emergency/ acute conditions Flashcards
COPD, AKI, HHS, DKA, acid base problems, acute bronchitis, lung cancer, cellulitis, urticaria, polymyalgia reumatica, psoriasis,
what is the nature of cough in COPD
productive
other causes od COPD other than smoking
alpha-1 antitrypsin + less cadmium coal cotton and cement
other X-ray fidning of copd
bullae that may mimic a pneumothorax
pathophysiology
bronchitis and emphysema
complication that can lead to peripheral oedema
right heart failure
how is COPD graded
FEV1 value (fev1/ fvc) is less than 70% always <80 stage 1- mild only if symptomatic
50-79 stage two moderate
30-47 stage 3 severe
<30 very severe
long term management of copd
saba or sama and if bad add LABA and LAMA and if asthmatic features ICS + LABA
MOST COmmon cause of exacerbration of COPD
haemophilus influenzae (bacterium) bacteria more common than viral
acute COPD management
nebulised SABA OR muscarinic antagonist and oxygen initial goal 88-92 on 28% venturi 4 l/min
if later found co2 nrmal then aim for 92-8
if type 2 resp failure bipap
presenting symptoms of DKA
abdo pain, polyuria, polydipsia, dehydration, kussmal respiration (deep hyperventilation)
diagnostic features of DKA
ketones> 3, acid< 7.3, glucose> 11 bicarb 15
Triggers of DKA
missed insulin, infection, MI!!
Pathophysiology of DKA
increased lipolysis leading to free fatty acids in blood ultimately converted to ketone bodies
what is a iatrogenic complication of DKA
cerebral oedema more common in young adults and children needs monitroing of focal neurological symmptoms
does HHS or DKA have higher mortality
HHS 20% VS DKA 1%
diagnostic features of HHS
v high glu» 30 no acidosis high serum osmolality, no ketones> 3, hypovolaemia
pathophysiology of HHS
glucose is so high leading to osmotic diuresis meaning glucose leaks from kidneys in urine driving water with it leading to dehydration high osmolality of serum ect
clinical symptoms of HHS
volume depletion: 1) dehydration, polyuria, polydipsia,
2) neuro: altered level of consciousness and focal neuro deficits
3) hyperviscosity leading ot MI STROKE , peripheral arterial thormbosis
4) Systemic: lethargy, nausia and vomiting
management of HHS
FLUID ressucitation, not too much though give slowly 0.9 normal saline only at the start
can add K if low - monitor this
insulin SHOULD NOT be started before glucose STOPS dropping on only fluids (NOOO DEXTROSEE THIS IS FOR DKA)
AKI symptoms
- can be low urine output (oliguria defined < 0.5 ml/kg/h)
- pulmonary and peripheral oedema can occur (fluid retention)
- arrhythmias can occur (high K)
- uraemic features such as encephalopathy or pericarditis)
AKI diagnostics
U+ E typicall stuff creatinine, urea, (na and k are affected but part of diagnostic guidelines )
creatinine > 50% increase in 7 days
creatinine
creatinine >26mmol/L in 48 h
or <0.5 ml/kg/hr output for more than 6 hours - in question may be framed as ml/hr so dont get confused
causes of AKI
pre renal intrinsic and post renal
1) hypoperfusion- hypovolaemia, stenosis
2) renal: glomerulonephritis, acute tubular necrosis ect
3) post renal: renal stone, BPH external compression of ureter- anything backlogging fluid into kidneys
general management AKI
supportive meaning give fluids but not too much to avoid overload
stop dangerous meds that may be contributing or that are toxic to kidneys (not directly contributing)
cardiac management AKI if needed
calcium gluconate IV
K balancing in AKI management
combined insulin and dextrose infusion for short term K shift from blood to cells and nebilised saba
removal of K is calcium resonium or loop diuretics
metabolic acidosis 2 types
normal anion gap or increased
explain metabolic acidosis with normal anion gap
CL is compensating for the drop in HCO3 and some examples are diarrhoea, renal tubular acidosis, addisson’s
anion gap calculation
NA + K - (HCO3 + CL)
EXPLAIn metabolic acidosis with high anion gap
here the drop in HCO3 is happening because of some other anion that is present in blood like a toxin so ex lactic acid in hypoxia or hypoperfusion or ketones in dka or alcoholic ketoacidosis, renal failure, toxins.
