Primary Care Flashcards
What is whooping cough?
infectious disease caused by gram negative bacterial BORDETELLA PERTUSSIS.
cough of “100 days”
transmission of whooping cough
respiratory secretions by cough or sneeze, contaminated objects
incubation period: 7-10 days
if untreated infectious for 21 days from symptom onset
immunisation for whooping cough
maternal whooping cough programme : 16-32 weeks of pregancy (upto 38)
6-1 vaccine to children aged 8,12,16 weeks
4-1 pre-school booster age 3,4 months old.
doesn’t give lifelong protection. wheens off over time
clinical features of whooping cough
catarrhal phase : 7-10 (range 4-21) after exposure. lasts 1-2 weeks. symptoms similar to urti : rhinorrhoea, malaise, mild cough, sore throat, conjunctivitis. fever is uncommon.
MOST INFECTIOUS STAGE IS CATARRHAL
Paroxysmal : 1-6 weeks (10weeks)
rapid,violent,uncontrolled coughing fits. - difficulty expelling thick mucus from tracheobronchial tree.
cough: increasing severity. worse at night (could be triggered by cold/noise) , after feeding, possible end in vomiting, associated central cyanosis.
sometimes inspiratory whoop. (short expiratory burst then inspiratory gasp)
infants spells of apnoea.
CONVALESCENT: 2-3 weeks. - gradually improves.
Diagnosing Whooping Cough - when to suspect?
suspect if acute cough lasting 14 days or more without apparent cause plus 1 or more of:
paroxysmal cough
inspiratory whoop
post-tussive vomiting
undiagnosed apnoeic attacks
suspect if clinical features plus:
- in contact with confirmed case within 21 days.
diagnosing whooping cough - lab tests
all ages: per nasal swab culture for BORDETELLA PERTUSSIS
pcr : all ages
serology : over 16
oral fluid testing (OFT) - 2-16 - test for anti-pertussis toxin immunoglobulin g (IgG). - OFT KIT SENT HOME.
IgG greater than 70 IU/ml or 70 aU
is whooping cough a notifiable disease?
YES - NOTIFY UKHSA WITHIN 3 DAYS
how would you manage whooping cough?
infants under 6 months - admit to hospital
notifiable disease - notify ukhsa
ORAL MACROLIDE:
clarithromycin (infant under 1 month)
azithromycin - child over 1 azi/clari
erythromycin - pregnant
non pregancy : azi/clari
where macrolides are contraindicated: CO-TRIMOXAZOLE. (NOT PREGNANT WOMEN OR INFANTS LESS THAN 6 WEEKS)
school exclusion: 48 hrs after abx start ( 21 days from symptom onset if no abx)
abx prophylaxis to household contacts.
complications of whooping cough
subconjunctival haemorrhage
pneumonia
bronchiectasis
seizures
pneumothrax ( increased intra-thoracic pressure bc of violent coughing)
umbilical/inguinal hernai, rectal prolapse (increased intra-abdominal pressure)
what is exanthem? (roseola infantum)
fever+ rash - nagayama spots
common disease of infancy caused by human herpes virus 6 (HHV6)
incubation period: 5-15 days.
affects children 6 months - 2 years.
no need for school exclusion
features of exanthem (roseola infantum)
high fever lasting a few days followed later by a maculopapular rash
Nagayama spots: papular exanthem on the uvula and soft palate.
febrile convulsions (10-15% of ppl)
diarrhoea and cough common
possible consequences of HHV6 infection
aseptic meningitis
hepatitis
what is gastroenteritis?
transient disorder due to enteric infection with virus, bacteria or parasites.
sudden onset diarrhoea, with/without vomiting.
could have fever, abdo pain
what is food poisoning?
illness caused by food/water consumption with bacteria.
Staphylococcus aureus
Bacillus cereus
Clostridium perfringens
travellers diarrhoea - what is it?
at least 3 loose to watery stools in 24 hrs with/without 1 or more of :
abdo cramps, fever, nausea, vomiting or blood in stool.
most common cause: e-coli
define acute diarrhoea
3 or more episodes of liquid or semi liquid stool in a 24 hour period lasting for less than 14 days .
stool takes shape of sample pot.
prolonged diarrhoea - over 14 days
define dysentery
acute infectious gastroenteritis with diarrhoea with blood and mucus
often fever and abdo pain
define antibiotic associated diarhoea
clinical infection
normal gut flora is disturbed by antibiotic use
certain strains of Clostridium difficile to grow
produce toxins
how is gastroenteritis spread?
person to person
faeco-oral
foodborne
environmental
airborne routes
viral causes of gastroenteritis
rotavirus - mc in children but reduced due to vaccine. person-to- person via faeco-oral route
symptoms: watery diarrhoea and vomiting, with/without fever, Abdo pain
vomiting settles 1-3 days , diarrhoea 5-7 days
infection in adults uncommon as immunity is long lasting
adenovirus - usually rti’s but can cause gastroenteritis in kids
norovirus - commonest cause in uk. all ages. immunity not long lasting
symptoms: 24-48 hours after infection and last for 12-60 hours
Sudden-onset nausea then projectile vomiting, watery diarrhoea. fever
headache
abdominal pain
myalgia
recovery - 1-2 days.
bacterial causes of gastroenteritis - campylobacter
Campylobacter jejuni/coli - MC - flu like prodome with abdo cramps, fever, possible bloody diarhoea, n+v.
