General Practise/Primary Care Flashcards

1
Q

What is Acne Vulgaris?

characterised by?

most common bacterium

common areas affected

A

Chronic Inflammatory Dermatosis

increased sebum production
follicle hyperkeratinisation
inflammation

triggered by Propionibacterium acnes

face neck upper trunk

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2
Q

Aetiology of Acne Vulgaris

A

Age : adolescents

Environment: diet, stress, pollutants

Genetics: FHX

Hormones: Androgens: testosterone, dehydroepiandrosterone sulfate - stimulated sebaceous gland activity.

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3
Q

Pathophysiology of Acne Vulgaris

A

Increased sebum production by increased androgens

lipid rich environment of sebaceous glands favouring skin micro-organism proliferation and therefore follicular occlusion.

keratinocyte proliferation further follicular occlusion. differentiation within pilosebaceous unit.

overgrowth of P.acnes

inflammation - release of IL-1/8, tnf-a cause papules,pustules,nodules,cysts

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4
Q

List of different lesions in Acne Vulgaris

A

Macules - flat skin marks
Papules - small skin lumps
Pustules - small skin lump with yellow pus
Comedomes - skin coloured papules blocked pilosebaceous unit
Blackheads - open comedomes
Ice pick scars - small indents in skin after acne lesion heal
Hypertrophic scars - small skin lump after acne lesion heal
Rolling Scars - irregular wave like skin after acne lesion heal

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5
Q

tell me a little about comedomes - acne

A

due to dilated sebacous follicle

closed - white - obstructed completely
open - black - partially obstructed

non inflammatory lesion.

hyperkeratinisation caused increased sebum production.

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6
Q

Tell me about papules and pustules - acne

A

when the follicle bursts releasing irritants

inflammation around blocked follicle- papules

papule - papule with pus because of neutrophil infiltration.

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7
Q

tell me a little about nodules and cysts - acne

A

severe inflammatory response.
macrophages,lymphocytes, plasma cells and tissue destruction causing fibrosis.

nodules - firm lumps under skin
cysts - fluctuant due to liquified necrotic material in fibrous tissue.

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8
Q

what would you see in drug induced acne

A

monomorphic

pustules in steroid use

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9
Q

what acne fulminans

A

severe acne with systemic upset like a fever

hospital admission required

oral steroids - tx

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10
Q

How would you treat Acne Vulgaris

A

mild - open/closed comedomes with/without sparse inflammatory lesions
moderate - widespread non-inflammatory and papules/pustules
severe: extensive inflammatory lesions

mild-moderate: 12 week course of topical combo therapy 1st line
1. fixed combo - topical adapalene + topic benzoyl peroxide
2. fixed combo - topical tretinoin + topical clindamycin
3. fixed combo - topical benzoyl peroxide + topical clindamycin

could use benzoyl peroxide as monotherapy if contraindicated

moderate- severe: 12 week course of:
1. fixed combo topical adapalene + topical benzoyl peroxide
2. fixed combo - topical tretinoin + topical clindamycin
3. fixed combo - topical adapalene + topical benzoyl peroxide+ either oral lymecycline/doxycycline
4. topical azelaic acid+ either oral lymecycline/doxycycline

oral isotretinoin: not pregnancy - specialist supervision

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11
Q

who would you avoid tetracycline in and why?

A

pregnancy
breastfeeding women
children under 12.

use erythromycin instead in pregnancy.

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12
Q

side effect of minocycline - acne tx

A

possible irreversible pigmentation

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13
Q

why should you give topical retinoid with oral abx

A

reduce the risk of abx resistance developing.

dont combine topical and oral abx

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14
Q

complication of long term abx use

how would you treat

A

gram negative folliculitis

tx: high dose oral trimethoprim

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15
Q

name an alternative to oral abx in women for acne tx?

side effects

A

combined oral contraceptive
combine with topical agents

dianette (co-cyprindiol) - anti-androgen properties.

increased risk of vte - use 2nd line - only for 3 months.

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16
Q

rules for administering abx - acne

A

don’t combine topical and oral abx
monotherapy with oral abx
mono with topical abx

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17
Q

what is acne conglobate?

A

rare and severe of acne found mostly in men that presents with extensive inflammatory papules, suppurative nodules and cysts on the trunk.

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18
Q

side effect of tetracycline

A

teeth discoloration if used in children under 8 years or pregnant.

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19
Q

side effect of isotretinoin

A

its potent oral retinoid used for severe acne

teratogenicity
hyperlipidaemia
hepatotoxicity

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20
Q

side effects of isotretinoin

A

dry skin and lips
photosensitivity of skin to sunlight
depression, anxiety, aggression and suicidal ideation.

rarely Steven-Johnson syndrome and toxic epidermal necrolysis

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21
Q

tell me a little bit about isotretinoin

A

retinoid
reducing inflammation and reducing bacterial growth.

teratogenic.

stop it at least a month before becoming pregnant.

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22
Q

What is Acute Bronchitis?

leading cause
resolve time

A

chest infection
self-limiting

inflammation of trachea and major bronchi

associated with oedematous large airways and sputum production.

resolves in 3 weeks.

viral infection - leading cause

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23
Q

Clinical Features of Acute Bronchitis

A

cough - could be productive
sore throat
rhinorrhoea
wheeze

most have normal chest exam some have:
low grade fever
wheeze

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24
Q

how would you investigate acute bronchitis

A

clinical diagnosis
crp testing to guide whether to give abx.

