Acute and Emergency Flashcards
Causes of transient or spurious non-visible haematuria
urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse
Causes of persistent non-visible haematuria
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
Nephrotic syndrome is a clinical complex characterised by a triad of:
- Proteinuria (> 3g/24hr) causing
- Hypoalbuminaemia (< 30g/L) and
- Oedema
Nephrotic syndrome can be primary (idiopathic) or secondary to systemic diseases. Common causes include:
Primary causes: Minimal change disease, focal segmental glomerulosclerosis (FSGS), membranous nephropathy.
Secondary causes: Diabetes mellitus, systemic lupus erythematosus (SLE), amyloidosis, infections (HIV, hepatitis B and C), drugs (NSAIDs, gold therapy).
Clinical features of urinary tract infections
dysuria
urinary frequency
urinary urgency
cloudy/offensive smelling urine
lower abdominal pain
fever: typically low-grade in lower UTI
malaise
in elderly patients, acute confusion is a common feature
Examples of neuropathic pain
diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disc
First line treatment for neuropathic pain
amitriptyline, duloxetine, gabapentin or pregabalin
What is used as rescue therapy in neuropathic pain?
Tramadol
What is the breakthrough dose of morphine?
1/6 of daily morphine
What drug is preferred in palliative care for patients with mild-moderate renal impairment?
Oxycodone
What does metastatic bone pain respond to?
Strong opioids, bisphosphonates or radiotherapy
Opioid side effects
Nausea, Drowsiness, Constipation
Causes of acute interstitial nephritis
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
Features of acute interstitial nephritis
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
Investigations of acute interstitial nephritis
sterile pyuria
white cell casts
Prerenal causes of AKI
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
Intrinsic causes of AKI
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
Post renal causes of AKI
kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter
Risk factors of AKI
chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over
Drugs that should be stopped in AKI
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
Common identified causes of anaphylaxis:
food (e.g. nuts) - the most common cause in children
drugs
venom (e.g. wasp sting)
Symptoms of anaphylaxis
- Swelling of throat and tongue
- Hoarse voice and stridor
- Respiratory wheeze
-Dyspnoea
-Hypotension
-Tachycardia
How often can adrenaline be repeated in anaphylaxis?
Every 5 minutes
What is refractory anaphylaxis
defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
IV fluids should be given for shock
expert help should be sought for consideration of an IV adrenaline infusion
Management following stabilisation of anaphylaxis
- Non sedating oral antihistamines
-Serum tryptase levels
Referred to specialist allergy clinic
-Prescribed 2 auto injectors
Definition of antepartum haemorrhage
Antepartum haemorrhage is defined as bleeding from the genital tract after 24 weeks pregnancy, prior to delivery of the fetus
Symptoms of placental abruption
shock out of keeping with visible loss
pain constant
tender, tense uterus*
normal lie and presentation
fetal heart: absent/distressed
coagulation problems
beware pre-eclampsia, DIC, anuria
Symptoms of placenta praevia
shock in proportion to visible loss
no pain
uterus not tender*
lie and presentation may be abnormal
fetal heart usually normal
coagulation problems rare
small bleeds before large
Is the cervical OS open or closed in threatened miscarriage
Closed
What is a missed (delayed) miscarriage and is the cervical OS open or closed?
a gestational sac which contains a dead fetus before 20 weeks without the symptoms of expulsion
mother may have light vaginal bleeding / discharge and the symptoms of pregnancy which disappear. Pain is not usually a feature
cervical os is closed
Is the cervical OS open or closed in inevitable miscarriage?
Open
What is incomplete miscarriage and is the cervical OS open or closed?
not all products of conception have been expelled
pain and vaginal bleeding
cervical os is open
Risk factors of miscarriage
advanced maternal age, with women over 35 having a significantly higher risk
a history of previous miscarriages
previous large cervical cone biopsy
lifestyle factors such as
smoking
alcohol consumption
obesity
medical conditions
uncontrolled diabetes
thyroid disorders,
Medical management of missed miscarriage?
