General Practise/Primary Care Flashcards
What is acute bronchitis?
self limiting LTRI
inflammation of bronchi and trachea.
Risk Factors of Acute Bronchitis
Smoking
Winter months
Contact with patients with RTI
Pathophysiology of Acute Bronchitis
Acute bronchial wall inflammation
causes increased mucous production and oedema = productive cough.
damage caused to the wall may take weeks to repair so the cough might last a little.
50% lasts over 2 weeks and 25% over a month. - post bronchitis syndrome.
Aetiology of Acute Bronchitis
Viral: same as urti’s
RSV
CORONAVIRUS
RHINOVIRUS
ADENOVIRUS
Presentation of Acute Bronchitis
Productive Cough - clear, discoloured or white sputum. cough usually less than 1 month.
Sore throat
Rhinorrhoea
Wheeze - not always. maybe on forced expiration
Low grade fever - systemic features should be absent
Bronchitis vs Pneumonia
Systemic features and dysnpoea, wheeze and productive cough - pneumonia
dullness, bronchial breathing and crepitations - pneumonia
if crackles for bronchitis will clear with cough
Criteria for Acute Bronchitis
None in stone by Macfarlane helps with diagnosis:
Acute : less than 21 days
Cant be explained otherwise
At least 1 of LTRI symptoms like sputum, chest pain or wheeze.
Cough main symptom.
Ix of Acute Bronchitis
Clinical diagnosis
CXR - RULE OUT PNEUMONIA IF UNSURE.
USE CRP TO GIVE BACK UP ABX
LESS THAN 20 MG/L - NO ABX
20-100 - DELAYED ABX
OVER 100 - IMMEDIATE ABX
PROCALCITONIN - new test for bacterial and viral infections. more effective for bacterial though.
Management of Acute Bronchitis
Self - limiting - doesnt require anything other than symptom mx.
Adequate fluid and analgesia (para/ibuprofen) - maybe honey cough syrup?
ABX - BE CAREFUL BC ITS SELF LIMITING AND YOU DONT WANT OVERUSE.
ONLY GIVE ABX IF :
PRE-EXISTING CO MORBID ISSUES OR IMMUNOSUPPRESSED.
OVER 65 WITH 2/ OVER 80 WITH 1 :
HOSPITAL IN LAST YR
T1DM/T2DM
CCF
ORAL CORTICOSTEROID USE CURRENTLY
CRP OVER 100 MG/L
What abx do you give in Acute Bronchitis ( if you give them)?
over 18 :
Doxycycline : 5 days - 1st day 200mg then 100mg OD for 4 days. NOT TO PREGNANT WOMEN.
ALTERNATIVE: AMOXICILLIN (PREGNANT) , ERYTHROMYCIN/CLARITHROMYCIN
12-17:
AMOX: 500MG 3*DAILY FOR 5 DAYS
ALTERNATIVE: ERYTHROMYCIN/CLARITHROMYCIN
What is Acute Stress Disorder? (ASD)
acute stress reaction within first 4 weeks after traumatic event.
something abnormal like sexual assault or car accident or robbery.
diff between asd and ptsd
asd is first 4 weeks and ptsd is after 4 weeks
asd vs adjustment disorder
adjustment disorder - state of stress inferring with social function after having to adjust your life due to life change maybe a death or seperation. not an abnormal thing though
asd - abnormal stressor (physical/mental) that shouldnt be experienced by human.
Presentation of ASD - ACUTE STRESS DISORDER
dsm-v criteria
- disassociation - feel out of it. out of time
- intrusive thoughts - nightmares/flashbacks
- negative mood
- avoidance - of like distressing memories or thoughts/feelings
- arousal - hypervigilant, insomnia, cant concentrate
Mx of acute stress disorder (ASD)
trauma - based CBT - 1st line - given to people with asd that affects daily function.
benzodiazepine - sometimes for acute symptoms like sleep disturbance or agitated. NOT LONG TERM (addictive)
nice recommends you don’t prevent PTSD
What is contact dermatitis?
allergic or irritant reaction - 2 types
irritant contact (ICD) OR allergic (ACD)
What is irritant contact dermatitis caused by?
direct toxicity to skin.
anyone in contact with irritant of sufficient conc for sufficient time. severity depends on this too.
can range from acute to chronic (single to repeated exposure)
metals
solvents
detergents
weak acid/alkalis
cement ( alkaline) - can even cause ACD because of dichromates presence.