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25
differentials for acute bronchitis
pneumonia if: sputum wheeze breathlessness - at least 1 focal chest signs - dullness to percussion, crepitations and bronchial breathing systemic features - malaise myalgia and fever
26
how would you manage acute bronchitis
analgesia fluids abx if: systemically unwell , pre-existing comorbidities crp of 20-100 - delayed prescription crp over 100 mg/L - abx immediate. DOXYCYCLINE - 1ST LINE . - not in kids or pregnant. - amoxicillin alternative
27
What is Acute Stress Reaction?
psychological shock following exposure to severe stress/traumatic event.
28
pathophysiology of acute stress reaction
acute disruption in homeostasis due to stress hyperarousal of sympathetic nervous system. releases adrenaline and cortisol physical and psychological symptoms.
29
Aetiology of Acute Stress Reaction
Genetic Predisposition : serotonin transporter gene and dopamine receptor D2 gene. Prior Psych Hx. Neurobiological faqctors: dysregulation of HPA axis and altered amygdala function traumatic incident. sudden life change socioeconomic status coping mechanisms social support lack of
30
differentials for acute stress reaction
panic disorder - intense fear, sweating, shaking but difference is trigger. panic attacks are recurrent unexpected but ASR is acute single episode. PTSD - both traumatic event. PTSD must be following 1 month after trauma. ASR resolves within 4 weeks. adjustment disorder - anxiety and depressed mood both. develops gradually over time to life stresses rather than acute traumatic event.
31
Clinical Features of Acute Stress Reaction
pt with traumatic event, cognitive behavioural and physiological responses. immediately after, can be few hours or days post trauma. cognitive: - confusion/disorientation - intrusive thoughts - derealisation and depersonalisation behavioural: -avoidance -hypervigilance physiological sx : - tachycardia and htn - sweating and trembling non-specific: - insomnia -irritability -fatigue -GI disturbances
32
how would you manage acute stress reaction?
immediate: - psychological 1st aid: calm supportive environment, basic needs met, active listening -if severe: possible short term benzodiazepines or antipsychotics. ongoing mx: - CBT -mindfullness -if sx persist: ptsd assess follow-up: - monitor - refer to mental health cultural consideration: - be sensitive educational resources: - pt education on ASR reduces fear and uncertainty. - give info on common reactions to trauma, coping strategies.
33
What is an allergy?
hypersensitivity of immune system to allergens which are proteins that the immune system see as foreign. these proteins are antigens
34
what is the skin sensitisation theory of allergy?
break in infants skin - allows allergens to cross the skin and react with immune system. child doesnt have contact with allergen from gi tract - absence of gi exposure to allergen.
35
name some conditions as a result of hypersensitivity reactions
asthma atopic eczema allergic rhinitis hayfever food allergies animal allergies
36
tell me about the coombs and gell classification
underlying pathology of different hypersensitivity reactions TYPE 1 - IGE antibodies to specific allergen trigger mast cells and basophils , release histamines and other cytokines. TYPE 2 - IGG AND IGM antibodies. react to allergen activate complement system, direct damage to local cells. eg: transfusion reactions, haemolytic disease of newborn. Type 3 - immune complexes accumulate, damage to local tissues. SLE, RA , henoch-schonlein purpura type 4 - cell mediated hypersensitivity caused by t lymphocytes. t cells inappropriately activated = inflammation= damage to lcoal tissue. eg: organ transplant rejection, contact dermatitis
37
investigations in allergy
skin prick testing RAST - bloods for total and specific immunoglobulin E (IgE) food challenge testing. - gold standard. takes time. skin prick and RAST assess sensitisation not allergy.
38
how does skin prick testing work?
drop of each allergen at marked points. with water control histamine control fresh needle makes tiny break in skin at site of allergen. after 15 mins size of wheals to each allergen checked. compare to controls
39
what is patch testing?
most helpful in allergic contact dermatitis. not for food allergy. latex perfume cosmetics plants. patch on pt skin. 2-3 days , skin reaction to patch checked.
40
what is RAST testing
measures total and allergen specific IgE quantities in blood. in eczema and asthma, itll come back positive for everything u test.
41
how would you manage allergy?
establish allergen and avoid hoover and change sheets stay indoors when high pollen prophylactic antihistamines give adrenaline auto-injector for at risk pt of anaphylaxis potentially immunotherapy? - exposure over months to allergen
42
following exposure how would you manage allergy?
antihistamine - cetrizine steroids - predinisolone , topical hydrocortisone or iv hydrocortisone intramuscular adrenaline - anaphylaxis antihistamine and steroid - dampen immune response.
43
What is an Anal Fissure? what is anoderm?
longitudinal tear in anoderm commonly caused by increased anal resting pressure, trauma and constipation anoderm is specialised squamous epithelium lining distal anal canal peak incidence: 30-40
44
Aetiology of Anal Fissure
young adults and middle aged. primary idiopathic - no clear cause. could be : increased anal resting pressure: elevated internal anal sphincter pressure. reduced blood flow to anorderm = ischemic injury. trauma - hard stools constipation/straining: increased pressure in anal canal. secondary anal fissure - underlying condition IBD - chrons and uc - inflammaiton in rectum and anus. infectious: STI eg syphilis, hsv, hiv malignancy: presenting sx of anal/rectal malignancy. other causes: iatrogenic during surgery, radiation proctitis.
45
what is a chronic anal fissure?
fibrosis and hypertrophy of anal papilla and sentinel pile formation. can get granulation tissue which further impairs healing process
46
classifying anal fissure where most anal fissures occur?
acute - less than 6 weeks chronic - more than 6 weeks 90% - posterior midline
47
Clinical Features of Anal Fissures
Pain - sharp severe localised to anus. during and after bowel movement most intense. mins to hours. can lead to avoidance of bowel movement and constipation. Bleeding - bright red on toilet paper or bowel. minimal, self-limiting. Pruritis ani : itching around anus - particularly in chronic constipation : avoid of bowel movements
48
key findings on physical examination of anal fissure patient Visual Inspection Gental Palpation DRE
Visual Inspection: erythema,oedema,discharge. linear tear in anoderm could have sentinel pile (hypertrophied skin tag) at distal end. Gental Palpation: localised tenderness or induration. sentinel pile could be small firm nodule DRE: with caution, extreme pain. assess tone of anal sphincter. check for mass, strictures or abnormalities.
49
How would you manage anal fissure?
if less than 6 weeks: - diet - high fibre high fluid - bulk forming laxative 1st line - if not lactulose - lubricant before shitting -topical anaesthetics -analgesia - NO TOPICAL STEROIDS over 6 weeks: - above techniques -topical gtn -1st line for chronic - if gtn not effective after 8 weeks then secondary care - surgery or botulinum toxin
50
What is Anaphylaxis?
life threatening systemic hypersensitivity reaction. type 1 hypersensitivity reaction IgE mediated.
51
how does anaphylaxis happen?
IgE stimulated mast cells to rapidly release histamine and other pro-inflammatory chemicals. = mast cell degranulation. u get rapid onset of sx. airway breathing circulation compromise.
52
triggers of anaphylaxis
variety of allergens foods - peanuts, tree nuts, fish milk eggs insect venom - bees wasps fire ants meds - penicillin , nsaids latex: natural rubber latex. idiopathic: unknown
53
clinical features of anaphylaxis airway breathing circulation issues
airway : swelling of throat and tongue - hoarse voice and stridor breathing: respiratory wheeze, dyspnoea circulation problems: hypotension, tachycardia 80-90% pts have skin and mucosal changes: generalised pruritus widespread erythematous or urticarial rash.
54
presentation of anaphylaxis
pt with hx of allergy - can be idiopathic tho rapid onset: - urticaria -itching -angio-edema - swelling around lips and eyes - abdo pain -sob -wheeze -swelling of larynx causing stridor -tachy -lightheaded -collapse
55
how would you manage anaphylaxis?# a b c d e
intramuscular adrenaline under 6 months : 100-150 micrograms- 0.1-0.15 ml 1 in 1000 6months-6yrs - 150 micro - 0.15ml 6-12 yrs - 300 micro 0.3ml 12+ - 500 micro 0.5 ml 1 in 1000 repeat every 5 mins if necessary. im - anterolateral aspect of middle third of thigh a - secure airway b - give ox if needed. salbutamol with wheeze c - iv fluids d - lie flat improve cerebral perfusion e - check for angiodema urticaria flushing