Oral mifepristone then 48 hours later misoprostol (vaginal, oral or sublingual)
Medical treatment of incomplete miscarriage
Single dose of misoprostol
Causes of recurrent miscarriages
antiphospholipid syndrome
endocrine disorders: poorly controlled diabetes mellitus/thyroid disorders. Polycystic ovarian syndrome
uterine abnormality: e.g. uterine septum
parental chromosomal abnormalities
smoking
First line treatment for animal bites
co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended
Common organisms after a human bite
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella
Treatment following human bite
Co-amoxiclav
What is lyme disease caused by and who spreads it
Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.
Early features of lyme disease (within 30 days)
erythema migrans
‘bulls-eye’ rash is typically at the site of the tick bite
typically develops 1-4 weeks after the initial bite but may present sooner
usually painless, more than 5 cm in diameter and slowlly increases in size
present in around 80% of patients.
systemic features
headache
lethargy
fever
arthralgia
Later features of lyme disease (after 30 days)
cardiovascular
heart block
peri/myocarditis
neurological
facial nerve palsy
radicular pain
meningitis
Investigations for lyme disease
-Diagnosed clinically if erythema migrans is present
-Enzyme linked immunosorbent assay antibodies to Borrelia Burgdorferi first line test
Management of Lyme disease
doxycycline if early disease. Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy)
people with erythema migrans should be commenced on antibiotic without the need for further tests
ceftriaxone if disseminated disease
Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)
Shockable rhythms
Ventricular fibrillation
Pulseless ventricular tachycardia
Non shockable rhythms
Asystole
Pulseless electrical activity
What drug do you give in non-shockable rhythms
Adrenaline 1mg and repeated every 3-5 minutes
What should be given to patients who are in VF/ pulseless VT after 3 shocks
Amiodarone
Reversible causes of cardiac arrest
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins
Features of acute coronary syndrome
chest pain
classically on the left side of the chest
may radiate to the left arm or neck
this may not always be present. Being elderly, diabetic or female makes an atypical presentation more likely
dyspnoea
nausea and vomiting
sweating
palpitations
Associations with aortic dissection
hypertension: the most important risk factor
trauma
bicuspid aortic valve
collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
pregnancy
syphilis
Features of aortic dissection
- Sharp chest/ back pain
- Pulse deficit
-Aortic regurgitation - Hypertension
- Non specific ECG changes
What is Boerhaaves syndrome
Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
Causes of myocarditis
viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin
Presentation of myocarditis
usually young patient with an acute history
chest pain
dyspnoea
arrhythmias
Investigations in pericarditis
bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP
ECG
tachycardia
arrhythmias
ST/T wave changes including ST-segment elevation and T wave inversion
Complications of pericarditis
heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication
Cyanotic congenital heart disease
tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia
Initial management of suspected cyanotic congenital heart disease
supportive care
prostaglandin E1 e.g. alprostadil
used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect
this can act as a holding measure until a definite diagnosis is made and surgical correction performed
4 Characteristics of TOF
ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta
Features of transposition of the great arteries
cyanosis
tachypnoea
loud single S2
prominent right ventricular impulse
‘egg-on-side’ appearance on chest x-ray
Classic presentation of extradural haematoma
patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury. The brief regain in consciousness is termed the ‘lucid interval’ and is lost eventually due to the expanding haematoma and brain herniation.
Imaging result of extradural haematoma
extradural haematoma appears as a biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.
