones)
- Reduced tissue turgor, hypotension + tachcardia

235
Q

What are the diagnostic blood concentrations of ketones, glucose and acid in DKA?

A

Ketones >3mmol/l
Random plasma glucoe >11.1mmol/l
pH<7.3 or <15mmol HCO3-

236
Q

What is the treatment for DKA?

A
  • in an emergency ABCDE
  • 1st line always fluid (dehydration is most likely cause of death)
  • then insulin (+ glucose and postassium)
237
Q

What are the FPG and OGTT values in IGT?

A

FPG >/= 6mmol/l
2hr OGTT 7.8-11mmol/l

238
Q

What are the FPG and OGTT in IFG?

A

FPG 6.1-6.9mmol/L
2hr OGTT <7.8mmol/l

239
Q

What are the potential complications of DKA?

A
  • cerebral oedema
  • adult respiratory distress syndrome
  • thromboembolism
  • aspiration pneumonia (drowsy/comatose patients)
  • death
240
Q

What is Hashimoto’s thyroiditis?

A

An autoimmune disease which causes the immune system to attack the thyroid gland resulting in permanent hypothyroidism

241
Q

What are the symptoms of Hashimoto’s thyroiditis?

A
  • goitre
  • tiredness
  • weight gain
  • muscle weakness
242
Q

Why can insulin treatment for DKA cause hypokalaemia and why is this dangerous?

A

insulin decreases potassium levels in the blood by redistributing K+ into the cells via increased Na/K pump activity causing low serum K+ levels –> hypokalaemia
low levels of K+ can cause arrhythmia, weakness (as the heart and muscles can struggle to contract)

243
Q

What is balanitis?

A

inflammation of the glans penis

sometimes extends to the underside of the foreskin which is known as balanoposthitis

244
Q

What is the treatment for balanitis?

A

gentle saline washes and ensuring washing under the foreskin
1% hydrocortisone

if caused by candidiasis, treat with topical clotrimazole for 2 weeks
oral flucloxacillin for bacterial balanitis
circumcision can help in cases of lichen sclerosus associated balanitis
lichen sclerosus and plasma cell balanitis of Zoon are managed with high potency topical steroids like clobetasol
dermatitis and circinate balanitis are managed with mild potency topical corticosteroids e.g. hydrocortisone

245
Q

What are the common causes of balanitis?

A

candidiasis - white non-urethral discharge
dermatitis (contact or allergic) - clear non-urethral discharge
dermatitis (eczema or psoriasis)
bacterial (most commonly staph spp.) - yellow non-urethral discharge
lichen planus - Wickam’s striae and violaceous papules
lichen sclerosus (rare)
plasma cell balanitis of Zoon (rare)
circinate balanitis (can be associated with reactive arthritis)

246
Q

What is chancroid? what are the ulcers like?

A

a tropical STD caused by haemophilus ducreyi which presents with painful genital ulcers associated with unilateral, painful inguinal lymph node enlargement

the ulcers typically have a sharply defined, ragged, undermined border

247
Q

What is the treatment for chancroid?

A

macrolide antibiotics - azithromycin, ceftriaxone or erythromycin

aminoglycosides e.g. gentamycin second line

248
Q

What is lymphogranuloma venereum?

A

STI caused by chlamydia trachomatis serotypes L1, L2 and L3

249
Q

What are 3 risk factors for lymphogranuloma venereum?

A

men who have sex with men
HIV
historically seen more in the tropics

250
Q

What are the 3 stages of lymphogranuloma venereum infection?

A

1: small painless pustule which later forms an ulcer
2: painful inguinal lymphadenopathy which can form fistulating buboes
3: proctocolitis (inflammation of the rectum and colon)

251
Q

What is the treatment for lymphogranuloma venereum?

A

doxycycline

252
Q

What are genital warts and what causes them?

A

also known as condylomata accuminata

small, slightly pigmented fleshy protuberances which may bleed or itch

caused by the many varieties of the human papillomavirus HOV, especially types 6 & 11

253
Q

What is the management for genital warts?

A

1st line: topical podophyllum or cryotherapy
2nd line: imiquimod cream

often resistant to treatment

254
Q

What are the routes of transmission of HIV?

A
  • Sexual
  • Vertical (in the womb, breast-feeding)
  • Blood or bodily fluids
255
Q

What are 5 scenarios when HIV testing takes place?