56
what is refractory anaphylaxis?
respiratory/cardio problems despite 2 doses of im adrenaline iv fluids for shock
57
once youve stabilised an anaphylaxis pt then what to do?
non sedating oral antihistamine- if urticaria - chlorphenamine/cetrizine can give steroid: iv hydrocortisone check serum tryptase levels - stay high 12 hrs following anaphylaxis - check if it actually was this adrenaline injector - give interim measure. - 2 of them - teach how to use
58
discharging after anaphylaxis
2 hrs after sx stopped if: - single dose 6 hrs : 2 doses or previous biphasic reaction 12 hrs: severe reaction over 2 doses. severe asthma. late night presentation.
59
how to use an adrenaline autoinjector?
remove safety cap on non needle end. - blue cap on epipen and yellow on jext grip device in a fist with needle pointing down. - orange in epi black on jext. - dont put thumb over end. adminster firmly jabbing into outer portion of mid thigh until device clicks. - can do thru clothing. epi hold for 3 seconds jext 10 seconds remove massage area 10 seconds phone ambulance. second dose after 5 mins if needed.
60
What is generalised anxiety disorder?
excessive worry about number of different events. sx persistent ocurring most days for at least 6 months and not caused by substance use or another condition. more females than men
61
clinical features of generalised anxiety disorder
excessive and persistent worry about events at least 6 months difficulty controlling worry restlessness , on edge fatigue irritable muscle tension sleep disturbance significant distress or impairement difficulty concentrating or mind going blank
62
what medications could trigger anxiety? alternative causes of anxiety?
salbutamol theophylline corticosteroids antidepressants caffeine cocaine hyperthyroidism cardiac disease phaeochromocytoma cushings substance withdrawal - alcohol, benzodiazepine
63
how would you manage generalised anxiety disorder?
monitor low intensity psychological intervention - self-help or group education high intensity psycological intervention - CBT/drug tx (1st line SSRI sertraline) - high specialist input - multi agency team
64
what is panic disorder?
recurring panic attacks. unexpected. worry about further attacks. maladaptive behaviour changes related to attacks - avoiding activities.
65
how would you manage panic disorder?
1. diagnosis 2. tx in primary care - cbt or ssri 1st line. if ci'd or no response after 12 weeks give imipramine or clomipramine. 3. review 4. refer to mental health 5. care in specialist mental health
66
presentation of panic attacks
sudden intense physical and emotion sx of anxiety. last short time like 10 mins max. physical sX: tension palpitations tremors sweating dry mouth chest pain sob diziines nausea emotional sx: panic, fear,danger,depersonalisation, loss of control
67
phobia examples closed space heights spider public speaking needles
extreme fear of situations - claustrophobia - closed space acrophobia- heights arachnophobia- spider glossophobia - public speaking trypanophobia - needles
68
what is the questionaire to assess severity of anxiety?
GAD-7 seven questions. 5-9 : mild anxierty 10-14 : moderate 15-21 = severe
69
why might propanolol be given in anxiety tx?
doesnt treat anxiety. nonselective beta blocker treats physical sx of anxiety. reduces SNS overactivity. stops palpitations tremors and sweating contraindication: ASTHMA - causes bronchoconstriction.
70
how do benzodiazepines work for anxiety? NOT RECOMMENDED TO USE
STIMULATE GABA RECEPTOR RELAXING EFFECT OF BRAIN.
71
What is obsessive compulsive disorder?
obsession: unwanted intrusive thought,image or urge. compulsion: repetitive behaviour or mental act that person driven to do. can be overt or seen by others.
72
Aetiology of ocd
genetic psychological trauma paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS) associations: depression schizophrenia sydenams chorea tourettes syndrome anorexia nervosa
73
Clinical Features of ocd
obsessive: - contamination fears - harm related obsession -unwanted sexual thoughts -religious/moral obligations -perfectionisms/symmetry compulsions: - cleaning/washing -checking rituals - counting/repeating rituals -ordering/arranging behaviour -mental neutralizing strategies
74
how would you diagnose ocd? Tx
yale brown obsessive compulsive scale - Y-BOCS : severity of obsessions and compulsions DSM-5 ICD-11 obsessive-compulsive inventory-revised: OCI-R : self report questionaire asesses severity. DBT
75
how would you manage ocd?
if functional impairement mild: - CBT and response prevention (ERP) - if not then SSRI or more intensive CBT if moderate functional impairement: - SSRI any but if body dysmorphic disorder then fluoxetine. or more intensive CBT including ERP if severe: - combined ssri and cbt ssri continue at least 12 months - prevent relapse if ssri ineffective try another can give clomipramine - TCA
76
WHAT IS ERP? - ocd?
psychological method expose pt to anxiety provoking situation stopping them engaging in their usual safety behaviour.
77
cycle of ocd
obsession anxiety compulsion temporary relief
78
how to measure bmi?
weight (kg) / heigh (m) squared underweight - under18.49 normal 18.5-25 overweight 25-30 obese class 1 30-35 2 - 35-40 3 - over 40
79
how would you manage obesity
diet and exercise med: orlistat (pancreatic lipase inhibitor) , liraglutide surgical
80
when can orlistat be prescribed? side effects
faecal urgency/incontinence flatulence bmi of 28 or more with associated risk factors or bmi of 30 or more continued weight loss eg 5% at 3mnths use for lss than1 yr.
81
what is liraglutide? when to use?
as adjunct for weight loss in class 2 obese glucagon like peptide 1 mimetic - use in t2dm once daily sub cut bmi at least 35 prediabetic hyperglycaemia
82
types of bariatric surgery primarily restrictive primarily malabsorptive mixed
primarily restrictive operations: laparoscopic-adjustable gastric banding - LAGB - 1st line for bmi 30-39 - less weight loss than malabsorption or mixed but fewer comps. - sleeve gastrectomy - stomach reduced to 15% of original size -intragastric baloon - baloon left in stomach for 6 months max primarily malabsorptive options: - biliopancreatic diversion with duodenal switch - only for very obese - bmi over 60 mixed: roux-en-y gastric bypass surgery - restrictive and malabsorptive
83
obesity in pregnancy is defined as:
bmi over or equal to 30 at first antenatal visit
84
Maternal Risks of obesity for pregnancy
miscarriage vte gestational diabetes pre-eclampsia dysfunctional labour, induced labour postpartum haemorrhage wound infections higher risk of C section
85
fetal risks of obesity - pregnancy
congenital anomaly prematurity macrosomia stillbirth increased risk of developing obesity and metabolic disorders in childhood neonatal death
86
Management of obesity in pregnancy
tell them not to diet. 5mg of folic acid rather than 400mcg screen for gestational diabetes with ogtt at 24-28 weeks if bmi 35 or more consultant led birth. if bmi 40 or more antenatal consultation with obs anaesthetist and make plan
87
What is the whooping cough? (pertussis)
gram negative bacterium bordetella pertussis causing infectious disease. children. cough of 100 days.
88
immunisation against whooping cough (pertussis)
routinely immunised at 2,3,4 months and 3-5 years. vaccination for pregnant women. neither infection nor immunisation = lifelong protection. 16-32 weeks pregnant give vaccine
89
features of whooping cough (pertussis)
catarrhal phase: sx similar viral urti. lasts 1-2 weeks. mild coryzal sx. - poss mild dry cough. paroxysmal phase: cough increases in severity. - worse at night, after feeding, ended by vomiting, associated central cyanosis. - inspiratory whoop: not always present - caused by forced inspiration against closed glottis. - infants: poss spells of apnoea. - persistent coughing may cause subconjunctival haemorrhages or even anoxia leading to syncope and seizures. - lasts between 2-8 weeks convalescent phase: - cough subsides over weeks to months
90
diagnostic criteria for whooping cough - pertussis
suspect if person has acute cough lasted for 14 days or more without another apparent cause and 1 of: - paroxysmal cough -inspiratory whoop -post-tussive vomiting -undiagnosed apnoeic attacks in young infants
91
how to diagnose whooping cough
per nasal/nasopharyngeal swab culture for bordetella pertussis - may take several days or weeks to come back PCR and serology are now increasingly used as their availability becomes more widespread per nasal with pcr - within 2-3 weeks. if cough present more than 2 weeks test for anti-pertussis toxin immunoglobulin G. - test in oral fluid of kids 5-16 and in blood over 17.
92