What is allergic contact dermatitis caused by ?
type 4 hypersensitivity reaction
dont need prior sensation.
rarer than icd
allergens typically haptens cause it. cause immune response when they bind to protein complex. they then move to epidermis and bind to langerhans cells in epidermis which are antigen presenting cells.
they also travel to regional lymph node sites to present cd4+ t cells which give a response in 48-96 hrs of re-exposure.
poison ivy
fragrance
metals - nickel
jewellery
hair dye
latex
dichromates - cement and leather
preservatives - hygiene and cosmetic product
risk factors of contact dermatitis
occupational exposure - labourer, dry cleaner, janitor, dry cleaner, farmer, food-industry worker, machine operator, cook
atopic dermatitis (excema)
Presentation of irritant contact dermatitis
presents minutes - hours of exposure to irritant. mild irritant days-weeks
commonly of face and hands. limited to site of exposure:
erythema
burning
pustules/acneiform lesions
ulceration (severe irritant)
Presentation of allergic contact dermatitis
prevents 24-72 hours after re-exposure (previous sensitised)
commonly dominant hand but can be anywhere.
often margin of hairline.
erythema
pruritis
bullae and vesicles
urticaria - with latex or certain food exposure.
Ix of contact dermatitis
Patch testing - present allergen to skin. will show inflammation - grade within 2-7 of application if +ve.
repeat open application test (ROAT)/ proactive use test (PUT) - 2* daily for 1 week.
stimulates contact dermatitis for leave on products like moisturisers or sunscreen or cosmetics
Mx of contact dermatitis
1st line - avoid irritant/allergen
emolient = icd - applied to affected area
hydrocortisone - only ACD - topical corticosteroid
How do insect bites affect you?
mosquitos, bed bugs and fleas have mouth piercing parts that pierce the skin.
horseflies lacerate the skin.
they have antigenic components in saliva cause local, systemic reactions. first time bite no reaction but after type 4 hypersensitivity reaction and after repetitive leads to inflamed and itchy maculopapules.
More concerningly, a type 1 hypersensitivity reaction may develop with a typical wheal and flare presentation. This develops within 20 minutes of the bite, and can sometimes lead to anaphylaxis.
how do insect stings affect you?
bees wasps hornets
inject venom from a sac attached to a stinger into the skin directly. - has allergen and histamine cause reaction.
Local - no more than 10cm from the site of exposure. Redness, swelling and pain are limited to the soft tissue solely.
Systemic - these are distant from the site, such as widespread redness, itching, uriticaria, angioedema. It is more likely to lead to anaphylaxis if there is airways and haemodynamic compromise.
presentation of insect stings and bites
local - swelling erythema pain
systemic - Uriticaria, rhinitis, wheeze, abdo pain, vomit, dizzi, angioedema, anaphylaxis
ix of insect stings and bites
clinical diagnosis
test for venom allergies in any pt with systemic reaction or anaphylaxis (skin-prick or venom specific IgE testing)) and if these are positive venom immunotherapy (VIT) need to be given.