2-3 days . happens from contaminated food, undercooked meat, untreated water, unpasturised milk
might mimic appendicitis.
comp: guillian-barre syndrome
parasitic causes of gastroenteritis
Amoebiasis - Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks
gardiasis - prolonged non bloody diarhoea
bacterial cause of gastroenteritis - staph aureus
short incubation period
severe vomiting
bacterial cause of gastroenteritis - cholera
profuse watery diarhoea
severe dehydration resulting in weight loss
not common in travellers
bacterial cause of gastroenteritis - shigella
bloody diarhoea, abdo pain, vomiting
bacterial cause of gastroenteritis - bacillus sereus
Two types of illness are seen
vomiting within 6 hours, stereotypically due to rice
diarrhoeal illness occurring after 6 hours
bacterial cause of gastroenteritis - e- coli
travellers - kids under 5
could be asx - could be bloody diarrhoea, Abdo cramps, fever, ,nausea, vomiting.
watery stools
10 days .
person-to-person via faeco-oral route, contaminated food, untreated water.
pass through home settings, school, care homes etc.
ABX CAUSE DIARHOEA
incubation period of diarhoea based on bacterium
Incubation period
1-6 hrs: Staphylococcus aureus, Bacillus cereus (6-14)*
12-48 hrs: Salmonella, Escherichia coli
48-72 hrs: Shigella, Campylobacter
> 7 days: Giardiasis, Amoebiasis
where would you typically see a venous ulceration?
just above medial malleolus
investigations of venous ulceration
ABPI - important in non healing ulcers because poor arterial flow affects healing.
less than 0.9 and more than 1.3 (indicate arterial disease due to calcification)
if less than 0.5 - severe arterial disease - compression ci’d.
if 0.5-0.8 - avoid compression
if 0.8-1.3 - then give compresssion.
management of venous ulceration
compression bandaging - 4 layer
oral pentoxifylline - peripheral vasodilator improves healing rate
small evidence using flavinoids
little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression
why would you get a venous leg ulcer?
sustained venous hypertension happens because of chronic venous insufficiency due to venous valve incompetence or an impaired calf muscle pump.
risk factors for venous leg ulcers
age
obesity
immobile
limited range of ankle function
previous ulcer
personal/family hx of varicose veins/dvt
female
define syncope
transient loss of consciousness due to global central hypoperfusion with
rapid onset,
short duration
spontaneous complete recovery.
types of syncope : reflex syncope (neurallly mediated)
vasovagal - triggered by emotion, pain or stress. “fainting”
situational - cough, micturition, gastrointestinal
carotid sinus syncope
types of syncope : orthostatic syncope
primary autonomic failure - Parkinson’s, Lewy body dementia
secondary autonomic failure - diabetic neuropathy, amyloidosis, uraemia
drug induced - diuretics , alcohol, vasodilators
volume depletion - haemorrhage, diarrhoea
types of syncope - cardiac syncope
arrhythmias : bradycardias (Sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural : Valvular, MI, hypertrophic obstructive cardiomyopathy
other: PE
how to evaluate syncope?
cardio exam
postural blood pressure reading: symptomatic fall in systolic bp >20 or diastolic >10 or decrease in systolic <90 is diagnostic.
give ecg for all pts.
patients with typical features, no postural drop and normal ecg dont require anything further.
what is postural drop?
drop in bp when you stand up after lying or sitting down.
What are varicose veins?
dilated tortuous superficial veins that occur secondary to incompetent venous valves.
allow blood to flow back, away from heart.
why do varicose veins occur in legs?
reflux in great saphenous vein and small saphenous vein.
risk factors of varicose veins
increasing age
female
pregnancy - uterus causes compression of pelvic veins
obesity
symptoms of varicose veins
aching
throbbing
itching
skin changes of varicose veins
varicose eczema - venous stasis - treat with steroid
haemosiderin deposition - hyperpigmentation
lipodermatosclerosis - hard/tight skin - champagne looking leg
atrophie blanche - hypopigmentation
complications of varicose veins
skin changes
bleeding
superficial thrombophlebitis - inflammatory process causing blood clot to form in veins.
venous ulceration
DVT
investigations for varicose veins
venous duplex ultrasound - will show retrograde venous flow
management of varicose veins
most don’t need surgery
conservative : leg elevation, weight loss, regular exercise, graduated compression stockings
possible treatments:
endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
foam sclerotherapy : irritant foam causes inflammatory response by reacting with vein wall. pushes blood out of area. = closure of vein
surgery: ligation/stripping
what is chickenpox?
primary infection with varicella zoster virus.
shingles is reactivation of dormant virus in dorsal root ganglion.
how is chickenpox (v-z-v) spread?
respiratory route
caught from someone with shingles
infectivity of chicken pox (v-z-v)?
4 days before rash until 5 days after rash first appeared (crusted over vesicular rash)
incubation period : 10-21 days.
clinical features of chicken pox (v-z-v)
fever initially
itchy rash starting on head/trunk before spreading.
1st macular, then papular, then vesicular.
systemic upset - mild
management of chicken pox v-z-v
supportive
keep cool, trim nails
calamine lotion
school exclusion : 1-2 days before rash appears (infective) continues until lesions dry and crusted over (5 days after rash onset)
immunocompromised patients and newborns with peripartum exposure : give them varicella zoster immunoglobulin (VZV).
if chicken pox develops : IV ACICLOVIR (considered)
complication of chicken pox vzv
secondary bacterial infection of lesion
NSAIDS INCREASE RISK
could be single infected lesion/small area of cellulitis - in some could be invasive group a strept soft tissue infection = could lead to necrotizing fasciitis
pneumonia
encephalitis
disseminated haemorrhagic chicken pox
arthritis, nephritis, pancreatitis - rare
what type of virus is varicella zoster?
herpes virus causing chickenpox
what is shingles?
acute unilateral painful blistering rash caused by reactivation of v-z-v
types of varicella zoster vaccine
1 - stops development of primary varicella infection - chicken pox - LIVE ATTENUATED VACCINE - VARILRIX/VARIVAX
2 - reduces incidence of herpes zoster (Shingles) caused by reactivation of vzv
who would you give the primary vzv vaccine to
healthcare workers who arent immune to vzv
contacts of immunocompromised patients (child whose parents is having chemo)
who is the shingles vaccine given to?
boost immunity of elderly people against herpez zoster.