how would you manage whooping cough? is it a notifiable disease?
infants under 6 months with suspected pertussis - admit notifiable disease oral macrolide - (clarithromycin, azithromycin or erythromycin) - if onset of cough is within previous 21 days to eradicate the organism give household contacts abx prophylaxis abx : doesnt alter course of illness school exclude: 48 hrs after commencing abx ( or 21 days from onset if no abx)
93
complications of whooping cough
subconjunctival haemorrhage pneumonia bronchiectasis seizures if cough really hard can pneumothorax vomit faint.
94
What is roseola infantum?
infancy caused by human herpes virus 6 incubation 5-15 days. affects children aged 6 months to 2 yrs. no need school exclusion
95
features of roseola infantum
high fever - lasting a few days followed later by: - maculopapular rash - nagayama spots: papular enanthem on uvula and soft palate -febrile convulsion in 10-15% - diarrhoea and cough commonly seen
96
possible consquences of hhv6 other than roseola infantum? main complication of it
aseptic meningitis hepatitis febrile convulsions due to high temperature. immunocompromised at risk of : - myocarditis -thrombocytopenia -Gullain barre syndrome
97
what is an exanthem?
eruptive widespread rash. 6 viral exanthemas : first,2,3,4,5,6 first: measles second: scarlet fever third: rubella (german measles) fourth: dukes disease 5th: parvovirus b19 6th: roseola infantum
98
tell me about measles caused by contagious? spread? sx start sx when does it resolve? isolated? notifiable?
measles virus. RNA paramyxovirus spread by aerosol tranmission infective from prodome until 4 days after rash starts. incubation: 10-14 days highly contagious via resp droplets. sx start 10-12 days after exposure with fever coryzal sx and conjunctivitis. koplik spots: greyish white spots on buccal mucosa. - 2 days after fever. pathognomic for measles. rash starts on face: behind ears, 3-5 days after fever. spread to rest of body. erythematous macular rash with flat lesions. self resolving: 7-10 days of sx. isolate kid until 4 days after sx resolve. notifiable disease - report to public health.
99
complications of measles
pneumonia diarhoea dehydration encephalitis meningitis hearing loss vision loss death
100
what is scarlet fever? associated with ? whats it caused by?
group a haemolytic streptococcus infection, usually tonsillitis. not virus. children 2-6 yrs old. peak at 4 respiratory route spread by inhaling or ingesting resp droplets or by direct contact with nose and throat discharges. caused by a exotoxin produced by streptococcus pyogenes (group a strep) bacteria.
101
presentation of scarlet fever features
red-pink blotchy macular rash with rough "sandpaper" skin that tarts on the trunk and spreads outwards. red flushed cheeks. - desquamination in later course of illness , esp around fingers and toes - fine punctuate erythema (pinhead) which generally appears 1st on the torso and spares the palms and soles. - children flushed with circumoral pallor. rash obvious in flexures. fever lethargy flushed face sore throat strawberry tongue cervical lymphadenopathy
102
treatment of scarlet fever
abx for underlying strep infection. phenoxymethylpenicillin (pen v ) for 10 days. notifiable disease. - report to public health. children no school until 24 hrs after starting abx.
103
other than scarlet fever what 2 other conditions can you have associated with group a strep infection?
post-streptococcal glomerulonephritis acute rheumatic fever
104
tell me about rubella its cause? contagious? spread/ sx start? incubation? presentation?
rubella virus - togavirus. after mmr its very rare. incubation: 14-21 days highly contagious respiratory droplets 2 weeks after exposure infectious from 7 days before sx appear to 4 days after onset of rash milder erythematous macular rash compared to measles. rash start on face and spread to rest of body. last 3 days. mild fever joint pain sore throat enlarged lymph nodes (lymphadenopathy) behind ears and back of neck.
105
mx of rubella
supportive. self limiting. notifiable disease no school 5 days after rash comes. avoid pregnant women non immune mothers: give MMR vaccination in post-natal period. dont give MMR vaccine to women known to be pregnant or attempting to become it!
106
comps of rubella
thrombocytopenia encephalitis dangerous in pregnancy: congenital rubella syndrome : triad of deafness blindeness and congenital heart disease
107
what is dukes disease?
no identifable organism viral or bacterial cause. 4th disease. non specific viral rashes.
108
parvovirus b19 tell me about it other names of it caused by presentation
5th disease slapped cheek syndrome erythema infectiosum caused by parvovirus b19 mild fever coryza non specific viral sx: muscle aches and lethargy. after 2-5 days, rash appears quite rapidly: diffuse bright red rash on both cheeks few days later reticular mildly erythematous rash affecting trunk and limbs appear can be raised and itchy. (Reticular means net-like)
109
management of parvovirus b19 do you need to stay off school?
self-limiting illness rash and sx fade over 1-2 weeks. manage supportively with plenty of fluids and simple analgesia. its infectious before rash forming once its formed its not so you dont need to stay off school.
110
what patients are at risk of complications complications of parvovirus b19
immunocompromised pregnant women sickle cell anaemia,thalassaemia,hereditary spherocytosis, haemolytic anaemia. so you do serology testing for parvovirus to confirm - check fbc and reticulocyte count for aplastic anaemia. aplastic anaemia encephalitis or meningitis pregnancy comps: fetal death rarely hepatitis, myocarditis or nephritis
111
women exposed early in pregnancy (before 20 weeks) what to do ? parvovirus
check maternal IgM and IgG
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other presentations of parvovirus
asymptomatic pancytopenia in immunosuppressed patients aplastic crises eg sickle cell disease - parvovirus b19 suppresses erythropoiesis for about a week so aplastic anaemia is rare unless there is chronic haemolytic anaemia - hydrops fetalis - parvovirus b19 in pregnant women can cross placenta in pregnant women. - causes severe anaemia due to viral suppression of fetal erythropoiesis = hf secondary to severe anaemia = accumulation of fluid in fetal serous cavities (ascites, pleural and pericardial effusions) - tx : intrauterine blood transfusions
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how would you diagnose scarlet fever?
throat swab - abx commence immediately dont wait for results
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scarlet fever is usually a mild illness but may be complicated by what and why?
otitis media : mc comp rheumatic fever: typically 20 days after infection acute glomerulonephritis: 10 days after infection invasive comps (bacteraemia, meningitis, necrotizing fasciitis) rare but might present acutely wit life-threatening illness
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features of measles
prodromal phase: - irritable -conjunctivitis -fever koplik spots: - typically develop before rash - white spots (grain of salt) on the buccal mucosa rash: - starts behind ears then to the whole body - discrete maculopapular rash becoming blotchy and confluent - desquamation that spares palms and soles might happen after a week diarhoea - 10% pts
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how would you investigate measles
IgM antibodies - within few days of rash onset
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how would you manage measles
mainly supportive admission considered in immunosuppressed or pregnant patients notifiable
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complications of measles
otitis media: mc comp pneumonia: mc cause of death encephalitis: typically occurs 1-2 weeks following onset of illness subacute sclerosing panencephalitis: very rare, might present 5-10 yrs following an illness febrile convulsions keratoconjunctivitis, corneal ulceration diarhoea increased incidence of appendicitis myocarditis
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how would you manage contacts of measles?
give within 72 hours if child not immunised against measles comes into contact with measles then MMR should be given. vaccine induced measles antibody develops more rapid that natural infection post.
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complications of rubella
arthritis thrombocytopenia encephalitis myocarditis
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features of rubella
prodome: low grade fever rash: maculopapular, initially on the face before spreading to whole body, usually fades by 3-5 day lymphadenopathy: suboccipital and postauricular
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features of congenital rubella syndrome?