Mx of insect bites and stings
remove stinger if you see it
small local reaction - nothing other than analgesia for pain and
chlorphenamine (antihistamine) for itching or hydrocortisone cream.
large local reaction - oral antihistamine and/or oral corticosteroids ( be careful of steroid bc wound could be infected)
systemic reaction - admit to a+e - treat for anaphylaxis in meantime. allergy specialist referral.
what do you mean by food allergy?
adverse reaction to proteins in food. common is peanuts, tree nuts, milk, eggs, fish , wheat, soya
can be genetic and environmental factors and can be IgE mediated (acute) or non ige (subacute/chronic)
presentation of food allergy
IgE mediated: minutes to 2 hrs of ingestion
Uriticaria
Angioedema
Acute rhinoconjunctivitis
Acute asthma
Anaphylaxis
Nausea and vomiting
Abdominal pain
Non IgE mediated:
Contact dermatitis
Dermatitis herpetiformis
Coeliac disease
Heiner syndrome (cow milk induced pulmonary disease)
Ix of Food Allergy
Skin Prick - 1st line. reproducible quick 15 mins, fast and cheap good sensitivity (only 50% specificity). positive allergens produce wheal over 3 mm compared to control is +ve
Serum Specific IgE immunoassay - expensive and longer for results
Food Challenges - best test but longer expensive and difficult bc you need staff to manage anaphylaxis if necessary
Mx of Food Allergy
Anaphylaxis treat accordingly.
Allergy action plan and avoidance.
What is an anal fissure?
tear in the squamous mucosal lining of the anal canal.
occur most common on posterior (90%) aspect of anal canal. anterior fissures often follow parturition in females.
lateral anal fissure suggests secondary cause.
tell me the 2 types of anal fissures and how they come about
High-pressure fissures - ischaemia due to high pressure in anal sphincter causes the fissure.
Low-pressure fissures - tends to happen in postpartum women.
classify anal fissures
acute - less than 6 weeks
chronic - over 6 weeks
primary - no underlying disease present
secondary - underlying disease like IBD
Risk Factors of anal fissures
main causes: inflammation and trauma.
major rf:
- constipation
- dehydration
- IBD
- chronic diarrhoea
Clinical Features/symptoms of anal fissures
Intense post-defecatory pain - most common. disproportionate to size of fissure.
Bleeding of fresh, bright red blood on wiping or after defecation.
Itching
fissures visible on dre but pt may refuse. can give anaesthetic.
possible sentinel pile at 6 and 12 o clock. small external lump with tear.
DD of anal fissure
haemorroids
CHRONS/UC
ANAL CANCER
Mx of Anal Fissure
medical : analgesia, topic anaesthetic, diet management (increase fluid and fibre intake if less than 1 week), laxative
if this dont work, gtn cream or diltiazem cream (CCB). increases blood flow to region and relaxes internal anal sphincter - promotes healing and reduces pain, applies less pressure on sphincter.
diltiazem is better tolerated by gtn cream is cheap. use for high pressure fissures.
CHRONIC: Topical glyceryl trinitrate is first-line treatment
surgical: chronic with medical mx not working after 8 weeks.
LATERAL SPINCTERECTOMY - DIVISION OF INTERNAL ANAL SPHINCTER RELIEVE PRESURE
What is acne vulgaris?
chronic inflammation of hair follicles and sebaceous glands in the dermis.
12-25 - resolves in mid 20’s
Risk Factors of Acne Vulgaris
Teenage - peak is 14 girl, 16 boy
Fhx
Genetics - hyperkeratosis can run in family. PCOS is increased androgen=increased sebum
Medication - androgens, corticosteroids
Physical Product - moisturiser, cosmetics block pores
Contact Acne - headband irritate skin
Excessive washing of skin - irritate skin
Stress - increased cortisol cause increased sebum secretion
NOT DIET
Ix and Diagnosis of Acne Vulgaris
Clinical
consider: endocrine screen
test testosterone, LH, FSH if hyperandrogenism is suspected: PCOS
Pathophysiology of Acne Vulgaris
Obstruction of the pilosebaceous follicle
factors that contribute: keratin plugs, sebum and bacterial overgrowth
KERATIN PLUGS - tiny clumps of dead keratinocytes,keratin and melanin. when keratinocytes produce to much keratin in hair follicles= hyperkeratosis. more keratin plugs = block hair follicle opening
SEBUM - RELEASED BY SEBACEOUS GLANDS RESPONDING TO INCREASED ANDROGEN PRODUCTION IN PUBERTY. CLOG UP FOLLICLES AND CAUSE BLOCKAGE LIKE KERATIN PLUGS.