all pts 70-79
live attentuated and given sub-cut
eg: zostavax
contradindication of secondary vzv vaccine ?
immunosuppresion
side effects:
injection site reaction
less than 1/10,000 ppl get chickenpox
which drugs can cause urticaria?
aspirin
penicillin
nsaids
opiates
what is urticaria?
local or generalised superficial swelling of skin.
mc cause: allergy but non-allergic causes are seen too.
release of histamine and other pro-inflammatory chemicals by mast cells in skin
features of urticaria?
pale pink raised skin. - described as “hives,wheals, nettle rash”
pruritic
management of urticaria
non-sedating antihistamine - loratidine/cetrizine - 1st line - continue for 6 weeks following episode of acute urticaria
sedating antihistamine - chlorphenamine - night time use - in addition to daytime one - if troubling sleep symptoms.
prednisolone - severe or resistant episodes
chronic urticaria: fexofenadine
uti’s in children - who is it more common in ?
until 3 months - boys more than girls bc of congenital abnormalities.
after 3 months - girls
presentation of uti based of age of child?
infant - poor feeding, vomiting, irritable
younger child - abdo pain, fever, dysuria (pain/buring/stinghing of urethra)
older child - dysuria, frequency, haematuria
what features would suggest an upper uti in a child?
temperature over 38 degrees
loin pain/tenderness
what are the nice guidlines for checking urine sample in a child?
check if any symptoms or signs suggestive of uti
with unexplained fever of 38 or higher - test urine after 24 hours at latest
with alternative site of infection but still unwell
how to collect urine in a child suspecting uti?
clean catch
if not : urine collection pads
if not: suprapubic aspiration
cotton wool balls, gauze, sanitary towels not suitable
how would you manage uti in children?
infant less than 3 months: refer immediately to paeds
over 3 months with upper uti : admit to hospital.
if not: oral abx like cephalosporin or co-amoxiclav 7-10 days
over 3 months with lower uti : oral abx for 3 days.
trimethoprim, nitrofurantoin, cephalosporin, amoxicillin.
bring child back if still unwell after 24-48 hrs.
abx prophylaxis not given after 1st uti but consider in recurring cases.
causes of uti in children
check for causes and damage to kidneys
causes:
e-coli (80%)
proteus
pseudomonas
predisposing factors for utis in children
incomplete bladder emptying:
- infrequent voiding
- hurried micturition
- obstruction by full rectum due to constipation
- neuropathic bladder
vesicoureteric reflux - flow of urine from back to ureters due to defective valves - high risk of kidney infection - upper uti
poor hygiene - not wiping from front to back in girls
what is vesicoureteric reflux?
abnormal backflow of urine from bladder into ureter and kidney.
common abornmality of urinary tract in kids.
35% of children develop renal scarring.
pathophysiology of vur - vesicoureteric reflux
ureters displaced laterally, entering bladder in a perpendicular fashion
shortened intramural course of ureter
vesicoureteral junction cant function adequately
primary : usually ureter has a long tube into the bladder and when the bladder fills the ureter is closed so no backflow. but here, the ureter tube is shorter so when the bladder fills the tube isnt closed and you get backflow.
secondary: obstruction in urinary tract. - increase in pressure.
due to recurring uti - ureter swell and close
-posterior urethral valve disorder
-flaccid neurogenic bladder - bladder cant contract to release urine.
possible presentations of vur - vesicoureteric reflux
antenatal period - hydronephrosis on USS
recurrent childhood UTI
Reflux nephropathy:
chronic pyelonephritis secondary to VUR
commonest cause of chronic pyelonephritis
renal scar may produce increased quantities of renin causing HTN
investigations of vesicoureteric reflux
Micturating cystourethrogram
dmsa scan - renal scarring
grading of VUR - vesicoureteric reflux
grade 1 - reflux into ureter only, no dilation
2 - into renal pelvis on micturition, no dilation
3 - mild/moderate dilation of ureter , renal pelvis and calyces
4 - dilation of renal pelvis and calyces with moderate ureteral tortuosity
5 - gross dilation of ureter , pelvis, calyces with ureteral tortuosity.
what is acute pyelonephritis?
type of UTI where 1/2 kidneys get infected
caused by ascending infection - e.coli fromm lower urinary tract.
could also be due to bloodstream spread of infection - SEPSIS
Clinical features of acute pyelonephritis
fevers, rigors,
loin pain
nausea, vomiting
symptoms of cystitis: dysuria, urinary frequency
investigations of acute pyelonephritis
mid-stream urine before starting abx
management of acute pyelonephritis
hospital admission considered
local abx guidlines
bnf recommend: broad-spectrum cephalosporin or a quinolone (for non-pregnant women) for 7-10 days
clinical features of uti (lower) in adults
dysuria
urinary frequency/urgency
cloudy/offensive smelling urine
lower abdo pain
fever: low grade in lower uti
malaise
in elderly patients, acute confusion
investigations for uti (lower) in adults
urine dipstick for :
women under 65, with no risk factors for complicated uti.
dont use for men, pregnant, catheterised.
urine culture for :
women over 65
recurrent uti (2 episodes in 6 months or 3 in 12 months)
men
pregnant women
visible/non-visible haematuria
what should you expect to see in uti (lower) in adults - urine dipstick?
positive for nitrite or leukocyte and rbc = uti likely
negative for nitrite and positive for leukocyte = uti just as likely as another diagnosis
negative for both = uti less likely
what are the lower urinary tract symptoms in men? (LUTS)
over 50
mc - secondary to BPH or prostate cancer.
voiding - hesitancy, poor or intermittent stream, straining, incomplete emptying, terminal dribbling
storage - urgency, frequency, nocturia, urinary incontinence
post micturition - dribbling. sensation of incomplete emptying
how would you examine for lower urinary tract symptoms in men ?
urinalysis - exclude infection = check for haematuria
digital rectal exam - size and consistency of prostate
PSA - possibly, but patient should be counselled first.