sensorineural deafness congenital cataracts congenital heart disease (pda) growth retardation hepatosplenomegaly purpuric skin lesions salt and pepper chorioretinitis microphthalmia cerebral palsy
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how would you diagnose rubella?
discuss with HPU IgM antibodies raised in women recently exposed to virus very difficult to distinguish rubella from parvovirus b19 clinically. important to check parvovirus b19 serology 30% risk of transplacental infection, with a 5-10% risk of fetal loss
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venous ulceration, typically seen where?
medial malleolus
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ix of venous ulceration how could you get a false negative result?
ankle-brachial pressure index (abpi) - important in non-healing ulcers to assess for poor arterial flow which could impair healing. "normal" abpi might be regarded as between 0.9-1.2. below 0.9: arterial disease. above 1.3: artieral disease. false negative result: secondary to arterial calcification (in diabetic)
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how would you manage venous ulceration?
compression bandaging - 4 layer - only tx that acc helps oral pentoxifylline - peripheral vasodilator, improves healing rate. small evidence base supporting use of flavinoids hydrocolloid dressing,topical growth factors, uss therapy and intermittent pneumatic compression - doesnt help
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What is bursitis?
Inflammation of a bursa, small fluid filled sac that cushions and reduces friction between bones, tendons and muscles around the joints.
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common locations of bursitis?
Shoulder (subcromial) - Overhead activities, repetitive arm movement Elbow (olecranon) - Leaning on elbows “student’s elbow” Hip (trochanteric) - Runners or prolonged standing Knee (prepatellar or anserine). Common in people who kneel often Heel (retrocalcaneal)
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how does bursitis occur and present?
Causes: - Friction from repetitive movements - Trauma - Inflammatory arthritis - Infection (Septic bursitis) Presentation: - Swollen, warm, tender, fluid filled - If infection: Hot, more tender, redness to surrounding skin, fever, features of sepsis. Consider septic arthritis if reduced ROM
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what do the various joint aspirations result suggest for bursitis?
Pus - Infection Straw coloured fluid - Less likely to be infeced Blood stained - Trauma, infection, inflammatory cause Milky - Gout/Pseudogout Fluid should be sent for MCS
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mx of bursitis?
Reduce activity of affected joint Ice Compression Elevation Analgesia Steroid injections and aspiration may help
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Functions of kidney
AWETBED Acid-base homeostasis Water balance Electrolyte balance Toxin/waste product removal Blood pressure control Ertyhropoietin D (vitamin D activation)
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bp targets in ckd
140/90 or 130/80 if coexisting diabetes ACEi used (reduce filtration pressure, less proteinuria)
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define aki
A sudden decline in kidney function leading to a rise in serum creatinine and fall in urine output. Dysregulation of - Fluid balance - Acid-base homeostasis - Electrolyte imbalance
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drugs to stop in AKI
DAAMN D - Diuretics A - ACEi/ARB A - Aminoglycosides M - Metformin N - NSAIDs ACEi/ARB protective in Chronic
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6 pre renal causes of AKI
Hypoperfusion Hypovolaemia (bleeding, reduced cardiac output (CHF), cardiogenic shock) Liver failure (hypoalbuminaemia) Renal artery blockage/stenosis ACEi & NSAID Sepsis causing systemic vasodilation Dehydration
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4 intrarenal causes of aki
Intrinsic disease of kidney Acute tubular necrosis Acute interstitial nephritis (these 2 can be drug induced) Glomerulonephritis Small vessel vasculitis
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4 post renal causes of aki
Obstruction to urinary outflow, causing back pressure into kidney. (Obstructive uropathy) - BPH - Urolithiasis - Cervical and prostate cancer - Bladder neck stricture
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electrolyte consequence of AKI
Hyperkalaemia and azotaemia (increased blood creatinine and urea) Metabolic acidosis
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Symptoms of pre renal AKI
Hypotension Reduced capillary refill Dry mucus membranes Reduced skin turgor Cool extremities
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intrarenal aki symptoms
Infection/ signs of underlying disease (vasculitis, glomerulonephritis etc)
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post renal aki symptoms
Loin to groin pain Haematuria Palpable bladder/prostate Prostatic urinary issues (dysuria, terminal dribbling, hesitancy)
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causes of acute tubular necrosis
Ischaemia - Pre renal disease Nephrotoxicity - (aminoglycosides, chemotherapy), contrast in CT, myoglobin, multiple myeloma
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define ckd
Progressive deterioration in renal function over at least 3 months characterised by eGFR of <60ml/min/1.73m²
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what 2 tests are considered in CKD classification?
eGFR and albumin:creatinine ratio
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how is eGFR used to stage ckd?
Stage 1 - >90 (normal) Stage 2 - 60-89 (mild reduction, only CKD if symptoms) Stage 3a - 45-59 (mild-moderate reduction) Stage 3b - 30-44 (moderate-severe reduction) Stage 4 - 15-29 (severe reduction) Stage 5 <15 (End stage kidney failure)
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how is albumin:creatinine ratio used to stage CKD?
Checks proteinuria to give A score A1 - <3mg/mmol A2 - 3-30mg/mmol A3 - >30mg/mmol
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what can be used as evidence of renal damage?
Albuminuria (ACR>3) Electrolyte abnormalities Histological abnormalities Structural abnormalities on imaging Kidney transplant history Urine sediment abnormalities
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at what egfr is metformin contraindicated?
<30ml/min/1.73² (stage 3b)
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causes of ckd
Most common: Diabetes and HTN Nephrotoxic drugs Glomerulonephritis Systemic disease e.g. rheumatoid arthritis/SLE
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how does ckd lead to its complications?
low eGFR = azotaemia (which can cause encephalopathy and pericarditis) Urea affects platelet function (bleeding) Uremic frost (urea crystals in skin) Kidneys normally activate vit D. No activation = hypocalcaemia = PTH secretion = bone resorption (renal osteodystrophy) Low fluid to kidney = RAAS activation = HTN HTN causing increased intraglomerular pressure - causing shearing and loss of selective permeability (protein/haematuria) Kidneys produce less EPO = Anaemia
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signs/symptoms of ckd
Asymptomatic at first Uraemic frost (tiny yellow white urea crystals on skin) Uraemia swallow (pale/brown colour on skin) Pallor Fatigue Lethargy Frothy urine Swollen ankles/oedema Increased bleeding
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what does anaemia, with low calcium and low phosphate imply?
ckd
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ix in ckd
Urine dipstick - Haematuria, glycosuria eGFR and urine albumin:creatinine ratio U&E FBC - Normocytic normochromic anaemia Bone profile/PTH - Ca2+ low, phosphate high, PTH high, ALP high Renal ultrasound Bilateral kidney atrophy (small kidneys)
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comps of ckd
Anaemia (EPO reduced) Osteodystrophy (decreased vit D activation) Neuropathy/encephalopathy Pericarditis
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mx of ckd
No cure except transplant, can only treat symptoms Anaemia - EPO + Iron Osteodystrophy - Vit D supplementation CVD - ACEi + statins Oedema - Diuretics (ACEi help in CKD but harm in AKI)
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what is RRT and what are its indications?
Renal replacement therapy - Persistent severe complications (electrolyte, oedema, uraemia) or Stage 5 CKD AEIOU Acidosis > 7.2 - Acidosis not helped by sodium bicarbonate Electrolytes K+>7mmol/L Intoxication - Stage 5 CKD Oedema Uraemic pathology - Encephalopathy, pericarditis etc
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what are the types of RRT?