Causes of hypoglycaemia
insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol
causes exaggerated insulin secretion
mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion
nesidioblastosis - beta cell hyperplasia
Features of hypoglycaemia
Sweating
Shaking
Hunger
Anxiety
NauseaWeakness
Vision changes
Confusion
Dizziness Convulsion
Coma
Treatment of hypoglycaemia in the hospital
If the patient is alert, a quick-acting carbohydrate may be given (as above)
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein
Causes of subarachnoid haemorrhage
intracranial aneurysm (saccular ‘berry’ aneurysms)
accounts for around 85% of cases
conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
arteriovenous malformation
pituitary apoplexy
mycotic (infective) aneurysms
Presentation of subarachnoid haemorrhage
headache
usually of sudden-onset (‘thunderclap’ or ‘hit with a baseball bat’)
severe (‘worst of my life’)
occipital
typically peaking in intensity within 1 to 5 minutes
there may be a history of a less-severe ‘sentinel’ headache in the weeks prior to presentation
nausea and vomiting
meningism (photophobia, neck stiffness)
coma
seizures
ECG changes including ST elevation
Investigation of subarachnoid haemorrhage
Non contract CT head
If normal and ofter 6 hours of symptom onset do a lumbar puncture- xanthochromia
Management of subarachnoid haemorrhage
bed rest
analgesia
venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)
vasospasm is prevented using a course of oral nimodipine
intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
Complications of subarachnoid haemorrhage
Re-bleeding
Hydrocephalus
Vasospasm
Hyponatraemia
Seizures
Typical presentation of subdural haemorrhage
involves a history of head trauma, which may range from minor to severe. Patients frequently exhibit a lucid interval followed by a gradual decline in consciousness.
Clinical features of subdural haemorrhage
- Altered mental state
- Focal neurological deficits
- Headache
- Seizures
Physical examination findings in subdural haemorrhage
- Papilloedema
- Pupil changes- unilateral dilated pupil
- Gait abnormality- ataxia
- Hemiparesis or hemiplegia
What imaging is done for subdural haemorrhage and what does it show
-CT Head
- Crescentic collection, not limited by suture lines
When shouldn’t hartmanns fluid be given
If the patient is hyperkalaemic
What fluid is routinely used in children
0.9% sodium chloride + 5% dextrose- potassium is added if required
Clinical features of Hyperosmolar hyperglycaemic state
- Comes on over days
- Clinical signs of dehydration
- Polyuria
- Polydipsia
- Lethargy
- Nausea and vomiting
- Altered consciousness
- Focal neurological deficits
- Hyperviscosity
Management of hyperosmolar hyperglycaemic state
- Fluid replacement - IV 0.9% sodium chloride solution
Complications of hyperosmolar hyperglycaemic state
- MI
- Stroke
Symptoms of life threatening asthma attach
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Normal pCO2- indicated exhaustion
What is acute bronchitis
a type of chest infection which is usually self-limiting in nature. It is a result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.
Symptoms of acute bronchitis
Cough
Sore throat
Rhinorrhoea
Wheeze
Low-grade fever
Treatment of acute bronchitis
- Analgesia
- Good fluid intake
- Antibiotic therpay- doxycycline
Features of acute coronary syndrome
chest pain
classically on the left side of the chest
may radiate to the left arm or neck
this may not always be present. Being elderly, diabetic or female makes an atypical presentation more likely
dyspnoea
nausea and vomiting
sweating
palpitations
What is bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation.
Features of bronchiectasis
- Persistent productive cough
- Dyspnoea
- Haemoptysis
- Coarse crackles
- Wheeze
- Clubbing
Features of lung cancer
persistent cough
haemoptysis
dyspnoea
chest pain
weight loss and anorexia
hoarseness
seen with Pancoast tumours pressing on the recurrent laryngeal nerve
superior vena cava syndrome
Clubbing
Cervical lymphadenopathy
Causative pathogens of pneumonia
Bacteria: e.g Streptococcus pneumoniae - the most common cause of community acquired pneumonia (CAP)
Virus
Fungus (e.g. Pneumocystis jiroveci
Risk factors for pneumonia
Aged under 5 or over 65-years-old
Smoking
Recent viral respiratory tract infection
Chronic respiratory diseases: e.g. cystic fibrosis and COPD
Immunosuppression: e.g. cytotoxic drug therapy and HIV
Patients at risk of aspiration: e.g. those with neurological diseases such as Parkinson’s disease or those with oesophageal obstruction
IV drug users
Other non-respiratory co-morbidities: e.g. diabetes and cardiovascular disease
Presentation of pneumonia
Symptoms:
A cough with purulent sputum (rust coloured/bloodstained)
Dyspnoea
Chest pain (may be pleuritic in nature)
Fever
Malaise
Signs:
Signs of systemic infection: High temperature, tachycardia, hypotension, confusion
Tachypnoea
Low oxygen saturation (below 95% or below 88% in patients with COPD)
On auscultation, there may be reduced breath sounds, bronchial breathing, and crepitations/crackles
Dullness on percussion (fluid)
What score is used in pneumonia
CURB65
Confusion (abbreviated mental test score <= 8/10)
urea > 7 mmol/L
Respiration rate >= 30/min
Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
Aged >= 65 years
What is a primary spontaneous pneumothorax
Occurs without underlying lung disease, often in tall, thin, young individuals. PSP is associated with the rupture of subpleural blebs or bullae.