A
  • Clinician indicated diagnostic testing
  • Routine screening in high prevalence locations
  • Antenatal screening
  • Screening in high risk groups
  • Patient initiated requests for testing
256
Q

What symptoms indicate risk of HIV infection?

A

With any recurrent, severe or unexplained medical condition HIV should be considered.
Common examples:
- multi-dermatomal shingles
- unexplained lymphadenopathy
- unexplained weight loss or diarrhoea, night sweats, pyrexia
- oral/oesophageal candidasis or hairy leukoplakia
- flu-like illness, rash, meningitis
- unexplained blood dyscrasias (disorders)

257
Q

What is a normal CD4 count?

A

500-1200 cells/mm3

258
Q

What is HIV?

A

Human Immunodeficiency virus, a lentivirus which uses reverse transcriptase to replicate. (retrovirus) Decimates the CD4 cell population over time causing immunodeficiency and viral load increases over time.

259
Q

When is the viral load counted as undetectable?

A

<50 copies/mL

260
Q

What are some examples of AIDS-defining illnesses associated with end-stage HIV infection? x6

A

Kaposi’s sarcoma (disease in which cancer cells are found throughout the GI tract and presents with purple patches on the skin)
Pneumocystis jivorecii pneumonia (PCP)
Cytomegalovirus infection
Candidiasis (oesophageal or bronchial)
Lymphomas
Tuberculosis

261
Q

What are the treatment options for HIV? what is the aim of treatment?

A

antiretroviral therapy medications e.g. protease inhibitors, integrase inhibitors, nucleoside reverse transcriptase inhibitors, entry inhibitors

usual starting regime = 2 NRTIs (e.g. tenofovir plus emtricitabine) plus a third agent e.g. bictegravir

aim of treatment is to achieve a normal CD4 count and undetectable viral load

262
Q

What are some additional management options for HIV patients?

A

prophylactic co-trimoxazole (for PCP)

close monitoring for cardiovascular risk factors due to increased risk

yearly cervical smears due to increased risk of HPV and cervical cancer

vaccinations

condom use to prevent spread

263
Q

What are the recommended guidelines for delivery in HIV positive patients according to viral load?

A

under 50 copies –> normal vaginal birth
over 50 copies –> consider pre-labour c-section
over 400 copies –> pre-labour c-section recommended

unknown viral load or >1000 copies –> IV zidovudine infusion during labour

264
Q

What are the usual choices of PEP and PrEP medications?

A

PEP is a combination of ART therapy: emtricitabine/tenofovir and raltegravir for 28 days

PrEP: emtricitabine/tenofovir

265
Q

What causes pubic lice?

A

pediculosis pubis is caused by Phthirus pubis, an obligate, blood-sucking ectoparasite found on pubic and perianal hairs and transmitted through sexual contact or occasionally contact with infected towels, clothing or bedding

266
Q

What is the presentation of pubic lice?

A

genital itching, usually worse at night
small blue macules or red papules may be seen at feeding sites
rust-coloured flecks of the lice’s faecal material may be seen on skin and underwear

267
Q

what is the management for pubic lice?

A

insecticides such as permethrin or malathion
decontamination of clothing and bedding and avoidance of close bodily contact until treatment is completed

268
Q

What is erectile dysfunction?

A

the persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance

it is a symptom and not a disease

269
Q

What factors favour an organic cause of erectile dysfunction? x3

A

gradual symptoms onset
lack of tumescence (swelling)
normal libido

270
Q

What features of erectile dysfunction favour a psychogenic cause x6

A

sudden symptoms onset
decreased libido
good quality spontaneous or self-stimulated erections
major life events
problems or changes in a relationship
previous psychological problems
history of premature ejaculation

271
Q

What are some risk factors for erectile dysfunction?

A

increasing age
cardiovascular disease risk factors e.g. obesity, diabetes mellitus, dyslipidaemia, metabolic syndrome, hypertension, smoking
alcohol use
drugs - SSRIs, beta-blockers

272
Q

What are the investigations for erectile dysfunction?

A

free testosterone (measured in the morning between 9-11am) - low or borderline it should be repeated with FSH, LH and prolactin and if any are abnormal referral to endo is indicated

273
Q

What is the management for erectile dysfunction?

A

Treat the cause
Lifestyle changes - stop smoking, lose weight, reduce alcohol consumption

274
Q

What are the medications used to treat erectile dysfunction?

A

phosphodiesterase inhibitors e.g. sildenafil improve relaxation of smooth muscle

vacuum erection devices

prostaglandins are used as second line drug therapy

penile prosthesis

275
Q

What are the management options for premature ejaculation?