Haemodialysis (most common) - Blood taken from artery, filtered and returned into vein at AV fistula. - 3x4 hours a week - Complications: hypotension, nausea, chest pain, infected catheter (sepsis) Peritoneal dialysis - Peritoneal catheterisation, exchange of solutes across peritoneal membrane - Done at home - Complications: Peritonitis, abdominal wall hernia
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causes of ckd mineral bone disease
Reduced 1-alpha hydroxylase activity (reduced vit D activation) Reduced renal excretion of phosphate (phosphate stimulates bone resorption)
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tx of ckd mineral bone disease
Reduced dietary phosphate (fish, meat, poultry) Vit D replacement (calcitriol is already 1-alpha-hydroxylated) Phosphate binders Bisphosphonates
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copd risk factors
Age (>40) Smoking (biggest) Air pollution Occupational exposure (coal, cement, dust, smelting) Frequent respiratory infections Gender (men) Alpha 1 anti-trypsin deficiency- (young patients presenting with COPD!!)
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O2 saturation targets for a normal person and for someone with an acute COPD exacerbation. And at what O2 sats is someone considered hypoxic
Normal: 95-100% COPD exacerbation: 88-92% (normal COPD maintained above 92%) Normal <94% COPD exacerbation <88%
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What 2 organisms usually cause infective exacerbations of COPD
H. influenza S. pneumoniae
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define chronic bronchitis
Inflammation of the bronchial tubes. Considered chronic when it causes a productive cough for at least 3 months a year for 2 years.
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Pathophysiology of chronic bronchitis
Overall - Hypersecretion - Ciliary dysfunction - Narrowed lumen Explanations: Irritation of epithelium of bronchi causes inflammation. This leads to hypertrophy and hyperplasia of the bronchial mucous glands in bronchi, and goblet cells in bronchioles. Epithelial layer becomes ulcerated, eventually replacing the columnar epithelium with squamous (metaplasia), and smoking makes cilia shorter and less mobile Chronic inflammation causes infiltration of epithelium, narrowing lumen. Shortened immobile cilia and narrow, easily blocked lumen predispose to infection
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explain the lung spirometry tests (4)
1) FVC (Forced vital capacity) - Max air volume in 1 breath (<80%) 2) FEV1 (Forced Expiratory Volume in 1 second) - Max air 1 second (<80%) 3) FEV1:FVC Ratio (<0.7 obstructive) 4) TLC (total lung capacity) (increased in COPD due to air trapping)
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signs/symptoms of chronic bronchitis
Blue Bloater - Chronic productive cough - Cyanosis - Dyspnoea on exertion - Usually overweight - Purulent sputum - Crackles, wheezes when breathing Hypoxia/aemia (insufficient oxygen in tissues/blood) and hypercapnia (high CO2)
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symptoms of co2 retention
drowsiness asterixis confusion cyanosis
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complications of chronic bronchitis
2ndary polycythaemia vera Pulmonary HTN due to reactive vasoconstriction to hypoxaemia Cor pulmonale due to chronic pulmonary HTN
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define emphysema
Damage to/destruction of the alveolar air sacs. This causes the alveoli to permanently enlarge and lose elasticity. This means the lungs are unable to recoil, so patients have trouble exhaling
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Pathophysiology of emphysema
Irritants trigger inflammation in lungs, releasing proteases (collagenases, elastases), which break down elastin. Normally, elastin prevents low pressure environment from collapsing. In emphysema, elastin is lost and airways collapse. This causes: - Air trapping distal to point of collapse - Airways stretch during inhalation but cant breath out fully. - Elastin loss also causes breakdown of thin alveolar walls (Septa), causing neighbouring alveoli to coalesce. This reduces the area for gas exchange.
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types of emphysema
Centriacinar - most common. Damages central/proximal alveoli in each acinus, in the upper lobes of lungs. Seen in smokers. Pan-acinar - Whole acinus affected. Seen in A1AT, affecting lower lobes. Para-septal - Distal alveoli, can cause a pneumothorax when alveoli rupture Irregular - Irregular acinar involvement. Scarring/fibrosis
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signs/symptoms of emphysema
Pink puffer - Pursed lip breathing - Barrel shaped chest - Hyperresonance on percussion - Downward displacement of liver - Dyspnoea, cough, weight loss
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imaging signs of emphysema
Increased anterior-posterior diameter Flattened diaphragm Increased lung field lucency
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signs of copd (6)
Barrel chest Hyperresonance on percussion Cyanosis Pursed lip breathing Wheezing/crackling Productive cough with purulent sputum
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what scale is used to assess breathlessness?
MRC dyspnoea scale. Breathlessness: 1 - on exercise 2 - on hurrying/slight hill 3 - walks slower than others/ has to stop to catch breath 4 - Stops to catch breath after 100m 5 - breathless on minimal activity (getting changed)
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ix in copd
Clinical diagnosis - Over 35, smoking history, signs/symptoms of COPD. Spirometry - FEV1<80% expected - FEV1/FVC <0.7, with no bronchodilator reversibility Chest X ray - - Flattened diaphragm - Hyperinflation - Bullae CHECK FBC - COPD causes chronic hypoxia -> polycythaemia vera.
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how is copd classified?
GOLD classification Goes down based on FEV1 e.g. FEV1>80% = 1 (mild), FEV1 50-79 = 2 (moderate) etc FEV1 49-30 = 3 (Severe) FEV1 <30 = 4 (very severe)
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name all 5 drugs used in copd tx
Bronchodilators: - Short acting Beta 2 agonist (salbutamol) - Long acting Beta 2 agonist (salmeterol) - - Short acting muscarinic antagonists (Ipratropium bromide) - Long acting muscarinic antagonists (Tiotropium) Inhaled corticosteroid (Beclometasone)
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tx algorithm of copd (inhalers)
1) SABA or SAMA 2) LABA and LAMA regularly (ICS if asthma features) 3) LABA + LAMA + ICS + SABA at any stage (can still be taken as required)
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other tx of copd
Long term Oxygen if sats below 92 at rest Oral Theophylline (bronchodilator) Oral mucolytic Prophylactic azithromycin!
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How does pulmonary hypertension cause cor pulmonale, and what are its clinical manifestations
Pulmonary vasoconstriction and HTN means right heart must pump against high pressures, eventually failing. Causes peripheral oedema, raised JVP, hepatomegaly
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comps of copd (4)
Cor pulmonale (RH failure secondary to pulmonary HTN) Pneumothorax Type 1/2 resp failure and respiratory acidosis Infections
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define copd exacerbation with abg finding
Acute worsening of symptoms, usually due to infective cause (H influenza, S pneumoniae). Shows respiratory acidosis (low pH and high CO2). Increased bicarbonate (HCO3-) shows compensation by kidney Treated with amox
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what are the criteria for bronchodilator reversibility?
> 12% increase in FEV1 AND volume increase >200ml post bronchodilator
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Define infective conjunctivitis?
Sore, red eyes associated with sticky discharge. Can be bacterial or viral Bacterial - Purulent discharge, eyes may be stuck together Viral - Serous discharge - Recent URTI - Preauricular lymph nodes
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how is conjunctivitis mx?
Self limiting but can be treated with Abx - Chloramphenicol drops or ointment - Drops every 2-3 hours, ointment QDS - Topical fusidic acid in pregnancy women BD!!
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how is conjunctivitis mx in contact lens users?
Topical fluoresceins to identify corneal staining Contact lens should NOT be worn No school exclusion
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What are the types of dermatitis and whats a common cause?