Excess keratin plugs/sebum or both , fills hair follicle but not full thing. Hair can come thru as its open to skin surface. = open comedome – black appearance – blackhead. – melanin in keratin plug gets oxidised when exposed to air = dark
BACTERIAL OVERGROWTH:
Bacteria live in follicles – Propionibacterium. If hair follicle gets plugged up = closed comedone. Bacteria grows, feasts overgrowth. Immune cells attack bacterial cells. This mix is white pus with red inflammation = whitehead/pimple
If follicle bursts, inflammatory lesions like papules/pustules form. Excessive inflammation = nodules, cysts. You can get inflammatory scarring (ICE-PICK/HYPERTROPHIC SCARS)
Clinical Manifestations of Acne Vulgaris
generally face neck and upper trunk
mild - mostly non inflamed lesions - open and closed comedones with few inflammatory lesions. whiteheads and blackheads.
moderate - more widespread. inflammatory papules and pustules
severe - widespread inflammatory pustules and papules and nodules, cysts . scarring potentially
what is a macule, papule , pustule?
macule - flat mark
papule - small lump
pustule - small lump with yellow pus
describe different types of scars
icepick
hypertrophic
rolling
icepick - after acne lesion heals small indentation in the skin
hypertrophic - after acne lesion heals small lump in the skin
rolling - irregular wave-like irregularity after acne heals
Mx of Acne Vulgaris
1st line - if mild/moderate do one of :
topical retinoid (slows sebum production) +/- benzoyl peroxide (reduce inflammation, unblock skin and is toxic to P.acnes bacteria)
topical abx - clindamycin. give benzoyl peroxide or topical retinoid (if no ci) prevent abx resistance
topical azelaic acid 20%
2nd line -
oral tetracycline (doxycycline,limecycline, oxytetracycline) - with topical retinoid or benzoyl peroxide (prevent abx resistance)
Combined oral contraceptive to women - alternative to oral abx - co-cyprindiol (danette) . increased risk of VTE so only use when other failed . use with topical therapy. stop after acne controlled for 3 months.
3rd line -
Accutane - isotretinoin oral - vit A analogue if scarring or pt unresponsive to 2 courses of Abx .
function of accutane
Reduce production of sebum – reduce inflammation and bacterial growth .
Ci: pregnancy to both topic and oral retinoids – TERATOGENIC
rules for abx use in acne vulgaris
dont use same abx longer than 3 months if inneffective move onto another
erythromycin in pregnancy
no tetracycline in pregancy/breastfeeding/under 12
minocycline avoid - irreversible pigmentation
always co-prescribe benzoyl peroxide and topic retinoid to avoid resistance.
dont give both oral and topical abx
comps of acne vulgaris
Acne fulminans – severe acne – systemic upset. Hospital admin – steroid tx
Post inflammatory change – hyperpigmentation/scarring
Retinoid SE – dry skin, photosensitivity,depression, teratogencicity
Depression and anxiety
Gram-negative folliculities – long term abx – tx with high dose oral trimethoprim
Other meds SE – isotretinoin and tetracycline cause intracranal HTN so don’t give both
What is anaphylaxis
type 1 hypersensitivity reaction.
igE activation causes mast cells to degranulate and release histamine and other pro-inflammatory mediators and you have ABC compromise.
non-anaphylactic allergy doesnt have ABC compromise
common allergens for anaphylaxis
food - nuts
meds - b-lactams - pencillin and nsaids. general anaesthetics too.
wasp and bee stings
could be idiopathic
Presentation of anaphylaxis
confusion, headache and loss of consciousness
swollen lips , tongue, eyes
fast heart rate
abdo pain, vomit
hives
wheezing,cough, difficulty getting air
rapid onset of allergy symptoms
urticaria
itching
angioedema
abdo pain
ABC impact from anaphylaxis