A

selective serotonin reuptake inhibitor (SSRI)
Sertraline, Paroxetine and fluoxetine

topical anesthetic to reduce penile sensitivity, eg. lidocaine-prilocaine cream (5%) applied 20-30 minutes before sexual activity

behavioural techniques - . ‘Stop-start’ techniques, thicker condoms
taking breaks during sex

Couples therapy advice

276
Q

What are some causes of dyspareunia in women?

A

infection - especially, trichomonas, vaginal candidiasis
vaginal atrophy - postmenopausal shrinkage; infrequent intercourse
psychological - vaginismus, fear, ignorance, previous painful intercourse
poor sexual stimulation
pelvic inflammatory disease
endometriosis

277
Q

What is the treatment for dypareunia in females?

A

Management typically focuses on treating underlying causes where appropriate

A penetration desensitisation programme is useful in dyspareunia and vaginismus

Fenton’s procedure - increase the dimensions of the introitus
intramuscular injection of botulinum toxin

Psychological therapy may be useful in some patients.

if psychosexual problems persist refer her to a psychosexual therapist

278
Q

What is retrograde ejaculation? what can cause it?

A

semen passes into the bladder rather than the urethra - complication of TURP or bladder neck incision

may also occur as a result of spinal injury or DM
the patient can usually achieve an orgasm but there is no ejaculate or the volume of the ejaculate is decreased
urine may be cloudy after having sex

279
Q

What is vaginismus, and what are some common causes?

A

vaginismus is usually apparent at vaginal examination - severe spasm of the vaginal muscles and adduction of the thighs

Common causes:
- fear of intercourse
- local pain
- past history of rape, abuse or severe emotional trauma
- defence mechanism against growing up

280
Q

What is the management of vaginismus?

A

progressive relaxation to manage anxiety

densensitisation - vaginal trainers and encouraging the woman to examine herself

physiotherapy hypnotherapy
topical lidocaine applied within the vagina
antidepressants

281
Q

What are the stages of hypertension?

A

1 - Clinic blood pressure from 140/90 to 159/99 mmHg or average HBPM from 135/85 to 149/95 mmHg

2 - Clinic BP ≥160/100 but <180/120 mmHg and HBPM average ≥150/95

3 - Clinic systolic BP ≥180 mmHg or clinic diastolic BP ≥120 mmHg

282
Q

What are the 3 categories of health behaviours? Give an example of each

A

Health behaviour = behaviour aimed at preventing disease e.g. eating healthily

Illness behaviour = behaviour aimed at seeking remedy e.g. going to the doctor

Sick role behaviour = any activity aimed
at getting well e.g. taking prescribed medications, resting

283
Q

What are the determinants of health?

A

environment (physical, social and economic)

genes

lifestyle

healthcare access

284
Q

Define equity and equality

A

equity = recognises each person has different circumstances and allocates the exact resources and opportunities needed to reach an equal outcome

equality = each individual or group of people is given the same resources or opportunities regardless of circumstance

285
Q

Give an example of equality but inequity

A

Flat government subsidy for travel to work of £5 per day

Some people’s travel costs more than others e.g.

£7 - £5 = £2 to pay
£14 - £5 = £9 to pay

286
Q

Define horizontal and vertical equity

A

Horizontal equity is equal treatment for equal need e.g. all individuals with pneumonia (assuming all other things equal) should be treated equally

Vertical equity is unequal treatment for unequal need e.g. individuals with common cold vs pneumonia need unequal treatment

287
Q

What are the 3 domains of public health practice?

A

Health improvement
= societal interventions aimed at preventing disease, promoting health and reducing inequalities

Health protection
= measures to control infectious disease risks and environmental hazards

Health care
= organisation and delivery of safe, high quality services for prevention, treatment, and care

288
Q

What are the 3 levels of public health interventions?

A

Ecological (population) level
e.g. clean air act

Community level e.g. creating playground for local community

Individual level e.g. childhood immunisations

289
Q

Define primordial and quaternary preventions

A

Primordial prevention is action to prevent risk developing in healthy people who are currently not at risk
e.g. laws/health promotion put in place to discourage and prevent substance misuse

Quaternary prevention is action to prevent over treatment of patients with a condition or disease
e.g. empowering individuals to seek own outcome and avoid over-treatment and medication dependence

290
Q

What is the difference between secondary and tertiary prevention? Give an example of each

A

Secondary is focussed on early detection of illness and either curing or preventing progression/ long-term effects
e.g. mammograms to detect breast cancer early

Tertiary is centred on preventing worse outcomes or complications of a
condition or disease
e.g. reducing or controlling the symptoms and morbidity of established cancer or the morbidity caused by cancer therapy.