causes of metabolic alkalosis
vomiting/ aspiration, DIURETICS, hypokalaemia, cushings
causes of resp acidosis
COPD and other resp exacerbratons but also opposite of resp alkalosis so here being calm instead of panic attacks ect so benzos and other sedatives
resp alkalosis
panic attack, PE, CNS disorders, altitude, pregnancy
acute bronchitis duration
around 3 weeks
acute bronchitis cough duration
25% of people have it for more than 3 weeks
difference between acute bronchitis and pneumonia
bronchitis does not have any chest exam findings like consolidation so dull on percussion ect vs pneumonia does and pneumonia almost always systemic upset or one of the more serious symptoms
most common viral or bacterial for acute bronch?
viral
how do you diagnose acute bronchitis?
clinically anf can use CRP if avaialable to guide ABx use
when ab for bronchitis
if systemically unwell or crp 20-100 and immediate ab if > 100
first and second line ab for acute bronchitis
doxycycline first and amoxicillin second
presentation of lung cancer
dry cough reccurent infections breathless haemoptysis VOICE HOARSENESS when pressing on reccurent laryngeal nerve, chest pain
physical exam findings of lung cancer
fixed monophonic wheeze, supraclavicular and cervical lymphadenopathy, clubbing, syperior vena cava syndrome
first line investigation lung cacner
chest xray
next lung cancer investigations if xray suggestive
chest ct, biopsy from bronchoscopy if central - this can be US guided or biopsy CT guided for peripheral
blood test finding in lung cancer
raised platelets
scan for staging and metastasis looking and determining if surgery in non small cell mostly
PET CT
management in lung cancer
surgical if suitable, partial or total lobectomy, paliative or curative radioherapy, chemotherapy (usually not that effective even for non small cell)
types of lung cancer and rank how common
1) adenocarcinoma - most common and most common for non smokers
2) squamous cell - commonly smokers
3) small cell- very strong association with smoking
4) karge cell- very rare and atypical
adenocarcinoma features
typically peripheral
most common for non smokers
gynecomastia
hypertrophic pulmonary osteoarthropathy
squamous features
common central
if it secretes any ectopic hormones most commonly TSH, parathyroid gormones
small cell features
common central
VERY COMMON ectopic hormones eg ADH- so low sodium, or ACTH
large cell features
may secrete b hCG and is not common and atypical large cells seen. on micrtoscopy undifferentiated
cellulitis presentation
red, well demarcated, very painful, usually 1 extremity, BULLAE AND BLISTERS WITH BAD DISEASE
systemic: i know them and also nausea
most common and second most common cellulits causative organisms
strep pyogenes
staph aureus
risk factors for cellulitis
skin opening eg insect bite or cut, T2D, obese, immunocopromised, previous cellulitis
how is cellulitis diagnosed
clinically
classification system of cellulitis
Eron classification (not elon like leon musk NOT lol)_
what are the classes of eron system and the management of each
1: no systemic disease and can be treated with oral flucloxacillin or oral clarythromicin or erythromycin (pregnant) no admission
2: some systemic involvement or a comorbidity that puts you at risk - unclear admission and treatment depends on if local nurses can do IV antibiotics
3: systemic involvement severe with tachy and hypolaemia or a co morbidity that is really bad and could interfere with treatment –oral coamoxiclav or IV clindamycin or IV Cefuroxine or IV ceftriaxone
4 is sepsis syndrome or severe infection such as necrotising fascitis – same as 3
urticaria presentation
“hives, weals,” spots, basically pruritic usually allergic
management of urticaria
initially non sedative antihistamine such as loratadine or cetirizine 6 weeks max
additional management of urticaria
sedative anti histamine such as chlorphenamine
urticaria treatment if severe persistent episodes
add pred course maybe for 5 days
psoriasis pathophysiology
mutlifactorial and not fully understood
genetics definitely at play since high concordance rate in identical twins and HLA-13 -17 believed to be involved B-17 cW 6
Immunological - abnormal t cell stimulation- th17 il17 - leading to keratinocyte proliferation
environmental- worsened with stress, trauma
better with sunlight
triggered by strep infection
types of psoriasis
plaque psoriasis: scaly red,
flexor psoriasis: not scaly
guttate psoriasis: red spots all over body, transient type and commonly caused by streptococcal nfection
pustular psoriasis common in palms and soles
other features of psoriasis
arhtritis and nail pitting and onycholysis
complications of psoriasis
increased incidence of:
arthritis
CVD
psychological distress
VTE
metabolic syndrome
polymyalgia reumatica presentation
proximal muscle stiffness, morning rapid onset within a month, NOT muscle weakness, usually >60 year old woman
other possible symptoms of ppolymyalgia reumatica
mild arthralgia, lethargy, depression, low grade fever, anorexia, night sweats
investigation findings of polymyalgia reumatica
high inflammatory markers such as CRP ESR but not other stuff like high CK or any other autoimmune AB
condition commonly associated with polymyalgia reumatica
temporal arteritis - 15% of patients with polymyalgia get it