What is secondary spontaneous pneumothorax
Occurs in patients with pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor
Features of pneumothorax
Symptoms tend to come on suddenly:
dyspnoea
chest pain: often pleuritic
Signs
hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia
Symptoms of tension pneumothorax
- Respiratory distress
- Tracheal deviation away from the side of the pneumothorax
- Hypotension
Causes of hypercalcaemia
- Primary hyperparathyroidism
- Malignancy
- Sarcoidosis
- Vitamin D intoxication
- Acromegaly
-Thyrotoxicosis
-Dehydration
-Addisons
-Pagets disease of the bone
Causes of hyperkalaemia
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion
ECG changes in hyperkalaemia
peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern
Treatment of hyperkalaemia
- IV Calcium gluconate
- Combined insulin/ dextrose infusion
Causes of hypernatraemia
- Dehydration
- Osmotic diuresis
- Diabetes insipidus
- Excess IV saline
Causes of hypocalcaemia
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
Treatment of hypocalcaemia
- IV Calcium gluconate
Signs of hypocalcaemia
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval
Trousseau’s sign
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
wrist flexion and fingers are drawn together
seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people
Chvostek’s sign
tapping over parotid causes facial muscles to twitch
seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people
Causes of hypokalaemia with alkalosis
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Causes of hypokalaemia with acidosis
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
Causes of hypomagnesaemia
drugs
diuretics
proton pump inhibitors
total parenteral nutrition
diarrhoea
may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia
e.g. secondary to hyperparathyroidism
calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s
Features of hypomagnesaemia
paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity
Causes of epistaxis
most cases of epistaxis tend to be benign and self-limiting. Exacerbation factors include:
nose picking
nose blowing
trauma to the nose
insertion of foreign bodies
bleeding disorders
immune thrombocytopenia
Waldenstrom’s macroglobulinaemia
juvenile angiofibroma
benign tumour that is highly vascularised
seen in adolescent males
cocaine use
the nasal septum may look abraded or atrophied, inquire about drug use. This is because inhaled cocaine
cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum.
hereditary haemorrhagic telangiectasia
granulomatosis with polyangiitis
Management of epistaxis
- Ask pt to sit with torso forward and mouth open
-Pinch cartilaginous area of nose firmly - Nasaptin to reduce crusting
-Cautery used initially if source of bleeding is visible - Packing if bleeding no visualised
- Sphenopalatine ligation in theatre
Features of corneal abrasion
-Eye pain
-Lacrimation
-Photophobia
-Foreign body sensation
-Decreased visual acuity
Investigation for corneal abrasion and management
Fluorescein staining and topical antibiotic therapy
Orbital compartment syndrome features and management
- Eye pain/ swelling
-Proptosis
-Rock hard eyelids
-Urgent lateral canthotomy to decompress orbit
What is subconjunctival haemorrhage
Bleeding of blood vessels into subconjuctive space
Risk factors of sunconjunctival haemorrhage
- Trauma
-Idiopathic
-Valsava manoeuvre
-Hypertension
-Bleeding disorders
-Drugs- aspirin , NSAIDs, anticoagulants
-Diabetes
-Arterial disease and hyperlipidaemia
What test should all patients have with suspected upper GI bleeding within 24 hours
Endoscopy
Management of variceal bleeding
- Terlipressin and prophylactic antibiotics at presentation