get the patient to:
urinary frequency-volume chart: distinguish between urinary frequency, polyuria, nocturia and nocturnal polyuria.
international prostate symptom score (IPSS) : assess impact on patients life. classify symptoms as mild, moderate, severe.
management of lower urinary tract symptoms in men - voiding symptoms
conservative measures: pelvic floor muscle training, bladder training, prudent fluid intake and containment products
if moderate or severe : alpha-blocker
if enlarged prostate and patient high risk of progression, 5-alpha reductase inhibitor offered
if enlarged prostate and moderate/severe symptoms give both alpha blocker and 5-alpha reductase inhibitor
if mixed symptoms of voiding and storage not responding to alpha blocker then antimuscaranic (anticholinergic) drug can be added.
management of lower urinary tract symptoms in men - overactive bladder
moderating fluid intake
bladder retraining poss
antimuscarinic drugs if symptoms persist. oxybutunin (immediate release), tolterodine (immediate release), darifenacin (once daily preperation)
mirabegron if 1st line drugs fail
management of lower urinary tract symptoms in men - nocturia
advise on moderating fluid intake at night
furosemide 40mg in late afternoon poss
desmopressin may be helpful
management of uti in adults : non pregnant women
trimethoprim or nitrofurantoin for 3 days
send urine culture if:
over 65
visible/non-visible haematuria
management of uti in adults: pregnant women
symptomatic:
urine culture
abx :
1st line: nitrofurantoin (avoid near term)
2nd line: amoxicillin or cefalexin
trimethoprim is teratogenic in 1st trimester avoid during pregnancy
asymptomatic bacteriuria: urine culture at 1st antenatal visit
immediate abx prescription or either nitrofurantoin(avoid near term), amoxicillin or cefalexin. 7 day course.
treat to avoid progression to acute pyelonephritis
further urine culture after treatment
which uti treatment med should be avoided in pregnancy and why?
trimethoprim - teratogenic in 1st trimester
how to treat uti in adults : men
abx for 7 days
trimethoprim or nitrofurantoin - 1st line unless prostatitis suspected
urine culture before abx start
how to treat uti in adults: catheterised patients
dont treat asx bacteria in catherterised pts.
if symptomatic treat with abx :
7 days rather than 3 day
consider removing or changing catheter asap if its been in place for 7 days.
if the bladder is still palpable after urination what should i think?
retention with urinary overflow
what is urinary incontinence
unintentional passing of urine
more common in elderly females
risk factors of urinary incontinence
advancing age
previous pregnancy and childbirth
high bmi
hysterectomy
fhx
classifications of urinary incontinence
overactive bladder/urge : detrusor overactivity. urge followed by uncontrollable leakage from few drops to complete bladder emptying
stress incontinence - leaking small amounts when cough or laugh
overflow incontinence - due to bladder outlet obstruction eg: enlarged prostate
mixed incontinence - urge and stress
functional incontinence:
comorbid physical conditions- pt cant get to bathroom
causes: dementia, sedating meds and injury/illness meaning decreased ambulation(walking from place to place independently)
investigations for urinary incontinence
bladder diaries - 3 days min
vaginal exam - exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (kegel exercises)
urine dipstick and culture
urodynamic studies
what are urodynamic studies?
management for urinary incontinence if urge incontinence is predominant?
bladder retraining - 6 weeks min
bladder stablising drugs: antimuscarinics 1st line
oxybutinin , tolterodine (immediate releases) or darifenacin (once daily preperation)
immediate release oxybutynin should be avoided in frail older women
mirabegron (beta-3-agonist) - poss useful if concern about anticholinergic side effects in frail elderly patient
management for urinary incontinence if stress incontinence is predominant?
pelvic floor muscle trainning - min 8 contractions 3 times daily for 3 months
surgery: retropubic mid-urethral tape procedures
duloxetine - poss to women if they decline procedures
what is duloxetine
combined noradrenaline and serotonin reuptake inhibitor
moa:
increased synaptic concentration of noradrenaline and serotonin within pudendal nerve
= increase stimulation of urethral striated muscles in the sphincter
= enhanced contraction
what is trigeminal neuralgia?
pain syndrome characterised by severe unilateral pain.
unilateral disorder
brief electric shock like pain
abrupt in onset and termination
limited to 1 or more division of trigeminal nerve
causes of trigeminal neuralgia
idiopathic mostly
could be compression of trigeminal roots by tumours or vascular problems.
how is the pain in trigeminal neuralgia evoked?
light touch : washing, shaving,smoking,talking, brushing teeth
areas susceptible to trigeminal neuralgia pain
small areaas in nasolabial fold or chin
red flag symptoms suggesting underlying cause of trigeminal neuralgia
sensory changes
deafness/other ear problems
hx of skin or oral lesions that could spread perineurally
pain only in opthalmic division of trigeminal nerve (eye socket, forehead and nose) or bilaterally.
optic neuritis
fhx of multiple sclerosis
age of onset before 40 yrs
management of trigeminal neuralgia
1st line: carbamazepine
failure to respond to treatment or atypical features (eg under 50) - refer to neurology
what is trichomonas vaginalis?
highly motile, flagellated protozoan parasite.