Irritant: Common, non allergic. Related to weak acid or alkali exposure. Often seen on hands. Erythema, crusting, vescicles rare Allergic: T4 Hypersensitivity. Less common. Often seen on head following hair dyes. Acute weeping eczema, predominantly affecting the margins of the hairline, rather than scalp. Potent topical steroid!!!!!! Cement is a common cause, due to alkaline nature. Dichromates in cement can cause allergic dermatitis too. Patch testing to differentiate
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What is gout with risk factors?
Monosodium urate crystal deposition in joints. MTP most common. Elderly Male Purine rich foods Obesity HTN Impaired kidney function T2DM Family history
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causes of gout
Increased uric acid production - Increased cell turnover (leukaemia, haemolytic anaemia) - Purine rich diet (shellfish, red meat, organ meat) - Obesity/metabolic syndrome Decreased excretion - CKD - Diuretics/aspirin/pyrazinamide - Lead toxicity
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what foods predispose to gout, what diet is protective?
High Purine diet can raise uric acid levels - Red meat - Seafood - Sugary beverages - Beer
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recommended diet with gout
high diary diet protective
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signs/symptoms of gout
Generally monoarticular (can be up to 4) joint swelling, tenderness, erythema. - Usually 1st MTP but can affect ankle, wrist, knee, small hand joints. Gouty tophi (nodular masses of urate crystals - massive lump under skin) can appear Flares last between 7-10 days, first 12 hours worst
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ix in gout
Joint x ray: - Joint effusion, preserved joint space. - Lytic lesions - Punched out erosions with sclerotic margins and overhanging edges - Loss of joint space is a very late sign Joint aspiration w/ polarised microscopy: - Needle shaped crystals with negative birefringence
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mx of gout general life advice acute flares prevention
General life advice: - Low purine, lose weight, avoid alcohol (especially beer) Acute flares: - NSAID+PPI OR colchicine OR steroid injection 2nd line Prevention: - Allopurinol (xanthine oxidase inhibitor)
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comps of gout caused by hyperuricaemia
Urate nephrolithiasis: Hyperuricaemia can cause urate renal stones
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define pseudogout
Pseudogout is an inflammatory arthritis caused by deposition of calcium pyrophosphatase crystals in synovium
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rf of pseudogout
Increasing age Female Previous joint trauma Hyperparathyroidism Hypomagnesaemia Hypophosphataemia Haemochromatosis Acromegaly
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pathophys of pseudogout
Also known as chondrocalcinosis. Calcium pyrophosphatase crystals trigger synovitis, most commonly in the knee, shoulder and wrist. Acute - mainly larger joints in elderly Chronic - Inflammatory RA-like symmetrical arthritis
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signs/symptoms of pseduogout
Usually indistinguishable from gout, except that knee, wrist, ankle are most affected - Inflammation: warm, swelling, erythema, pain and joint stiffness
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ix in pseudogout
X ray: Chondrocalcinosis (suggestive but not diagnostic, absence doesn’t exclude) Joint aspiration w/ polarisation: Weakly positively birefringent rhomboid shaped crystals Also check: Bone profile/PTH, Iron studies, serum magnesium to check cause
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mx of pseudogout
Acute - NSAID or colchicine or corticosteroid injection - Cool packs + rest Chronic - DMARD (methotrexate) or joint replacement
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main differential of crystal athropathies
septic arthritis
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gout vs pseduogout joint aspiration
Gout - Negative birefringent needle shaped crystals Pseudogout - Positively birefringent rhomboid shaped crystals
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define osteoarthritis
Non inflammatory, progressive synovial joint damage caused by wear and tear of most commonly used joints.
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joints commonly affected in osteoarthritis?
Knees Hips Sarco-ileac joints Wrist Carpometacarpal Interphalangeal
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risk factors for osteoarthritis
Age Female sex Raised BMI/obesity Joint injury/trauma Joint malalignment (congenital or not)
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pathophys of osteoarthritis
Usually, cartilage breakdown and production by chondrocytes is under balance. In OA, chondrocytes secrete more metalloproteinases (degrading enzymes) leading to loss of Type 2 cartilage. (Type 1 has less elasticity) IL-1 and TNF-a also stimulate metalloproteinase production and inhibit collagen production. Causes decreased joint space, which causes damage to bones on movement. Bone attempts to repair itself with type 1 collagen but causes bony overgrowths
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signs/symptoms of osteoarthritis?
Asymmetrical non inflamed joint pain, which gets worse as the day goes on Herbeden’s nodes (DIP Swelling) Bouchard’s nodes (PIP swelling) Fixed flexion deformity of carpometacarpal Joint pain worse with activity Mechanical locking Joint stiffess, tenderness, crepitus (crunching sensation when moving) NO EXTRA ARTICULAR MANIFESTATIONS
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typical presentation of osteoarthritis
> 45 years old Typical activity related pain No morning stiffness (<30 mins)
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ix in osteoarthritis
1st - X ray (LOSS) L - Loss of joint space O - Osteophytes (bony overgrowths) S - Subchondral sclerosis S - Subchondral cysts
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non pharmacological treatments of osteoarthritis
Weight loss Low impact exercise Physiotherapy Occupational therapy Heat/cold packs at site of pain Orthotics (helps with foot issues)
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pharmacological tx of osteoarthritis
1st - Oral paracetamol, topical capsaicin, topical NSAID Topical NSAID first for knee Others: - Intra articular steroid injection - Joint replacement
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define prostate cancer with 4 risk factors
Adenocarcinoma of the prostate gland (usually peripheral zone). Associated with BRCA1 and BRCA2 Age Afro Caribbean Family history
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signs/symptoms of prostate cancer
LUTS- Voiding: Hesitancy, weak stream, straining, dysuria, incomplete emptying, terminal dribbling. Storage: Urgency, frequency, nocturia, incontinence Bone pain (if metastasised to bone) Wight loss, fatigue, night sweats
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ix of prostate cancer
DRE: Hard, asymmetrical, nodule, irregular prostate with loss of median sulcus PSA Transrectal ultrasound Prostate Biopsy - GOLD. Used with Gleason score. Bone scan to check for bone metastasis (Lesions)
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what scoring system is used in prostate cancer?
Gleason scoring - Uses biopsy to grade prostate cancer 1-5 1 - Well differentiated cancer 5 - Anaplastic (Extremely poorly differentiated) 1st and 2nd most prevalent histological patterns graded and added together to give score out of 10.
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mx of prostate cancer?
Local - prostatectomy Active surveillance if >70 or not severe If metastatic - Radiotherapy - Hormone therapy (GnRH e.g. Goserelin) or bilateral orchidectomy (remove testicles) - reduce testosterone - Androgen receptor blocker
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other causes of raised psa
bph prostatitis uti vigorous exercise recent ejaculation
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what is infectious mononucleosis, what its cause and association
AKA Glandular fever Caused by EBV and associated with Hodgkin’s, Burkitt’s and nasopharyngeal carcinoma
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presentation of glandular fever
Classic triad Fever, pharyngitis, lymphadenopathy Usually presents in adults and young children Shows atypical lymphocytes on blood film Investigated with monospot test/agglutination test
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how does glandular fever spread and what are its complications?
Spread through saliva (kissing, sexual activity) Lifelong latent infection, can cause chronic fatigue
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what is lyme disease?