291
Q

Define primary prevention and give an example

A

Preventing development of a health problem when risk exists
e.g. targeted education, health promotion against recreational substance misuse

292
Q

What are the 4 stages of the planning cycle?

A

Needs assessment
Planning
Implementation
Evaluation

293
Q

What are the 5 levels in Maslow’s triangle?

A

Self-actualisation (achieving one’s full potential, including creative activities)

Esteem needs (prestige and feeling of accomplishment)

Belongingness and love needs (intimate relationships, friends)

Safety needs (security, safety)

Physiological needs (food, water, warmth, rest)

294
Q

What are the 4 categories in Bradshaw’s taxonomy of social need?

A

Felt (individual perceptions of variation from normal health)

Expressed (individual seeks help to overcome variation in normal health (demand))

Normative (professional defines intervention appropriate for the expressed need)

Comparative (comparison between severity, range of interventions and cost)

295
Q

What are the 3 approaches to health needs assessment?

A

epidemiological

corporate

comparative

296
Q

What are the leading causes of death in the UK? x5

A

Dementia and Alzheimer’s disease
Ischaemic heart disease
Chronic lower respiratory diseases
Cerebrovascular diseases
Malignant neoplasm of trachea, bronchus and lung

297
Q

What are the 4 factors which influence perceptions of risk?

A
  1. Lack of personal experience with the problem
  2. Belief that the problem is preventable by personal action
  3. Belief that if the problem has not happened by now, it’s not likely to
  4. Belief that problem is infrequent
298
Q

What are the reasons for change stated in the health belief model (Becker 1974)?

A

individuals will change if they:

  • Believe they are susceptible to the condition in question (e.g. heart disease)
  • Believe that it has serious consequences
  • Believe that taking action reduces susceptibility
  • Believe that the benefits of taking action outweigh the costs
299
Q

What is intention determined by in the theory of planned behaviour (Ajzen 1988)?

A
  • A person’s ATTITUDE to the behaviour e.g. I don’t think smoking is a good thing
  • The perceived social pressure to undertake the behaviour, or SUBJECTIVE NORM e.g. important people in my life want me to give up smoking
  • A persons appraisal of their ability to perform the behaviour, or their PERCEIVED BEHAVIOURAL CONTROL e.g. I believe I have the ability to give up smoking
300
Q

What are some limitations of the theory of planned behaviour?

A

Lack of a temporal element and direction or causality

Doesn’t take into account emotions such as fear, threat, positive affect

Doesn’t explain how attitudes, intentions and perceived behavioural control interact

301
Q

What are the stages in the transtheoretical model of behaviour change?

A

Pre-contemplation (not ready yet)

Contemplation (thinking about it)

Preparation (getting ready)

Action (doing it)

Maintenance (sticking with it)

[Relapse]

302
Q

What are some limitations of the transtheoretical model of behaviour change?

A

not all people move through every stage or in that order

change might operate on a continuum rather than in discrete stages

doesn’t take into account values, habits, emotions, culture, social and economic factors

people often change their behaviour in the absence of planning/intentions can change over a very short time period

303
Q

What is the motivational interviewing model?

A

a counselling approach for initiating behaviour change by resolving ambivalence

clinical impact shown in problem drinkers

304
Q

What is the nudge theory of behaviour change?

A

“nudge’ the environment to make the best option the easiest e.g. opt out schemes such as pensions, fruit next to checkouts

weak evidence to support efficacy of nudging in improving population health

305
Q

What is malnutrition?

A

deficiencies , excess or imbalances in a person’s intake of energy and/or nutrients. Includes undernutrition and weight excess, obesity and diet-related non-communicable disease like heart disease, stroke, diabetes,

306
Q

What chronic medical conditions require nutritional support?

A

Cancer
Cystic fibrosis
Coeliac disease
Inflammatory bowel diseases
Types 1 and 2 Diabetes Mellitus
Faltering growth
Eating disorders
Overweight, obesity
Management of sarcopenic obesity in elderly patients

307
Q

What are the 4 dimensions of food insecurity?

A

Availability
Access
Utilisation
Stability

Phase 3A (10 decks)

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