STI
features of trichomonas vaginalis?
vaginal discharge : offensive , yellow/green, frothy
vulvovaginitis
strawberry cervix
ph over 4.5
in men is usually asx but could cause urethritis
investigation for trichomonas vaginalis
microscopy of a wet mount shows motile trophozoites
management of trichomonas vaginalis
oral metronidazole 400-500mg for 5-7 days
bnf supports using one off dose of 2g metronidazole
difference between bacterial vaginosis and trichomonas vaginalis
bacterial vaginosis has thin white discharge and microscopy shows clue cells
trichomonas : frothy yellow-green discharge, vulvovaginitis, strawberry cervix, wet mount: motile trophozoites
they both have: offensive vaginal discharge, ph over 4.5 vaginal, treat with metronidazole
what is bacterial vaginosis?
overgrowth of predominately anaerobic organisms like GARDNERELLA VAGINALIS.
consequently fall in lactic acid producing aerobic lactobacilli = raised vaginal ph
not sti but only seen in sexually active women
featurs of bacterial vaginosis
vaginal discharge : white thin homogenous (fishy)
asx in 50%
amsels criteria for diagnosis of bacterial vaginosis - 3 of 4
3 of 4 of these:
thin white homogenous discharge - fishy
clue cells : microscopy (stippled vaginal epithelial cells)
ph of vagina over 4.5
positive whiff test (addition of potassium hydroxide = fishy odour)
how to manage bacterial vaginosis ?
asx woman: no treatment
sx: oral metronidazole for 5-7 days (70-80% cure), relapse rate over 50% in 3 months. if adherence an issue give 2g metronidazole single dose.
alternative topic metronidazole or topical clindamycin
pregnant: dont give metronidazole increased risk of preterm labour , low birth weight, chorioamnionitis, late miscarriage
previous taught oral metro should be avoided in 1st trimester and topical clindamycin used instead.
recent guidlines say oral metro is used throughout pregancy.
if asx: speak to obs if tx indicated
if sx: either oral metro for 5-7 days or topical tx.
dont give higher, stat dose of metro
how would treatment differ for a pregnant women with trichomonas vaginalis?
if breastfeeding or symptomatic pregnant:
oral metronidazole 400-500mg twice a day for 5-7 days.
dont give high dose 2g single dose.
asx pregnant: specialist advice needed.
what is chronic urticaria?
autoimmune
autoantibodies target mast cells , trigger to release histamine.
could be chronic idiopathic, chronic inducible(induced by triggers), autoimmune (autoimmune condition like sle)
tx: fexofenadine
where in women would trichomoniasis be found?
vagina
urethra
paraurethral glands
vertical transmission from mother to baby during vaginal delivery
a sore throat could be inflammation of what?
pharyngitis
tonsilitis
laryngitis
what tests should you not carry out in a patient with sore throat routinely?
throat swab and rapid antigen tests
managament of sore throat (tonsilitis)
paracetamol/ibuprofen - pain relief
abx not routinely (if centor 3 or more or feverpain is over 4)
single dose of oral corticosteroid might reduce severity and duration of pain(not in uk guidelines)
give the indications for giving abx in tonsilitis
features of marked systemic upset secondary to acute sore throat
unilateral peritonsilitis
hx of rheumatic fever
increased risk from acute infection (child with diabetes or immunodeficiency)
pt with acute sore throatacute pharyngitis/acute tonsilitis when 3 or more centor criteria present
what is the scoring system for sore throat?
centor criteria
fever pain criteria
how to use the centor criteria for sore throaT?
1 point for each:
tonsillar exudate prescence
hx of fever
absence of cough
tender anterior cervical lymphadenopathy or lymphadenitis
0,1,2 - 3-17% likelihood of isolating streptococci
3,4 - 32-56%
how would you use feverpain criteria for sore throat? (tonsilitis)
1 point for each
fever over 38
purulence (pharyngeal/tonsillar exudate)
attend rapidly - 3 days or less
severely inflamed tonsils
no cough or coryza
0,1 - 13-18%
2,3 - 34-40%
4,5 - 62-65%
if abx are indicated in tx of sore throat(tonsilitis) what would you give?
phenoxymethylpenicillin (10day course) or clarithromycin (if penicillin allergic)
causes of tonsilitis
mc: group a streptococcus (streptococcus pyogenes)
2nd mc: streptococcus pneumonia
poss:
haemophilus influenza
moraxella catarrhalis
staphyloccocus aureus
in the pharynx (at back of throat), there is a lymphoid tissue ring whats it called?
waldeyers tonsillar ring
what is the waldeyers tonsillar ring made of> (lymphoid tissue in pharynx)?
adenoids
tubal tonsils
palatine tonsils (infected and enlarged in tonsilitis)
lingual tonsil
which area of lymphoid tissue is typically infected and enlarged in tonsilitis?
palatine tonsils
complications of tonsilitis
otitis media
quinsy- peritonsillar abscess (between one of tonsils and wall of throat)
rheumatic fever and glomerulonephritis very rare
indications for tonsillectomy
only if :
sore throats due to tonsilitis not recurrent urti
7 episodes per yr for 1 year, 5 per yr for 2 years, or 3 per year for 3 yrs. with no other explanation
episodes of sore throat disabling and prevent normal functioning
obstructive sleep apnoea,stridor,dysphagia
quinsy
recurrent febrile convulsions secondary to tonsilitis
complications of tonsillectomy
primary (<24 hrs) - haemorrhage 2-30% (6-8 hours after) - due to inadequate haemostasis, pain . SURGERY
secondary (24hrs - 10days) - haemorrhage - due to infection, pain(may increase for upto 6 days) tx: admit and abx. severe bleed =surgery.
how would you define a tension type headache?
episodic primary headache
characteristic type features of tension type headache?
tight band around head or pressure sensation.
BILATERAL - migraine is unilateral
lower intensity than migraine
no aura, no nausea/vomiting or not aggravated by routine physical activity
could be stress related
could have migraine and tension together
how would you define a chronic tension type headache?
tension headache 15 days or more days per month
management of tension type headache
acute: aspirin, paracetamol or nsaid : 1st line
prophylaxis: 10 sessions of acupuncture over 5-8 weeks
low dose amitriptyline for prophylaxis. (nice dont support but used in uk)
how would you define migraine?
common type of primary headache.