-Band ligation for oesophageal varices
-Transjugular intrahepatic portosystemic shunts if bleeding isn’t controlled
Prophylaxis of variceal haemorrhage
-Propanolol
-Endoscopic variceal band ligation
-Transjugular intrahepatic portosystemic shunt
Headache red flags
compromised immunity, caused, for example, by HIV or immunosuppressive drugs
age under 20 years and a history of malignancy
a history of malignancy known to metastasis to the brain
vomiting without other obvious cause
worsening headache with fever
sudden-onset headache reaching maximum intensity within 5 minutes - ‘thunderclap’
new-onset neurological deficit
new-onset cognitive dysfunction
change in personality
impaired level of consciousness
recent (typically within the past 3 months) head trauma
headache triggered by cough, valsalva (trying to breathe out with nose and mouth blocked), sneeze or exercise
orthostatic headache (headache that changes with posture)
symptoms suggestive of giant cell arteritis or acute narrow-angle glaucoma
a substantial change in the characteristics of their headache
Features of influenza
fever greater than 38ºC
myalgia
lethargy
headache
rhinitis
sore throat
cough
diarrhoea and vomiting
Triad of pre-eclampsia
- New onset hypertension
-Proteinuria
-Oedema
Complications of pre-eclampsia
-Eclampsia
-Fetal complications- prematurity and intrauterine growth retardation
-Liver involvement
-Haemorrhage
-Cardiac failure
Risk factors of pre-eclampsia
- Hypertensive disease in previous pregnancy
-CKD
-Autoimmune disease
-Diabetes
-Chronic hypertension
-First pregnancy
-Over 40
-High BMI
-Family history
-Multiple pregnancy
How to reduce the risk of pre-eclampsia
-Aspirin daily from 12 weeks gestation until birth
Treatment of pre-eclampsia
-Oral labetalol or nifedipine if asthmatic
-Delivery of baby is definative
What vessels are affected in temporal arteritis
-Medium and large sized vessels
Features of temporal arteritis
- Headache
-Jaw claudication
-Vision loss
-Tender palpable temporal artery
-Aching, morning stiffness in proximal limb weakness
-Lethargy, depression, fever, anorexia, night sweats
Investigations in temporal arteritis
-ESR/ CRP
-Temporal artery biopsy- skip lesions
Treatment of temporal arteritis
-High dose prednisolone if no vision loss
-IV methylprednisolone if vision loss
-Bone protection- bisphosphonates
Treatment for paracetamol overdose
- Activated charcoal
-N acetylcysteine
-Liver transplant
Treatment for opioid overdose
Naloxone
Symptoms of lead poisoning
- Abdominal pain
-Peripheral neuropathy
-Fatigue
-Constipation
-Blue lines on gum margin
Definition of postpartum haemorrhage
Blood loss of more than 500ml after vaginal delivery and may be primary or secondary
Causes of primary postpartum haemorrhage
-Tone- uterine atony
-Trauma- perineal tear
-Tissue- Retained placenta
-Thrombin- clotting/ bleeding disorders
Risk factors of primary postpartum haemorrhage
previous PPH
prolonged labour
pre-eclampsia
increased maternal age
polyhydramnios
emergency Caesarean section
placenta praevia, placenta accreta
macrosomia
Treatment of postpartum haemorrhage
-ACB approach
-Palpate the uterine fundus and rub it to stimulate contractions
-IV oxytocin
-IV ergometrine
-Carboprost IM
-Misoprostol sublingual
-Intrauterine balloon tamponade
What is secondary postpartum haemorrhage and what causes it
Secondary PPH occurs between 24 hours - 12 weeks. It is typically due to retained placental tissue or endometritis.
What are anal fissures
longitudinal or elliptical tears of the squamous lining of the distal anal canal. If present for less than 6 weeks they are defined as acute, and chronic if present for more than 6 weeks.