Caused by spirochaete Borrelia burgdorferi and spread by ticks. <30 days - Bulleye rash (erythema migrans), usually 1-4 post bite. Painless, >5cm and slowly grows. - Headache, lethargy, fever, arthralgia > 30 days - Heart block, peri/myocarditis, meningitis
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ix and mx of lyme disease?
Can be diagnosed if erythema migrans (bullseye rash) seen ELISA Antibodies to Borrelia burgdorferi Managed with tick removal (tweezer) and washing. If Lyme disease, doxycyline, with amox as alternative Jarisch-Herxheimer reaction (fever, rash, tachycardia, after first dose) possible
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define reactive arthritis?
Reactive arthritis (Reiter’s syndrome) refers to synovitis following a infection in other part of body. Most commonly gastroenteritis or STIs. Affects men 30-50x more than women
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causes of reactive arthritis
STI - Chlamydia - Gonorrhoea Gastroenteritis - Salmonella - Shigella - Campylobacter - Yersinia enterocolitica
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signs and symptoms of reactive arthritis
“Cant see, pee, climb a tree” Urethritis, arthritis (of lower leg), conjunctivitis Acute, asymmetrical monoarthritis, typically of lower leg. - Warm swollen join - Keratoderma blennorhagica - Mouth ulcers
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ix of reactive arthritis
“Hot joint” policy - assume warm swollen joint is septic - Joint aspiration - Culture and gram stain. Should show no organism, excludes differential (Septic arthritis). - ESR/CRP raised - RF/ANA negative Sexual health review/stool test will be diagnostic of underlying cause X ray: - Enthesitis - Sacroiliitis with periosteal reaction
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mx of reactive arthritis
Give antibiotics and aspirate joint NSAID, Steroids Methotrexate
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describe oral candidiasis
Creamy white/yellow spotty plaque adhered to oral mucosa. May be bleeding and redness under this. Most commonly found on buccal mucosa, tongue and palate. Can also present atrophic with a burning pain or under dentures (denture stomatosis - negative test on mucosa but positive on dentures)
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mx of oral candidiasis
topical antifungals: 1st line for mild to moderate: - nystatin suspension -miconazole gel systemic antifungals: severe or refractory case: - oral fluconazole
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What are diverticula?
A diverticulum is an outpouching of colonic mucosa and underlying connective tissue of colon wall. Usually 0.5-1cm. Usually caused by weakness in circular muscle that become larger gaps over time, causing mucosal herniation through the gap.
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Where are diverticula most likely to occur?
Sigmoid (MC) also right colon (ascending/transverse) Through colonic weak points such as where blood vessels pass through muscle, or gaps in taeniae coli muscle
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Give the type of diverticular disease
Diverticulosis - Presence of diverticula, asymptomatic patient Diverticular disease - Diverticula cause milder symptoms, e.g. intermittent abdominal pain without inflammation or infection Diverticulitis - Diverticula become inflamed and infected, causing more severe symptoms
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what is a false diverticulum?
Not all layers involved in the outpouching (in true diverticula, ALL Layers involved) False are most common.
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causes/risk factors of diverticular disease
Low fibre diet Old age NSAID Connective tissue disorders (Ehlers-Danlos/Marfans) Obesity Smoking
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what are 2 possible consequences of diverticula?
Blood vessels supplying colon can rupture, allowing blood into lumen, causing haematoschezia Diverticula themselves can rupture, causing fistula formation, usually with bladder (colovesicular fistula), causing gas in bladder or stool in urine
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signs/symptoms of diverticulitis?
Asymptomatic - Detected incidentally on colonoscopy Diverticulosis: - LLQ abdominal pain - Rectal bleeding possible Diverticulitis: - LLQ/LIF pain and guarding (If Sigmoid. Right sided if right colon affected) - LIF tender mass (if abscess) - Constipation - Fresh rectal bleeding - Diarrhoea
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ix in diverticulitis
CT abdomen/pelvis with contrast - Identify divertcula/diverticulitis and complications
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differentials for diverticulitis
Colorectal cancer Appendicitis UTI Pyelonephritis
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mx of diverticulitis
Diverticulosis - No treatment Diverticular disease - Increase fibre, hydration, cut out smoking. Analgesia such as paracetamol and anti-spasmodic such as mebeverine may be used Diverticulitis: - Analgesia/anti-spasmodic. Fluid or low residue diet, to rest bowel. - Co- amoxiclav - Surgery if complications
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comps of diverticulitis
Colovesical fistula - Faecaluria, pneumaturia (stools and gas in urine) Abscess Perforation/ rupture onto peritoneum -> Bacterial peritonitis Bowel obstruction
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Define haemorrhoids/piles
Haemorrhoids are normally spongy vascular structures in anal canal that act as cushions for stool as it passes through. Haemorrhoidal disease (haemorrhoids) is when they get swollen and inflamed
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classifications of haemorrhoids
Internal - above dentate line External - below dentate line Internals graded 1 - No protrusion out of anal canal 2 - Protrusion during stool passage but retract 3 - Protrude, dont retract but can be pushed in 4 - Prolapsed haemorrhoids that cannot be pushed in
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causes of haemorrhoids
Recurrent increased abdominal pressures - Straining during bowel movements - Chronic diarrhoea, constipation - Congestion from pelvic tumour
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signs/symptoms of haemorrhoids and investigations
Internal: Usually asymptomatic, can be slightly uncomfortable, and have fresh red blood External: Very painful, patients cant sit. Have discharge, swelling and itching. Rectal exam and proctoscopy for internal
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mx of haemorrhoids
1 - Increase fibre/fluids - Stool softeners - Topical analgesia or steroids 2/3/4 - Rubber band litigation, sclerotherapy or surgical treatment
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Define Polymyalgia Rheumatics
older people muscle stiffness and raised inflammatory markers.
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features of polymyalgia rheumatics
over 60 rapid onset - under a month aching, morning stiffness in proximal limb muscles - WEAKNESS NOT A SX OF IT. - mild polyarthralgia, lethargy, depression, low grade fever, anorexia, night sweats
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ix for polymyalgia rheumatics
raised inflammatory makrers - eg - esr over 40mm/hr creatinine kinase and EMG normal
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tx of polymyalgia rheumatica
prednisolone - 15mg/od they respond dramatically to steroids. if they dont respond: alternative diagnosis
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What is chronic rhinosinusitis
inflammatory disorder of paranasal sinuses and linings of nasal passages that last over 12.
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predisposing factors to chronic rhinosinusitis
atopy: hay fever, asthma nasal obstruction e.g. Septal deviation or nasal polyps recent local infection e.g. Rhinitis or dental extraction swimming/diving smoking
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features of chronic rhinosinusitis
facial pain: frontal pressure pain worse on bend forward nasal discharge: clear if allergic/vasomotor. thicker, purulent if secondary infection nasal obstruction: mouth breathing post nasal drip: could produce chronic cough
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how would you manage chronic rhinosinusitis
avoid allergen intranasal corticosteroids nasal irrigation with saline solution
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name 3 red flag symptoms associated with chronic rhinosinusitis
unilateral sx persistent sx: despite compliance with 3 months of tx epistaxis
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do acute sinusitis