UNILATERAL SEVERE THROBBING
nausea, photophobia, phonophobia
attack upto 72 hrs. - go to darkened quiet room during.
classic precipated by aura (1/3)
what is quinsy and why might you get it?
peritonsillar abscess (between one of tonsils and wall of throat)
complication of tonsillitis
what is an aura?
before migraine (fully reversible)
visual , progressive , last 5-60 minutes
transient hemianopic disturbance or a spreading scintillating scotoma (bright light abnormality blind spot) JAGGED CRESCENT
epidemiology of migraine
3 times more common in women
6% men 18% women
triggers of migraine
tiredness stress
alcohol
combined oral contraceptive pill
lack of food /dehydratin
cheese
chocolate
red wine
citrus fruit
menstruation
bright light
could you explain the migraine diagnostic criteria?
A: min 5 attacks fulfilling criteria b-d
B: headache lasting 4-72 hrs (untreated or unsuccessfully treated)
C: headache with at least 2 of : unilateral location, pulsating quality, moderate or severe pain intensity, aggravation by or causing avoidance of routine physical activity
D: during headache : nausea and/or vomit. photophobia and phonophobia
E: not attributed to any other disorder.
what is a hemiplegic migraine?
variant of migraine
motor weakness is a manifestation of aura in some attacks.
half patient have strong fhx.
VERY RARE . adolescent females
management of migraine
acute 1st line: oral triptan and nsaid or oral triptan and paracetamol
young people 12-17: nasal triptan over oral?
if above not effective/tolerated - non-oral metoclopramide or prochlorperazine. consider added non-oral nsaid/triptan.
why should you be careful prescribing metoclopramide in young patients (migraine)?
acute dystonic reactions could develop
dystonia(unintentional sustained muscle contractions)
prophylaxis
if migraine impact on qol and adl.
propranolol
topiramate : avoid in women of childbearing age - TERATOGENIC poss? - reduce effectiveness of hormonal contraceptives
amitryptiline
if these fail : course of 10 sessions of accupuncture over 5-8 weeks.
for some ppl: riboflavin (400mg once a day) help in reducing frequency and intensity
poss by specialist (not nice recommended) : candesartan , monoclonal antibody like erenumab (directed against calcitonin gene-related peptide receptor)
general rule for treating migraine
5-ht receptor agonist for acute treatment
5-ht receptor antagonist for prophylaxis
what would you give to a patient with predictable menstrual migraine?
frovatriptan (2.5mg twice a day)
or
zolmitriptan (2.5 mg twice or 3 times daily) - “mini prophylaxis)
what aura symptoms are atypical and would prompt further investigation (migraine)?
motor weakness
double vision
visual symptoms of 1 eye
poor balance
decreased gcs
how would you manage migraine during pregnancy?
paracetamol 1g : 1st line
nsaids : 2nd line - in 1st and 2nd trimest
avoid ASPIRIN AND OPOIDS eg: codeine
can you give combined oral contraceptive pill to a migraine patient and why ?
NO - contrindicated
increased risk of stroke
some women have increase migraine around menstruation , how to manage?
mefanamic acid or
combo of aspirin para and caffeine.
triptans also for acute situation.
can you do hormone replacement therapy for migraine pt?
yes but may make migraine worse
what is syphillis? (bacterium causing it)
sti caused by spirochaete treponema pallidum
characterise infection by primary secondary adn tertiary stags.
incubation period: 9-90 days
what features would you see in primary stage of syphillis?
chancre - painless ulcer at site of sexual contact
local non tender lymphadenopathy
often not seen in women (lesion could be on cervix)
what features would you see in secondary stage of syphillis?
occurs 6-10 weeks after primary infection
systemic symptoms
rash on trunk palms and soles
buccal snail track ulcers (30%)
condylomata lata ( painless, warty lesions on genitalia)
what features would you see in tertiary stage of syphillis?
gummas
ascending aortic aneurysms
general paralysis of the insane (memory language mood)
tabes dorsalis - slow degeneration of nerve cells and fibes that carry sensory info to brain
argyll - robertson pupil - smaller, irregular than normal pupils that dont constrict when exposed to light. constrict when focused on near object
what features would you expect in congenital syphillis?
keratitis - inflamed cornea
saddle nose
deafness
saber shins - anterior bowing of tibia
rhagades - linear cracks/fissures in skin - angles of mouth or anus
blunted upper incisor teeth (hutchinson teeth) - mulberry molars
how would you investigate for syphillis?
treponema pallidum is a very sensitive organism and cant be grown on artificial media.
diagnosis on clinical features, serology, microscopic exam of infected tissue.
serology:
- non treponemal tests - not specific to syphillis - possible false positives.
based on reactivity of serum from infected patients to a cardiolipin-cholestrol-lecithin antigen .
becomes negative after tx.
asses antibody quantity produced. eg: Rapid Plasma Reagin (RPR) and VDRL
- treponemal specific tests : more complex/expensive by specific. qualitiive only , reported as “reactive” or “non-reactive”. eg: (TP-EIA)
if both positive : active syphillis
if non positive and specific negative - false positive - due to sle or pregnancy
if negative non-trep and positive trep : successfully treated syphillis
bmi equation
weight kg / height m (2)
management of obesity
stepwise :
conservative: diet, exercise
medical: orlistat , liraglutide
surgical
MoA of orlistat
pancreatic lipase inhibitor
adverse effects: faecal urgency/incontinence and flatulence.
only prescribe as part of overal plan of management obesity for adult with :
bmi of 28 or more with associated rf
bmi of 30 or more
continued wt loss (eg5% at months)
orlistate normally used less than 1 yr
MoA of liraglutide
glucagon-like peptide 1 - (GLP-1) mimetic - used to manage T2DM
1 daily subcut injection
when used in t2dm it noted to cause wt loss.
use if:
bmi of 35 or more
prediabetic hyperglycaemia (hba1c 42-47)
give causes of false positive non-treponemal cardiolipin testd
pregnancy
sle , antiphospholipid syndrome
hiv
malaria
leprosy
tb
how would you manage syphilis?