Risk factors of anal fissure
-Constipation
-IBD
-Sexually transmitted infections
Symptoms of anal fissures
painful, bright red, rectal bleeding
around 90% of anal fissures occur on the posterior midline.
if the fissures are found in alternative locations then other underlying causes should be considered e.g. Crohn’s disease
Management of anal fissure
-Soften stool
-Lubricants
-Topical anaesthetics
-Analgesia
-Topical GTN
-Surgery
Features of intussusception
intermittent, severe, crampy, progressive abdominal pain
inconsolable crying
during paroxysm the infant will characteristically draw their knees up and turn pale
vomiting
bloodstained stool - ‘red-currant jelly’ - is a late sign
sausage-shaped mass in the right upper quadrant
Investigation of intussusception
-Ultrasound- target like mass
Treatment of intussusception
-Air enema
-Surgery
Investigations for rectal bleeding
-Digital rectal exam
-Procto-sigmoidoscopy
-Colonoscopy
How to diagnose epididymal cyst and what is the management
-Ultrasound and supportive management or surgical removal
What is a hydrocele and what is the main feature
-Accumulation of fluid within the tunica vaginalis
-Transilluminates with a pen torch
What is a varicocele, what is the main investigation and main feature
-Abnormal enlargement of testicular veins
-Ultrasound with doppler
-Bag of worms
Risk factors for testicular cancer
-Cryptorchidism
-Infertility
-Family history
-Kleinefelters syndrome
-Mumps orchitis
Main feature of testicular torsion
-Cremasteric reflex lost
-Elevation of testis does not ease pain
Risk factors for suicide
male sex (hazard ratio (HR) approximately 2.0)
history of deliberate self-harm (HR 1.7)
alcohol or drug misuse (HR 1.6)
history of mental illness
depression
schizophrenia: NICE estimates that 10% of people with schizophrenia will complete suicide
history of chronic disease
advancing age
unemployment or social isolation/living alone
being unmarried, divorced or widowed
Risk factors for completing suicide
efforts to avoid discovery
planning
leaving a written note
final acts such as sorting out finances
violent method
Protective factors of suicide
family support
having children at home
religious belief
Sepsis 6
- Administer oxygen: Aim to keep saturations > 94% (88-92% if at risk of CO2 retention e.g. COPD)
- Take blood cultures
- Give broad-spectrum antibiotics
- Give intravenous fluid challenges
NICE recommend a bolus of 500ml crystalloid over less than 15 minutes - Measure serum lactate
- Measure accurate hourly urine output
Types of shock
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic
Pathogen causing egiglottitis
Haemophilus influenza type B
Features of epiglottitis
rapid onset
high temperature, generally unwell
stridor
drooling of saliva
‘tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
What sign is shown on xray for epiglottitis and what is the management
-Thumb sign
-IV antibiotics
-Endotracheal intubation
What causes croup and what is the management
-Parainfluenza virus
-Dex single dose
Treatment for cocaine toxicity
Benzodiazepines
Symptoms of acute angle closure glaucoma
severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
Management of acute angle closure glaucoma
-Pilocarpine
-Timolol
-Apraclonidine
-IV acetazolamide
-Laser peripheral iridotomy
What is the most common cause of blindness in the UK
- Age related macular degeneration
Risk factors for age related macular degeneration
- Age
-Smoking
-Family history
Investigations for age related macular degeneration
- Slit lamp microscopy
-Fluorescein angiography
-Optical coherence tomography
Treatment of age related macular degeneration
-Vascular endothelial growth factor
Features of anterior uveitis
acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired
Conditions associated with anterior uveitis
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen
Treatment of anterior uveitis
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
Causes of cataracts
Age
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
What is central retinal artery occlusion due to?
-Thromboembolism or arteritis
Features of central retinal artery occlusion
sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina
Investigation and management of corneal abrasion
-Fluorescein staining and topical antibiotics
Causes of optic neuritis
multiple sclerosis: the commonest associated disease
diabetes
syphilis
Treatment of optic neuritis
-High dose steroids
Risk factors of scleritis
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
Treatment of scleritis
-Same day assessment by ophthalmologist
-Oral NSAIDs
Common causes of sudden painless loss of vision
ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
retinal migraine