1st line: intramuscular benzathine penicillin
alternative: doxycycline
nontreponemal titres need to be monitored after tx: fourfold decline in titres adequate.
what could happen as a result of syphillis tx?
jarisch-herxheimer reaction.
fever , rash, tachy, after 1st dose of abx.
not anaphylaxis bc no wheeze, hypotension.
due to endotoxins following bacterial death and typically occurs within a few hrs of tx.
no tx other than antipyretics. (remove fever)
give 2 causes of argyll robertson pupil
syphillis
diabetes mellitus
accomodation reflex present by pupillary reflex absent
small irregular pupils
no response to light by response to accomodate.
what is bariatric surgery?
surgery for obese that fail to lose weight with lifestyle and drugs.
nice reccomend for bmi 40-50 but over 30 is possible.
also with other conditions that may be caused by it like t2dm, htn.
types of bariatric surgery
primary restrictive operations : LAGB, SLEEVE, INTRAGASTRIC
Primarily malabsorptive operations : biliopancreatic diversion with duodenal switch (bmi>60)
mixed operations : Roux-en-Y gastric bypass surgery (restrictive and malabsorptive)
types of primary restrictive operations : bariatric surgery
LAGB - laparoscopic adjustable gastric banding: fewer comps but less weight loss. 1st line : bmi 30-39
sleeve gastrectomy - stomach reduced to 15% of original size
intragastric baloon: baloon can be left in stomach max 6 months.
how does the biliopancreatic diversion with duodenal switch work?
1st: sleeve gastrectomy, leave tube shaped stomach like banana.
valve that releases food to small intestine stays (pyloric valve) with small part of small intestine that connects to duodenum(stomach)
The second step bypasses the majority of the intestine by connecting the end portion of the intestine to the duodenum near the stomach. A BPD/DS both limits how much you can eat and reduces the absorption of nutrients, including proteins and fats.
bile duct - function
produces bile - bile emulsifies fat
connects organs to digestive system
how would you define obesity in children?
look at centiles
bmi at 91st centile or above - tailored clinical intervention
bmi at 98th centile or above - assess for comorbidity
causes of obesity in children
mc: lifestyle
more likely : asian 4* than white, female, taller kids
growth hormone deficiency
hypothyroidism
downs syndrome
cushings syndrome
prader-willi syndrome
name some consequences of obesity in children
orthopaedic problems : blounts disease (bowing of tibia), slipped upper femoral epiphyses
sleep apnoea
benign intracrainal htn
long term: increased chance of t2dm , htn, ihd
what is chronic rhinosinusitis
1/10 ppl affected.
inflammatory disorder of paranasal sinuses and lining of nasal passages lasting 12 or more weeks.
predisposing factors for chronic rhinosinusitis
atopy - hayfever, asthma
nasal obstruction - septal deviation or nasal polyps
recent local infection - rhinitis or dental extraction
swimming/diving
smoking
features of chronic rhinosinusitis
facial pain
nasal discharge : clear if allergic/vasomotor. thicker, purulent discharge suggests secondary infection
nasal obstruction: eg : mouth breathing
post-nasal drip: may produce chronic cough
how would you manage recurrent or chronic sinusitis
avoid allergen
intranasal corticosteroids
nasal irrigation with saline solution
what would be some red flag symptoms for someone with chronic rhinosinusitis
unilateral symptoms
persistent symptoms despite 3 months tx
epistaxis (nose bleed)
what is acute sinusitis?
inflammation of mucus membranes of paranasal sinuses.
sinuses are usually sterile - mc infectious agents:
steptrococcus pneumoniae,
haemophilus influenzae
rhinovirus
name some predisposing factors for acute sinusitis
nasal obstruciton - septal deviation or nasal polyps
recent local infection - rhinitis or dental extraction
swimming/diving
smoking
features of acute sinusitis
facial pain : frontal pressure pain worse on bending forward
nasal obstruciton
nasal discharge : thick and purulent
how would you manage acute sinusitis?
analgesia
intranasal decongestants or nasal saline (evidence limited)
nice: intranasal corticosteroids if symptoms over 10 days.
oral abx not needed but poss for severe presentation.
if so :
1st line: phenoxymethylpenicillin, co-amoxiclav if systemically unwell.
double sickening may be seen, where initial viral sinusitus worsens due to secondary bacterial infection
what is reactive arthritis?
arthritis developing following infection where organism cant be recovered from joint
“cant see , pee, climb a tree”
hla-b27 associated seronegative spondyloarthropathy.
encompasses reiters syndrome : urethritis, conjunctivitis, arthritis.
epidemiology of reactive arthritis
post-sti form much more in men - 10/1
post-dysenteric form equal sex incidence (intestine infection causing blood/mucus)
organisms most commonly associated with reactive arthritis
post-dysenteric form:
- shigella flexneri
- salmonella typhimurium
- salmonella enteritidis
- yersinia enterocolitica
- campylobacter
post-sti form
chlamydia trachomatis
how would you manage reactive arthritis
symptomatic : analgesia, nsaids, intra-articular steroids
sulfasalazine and methotrexate sometimes for persistent disease
symptoms rarely last over 12 months
features of reactive arthritis
time course : develops within 4 weeks of initial infection - symptoms 4-6 months last - 1/4 patient recurring episodes whilst 10% chronic disease.
arthritis typically asymmetrical oligoarthritis of lower limbs
dactylitis
symptoms of urethritis
eye : conjunctivities , anterior uveitis
skin :
circinate balanitis - painless vesicles on coronal margin of prepuce
keratoderma blenorrhagica - waxy yellow/brown papules on palms and soles
what is psoriasis?
chronic skin disorder.
red scaly patches on skin (extensor surfaces).
patients with it are at increase risk of arthritis and cardiovascular disease
pathophysiology of psoriasis
multifactorial
genetic : hla-b13, hla b-17 and hla -cw6. strong concordance with identical twins
immunological :
- abnormal t cell activity stimulates keratinocyte proliferation.
environmental: worsened by skin trauma, stress or triggered by strep infection or improved by sunlight.
subtypes of psoriasis
plaque psoriasis - mc subtype - well-dermacated red scaly patches affected the extensor surfaces, sacrum and scalp
flexural - contrast to plaque psoriasis you have SMOOTH skin
guttate - transient psoriatic rash triggered by strep infection. multiple red teardrop lesions on body
pustular - palms and soles
other features of psoriasis
nail signs : pitting , onycholysis
arthritis
complication of psoriasis
psoriatic arthropathy (10%)
increased incidence of metabolic syndrome
increase incidence of cardiovascular disease
increase incidence of VTE
psychological stress
what nail changes may be seen in psoriasis?
pitting
onycholysis
subungal hyperkeratosis
loss of the nail
nail changes affect fingers and toes.
there is an association with this and psoriatic athropathy - 80-90% of pts with psoriatic arthropthy have nail changes.
exacerbating factors of psoriasis
alcohol
trauma
drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACEi , infliximab
withdrawal of systemic steroids
which type of infection could trigger guttate psoriasis?
streptococcal infection
how would you manage psoriasis?
step wise
regular emoilents - reduce scale loss and pruritus
1st line:
potent corticosteroid once daily + vit d analogue once daily
apply seperately one morning one night
upto 4 weeks as initial tx
2nd line: if no improvement after 8 weeks offer: vit d analogue twice daily
3rd line: if no improvement after 8-12 weeks then offer either:
potent corticosteroid applied twice daily for upto 4 weeks or
coal tar preperation once or twice daily
short acting dithranol can also be used
what secondary care management could you do for psoriasis?
phototherapy - narrowband uv B light. 3 times a week.
photochemotherapy also - psoralen + uv A light (PUVA)
adverse effects : skin ageing, SCC(not melanoma)
systemic therapy:
oral methotrexate 1st line - useful for associated joint disease
ciclosporin
systemic retinoids
biological agents: infliximab, etanercept, adalimumab
ustekinumab (il-12/23 blocker) - showing promise in early trials
how would you manage psoriasis on the scalp?
potent topical corticosteroid once daily for 4 weeks.
if no improvement after 4 weeks use diff formulation of potent corticosteroid (shampoo/mouse) and/or topical agent to remove adherent scale (salicylic acid, emollients and oils) before application of potent corticosteroid
how would you manage psoriasis on the face, flexural and genital areas>?
mild or moderate potency corticosteroid once or twice daily for max 2 weeks
side effects of topical steroids
skin atrophy
striae
rebound symtpoms
systemic side effects when used on over 10% of body SA
scalp face and flexures (dont use for 1-2 weeks/month)
4 week break for them
no longer than8 week at a tame for potent and 4 for very potent
give some examples of vit d analogues
cacipotriol (dovonex)
calcitriol
tacalcitol
how do vit d analogues work
decreased cell division and differentiation = decreased epidermal proliferation
can use long term.
no smell/stain
reduce scale and thickness not erythema
avoid in pregnancy
max amount for adult 100g
how does dithranol work ? (psoriasis tx)
inhibits dna synthesis
wash off after 30 mins
adverse effects include burning, staining
features of chronic plaque psoriasis
80% of presentations in practise
erythematous plaque - silvery white scale
extensor surfaces- elbow,knees. also scalp trunk buttocks , periumbilical
clear delineation between normal and affected skin
1-10cm in size.
if scale removed, red membrane with pinpoint bleeding (AUSPITZ SIGN)
how would you identify guttate psoriasis?
tear drop
2 types of contact dermatitis
irritant contact : common non allergic - weak acid/alkali cause. detergent = erythema (no crusting/vesicles)
allergic contact: type 4 hypersensitivity. head following dyes?
acute wheeping eczema - tx with potent steroid. - margins of hairline
other cause: cement - its alkaline- irritant. dichromates (allergic contact)
what is polymyalgia rheumatica
elderly condition characterised by muscle stiffness and raised inflammatory markers.
closesly related to temporal arteritis. underlying cause not known.
features of polymyalgia rheumatica
patient over 60
rapid onset under 1 month
aching
morning stiffness in proximal limb muscles - weakness isnt considered a symptoms of it.
mild polyarthralgia, lethargy, depression, low grade fever, anorexia, night sweats
how would you investigate for polymyalgia rheumatica
raised inflammatory markers esr>40
creatine kinase and EMG normal
how would you treat polymyalgia rheumatica
prednisolone eg 15mg/od
pts should respond dramatically if not poss alternative diagnosis
3 main patterns of presentation in patients with peripheral arterial disease
intermittent claudication
critical limb ischaemia
acute limb-threatening ischaemia
features of acute limb threatening ischaemia
6 P’S
pale
pulseless
painful
paralysed
paresthetic
“perishing with cold”
how would you investigate for PAD/PVD?
handheld arterial doppler exam.
if doppler signs present , ABPI do
figure out whether ischaemia is because of thrombus (rupture of atherosclerotic plaque) or embolus (secondary to af)
for PAD, what factors would be suggestive that a thrombus has caused ischaemia?
pre-existing claudication with sudden deterioration
no obvious source of emboli
reduced/absent pulses in contralateral limb
evidence of widespread vascular disease (MI, STROKE, TIA, PREVIOUS VASCULAR SURGERY)
for PAD, what factors would be suggestive that an embolus caused ischaemia?
sudden onset of painful leg - under 24 hrs
no hx of claudication
clinically obvious source of embolus - af, recent mi
no evidence of peripheral vascular disease - normal pulses in contralateral limb
evidence of proximal aneursym - abdominal or popliteal
how would you manage PAD
INITIAL:
abc
analgesia : iv opoids
intravenous unfractionated heparin - prevent thrombus propagation, particularly if pt not suitable for surgery.
vascular review
definitive:
intra-arterial thrombolysis
surgical embolectomy
angioplasty
bypass surgery
amputation: for pts with irreversible ischaemia
