Acute and Emergency Flashcards by Hollie Peach

Causes of transient or spurious non-visible haematuria

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

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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

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Nephrotic syndrome is a clinical complex characterised by a triad of:

Proteinuria (> 3g/24hr) causing
Hypoalbuminaemia (< 30g/L) and
Oedema

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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).

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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

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Examples of neuropathic pain

diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disc

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First line treatment for neuropathic pain

amitriptyline, duloxetine, gabapentin or pregabalin

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What is used as rescue therapy in neuropathic pain?

Tramadol

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What is the breakthrough dose of morphine?

1/6 of daily morphine

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What drug is preferred in palliative care for patients with mild-moderate renal impairment?

Oxycodone

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What does metastatic bone pain respond to?

Strong opioids, bisphosphonates or radiotherapy

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Opioid side effects

Nausea, Drowsiness, Constipation

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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

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Features of acute interstitial nephritis

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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Investigations of acute interstitial nephritis

sterile pyuria
white cell casts

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Prerenal causes of AKI

hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

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Intrinsic causes of AKI

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

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Post renal causes of AKI

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

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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

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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

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Common identified causes of anaphylaxis:

food (e.g. nuts) - the most common cause in children
drugs
venom (e.g. wasp sting)

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Symptoms of anaphylaxis

Swelling of throat and tongue
Hoarse voice and stridor
Respiratory wheeze
-Dyspnoea
-Hypotension
-Tachycardia

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How often can adrenaline be repeated in anaphylaxis?

Every 5 minutes

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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

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Management following stabilisation of anaphylaxis

Non sedating oral antihistamines
-Serum tryptase levels
Referred to specialist allergy clinic
-Prescribed 2 auto injectors

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Definition of antepartum haemorrhage

Antepartum haemorrhage is defined as bleeding from the genital tract after 24 weeks pregnancy, prior to delivery of the fetus

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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

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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

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Is the cervical OS open or closed in threatened miscarriage

Closed

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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

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Is the cervical OS open or closed in inevitable miscarriage?

Open

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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

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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,

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Medical management of missed miscarriage?

Oral mifepristone then 48 hours later misoprostol (vaginal, oral or sublingual)

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Medical treatment of incomplete miscarriage

Single dose of misoprostol

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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

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First line treatment for animal bites

co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended

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Common organisms after a human bite

Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella

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Treatment following human bite

Co-amoxiclav

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What is lyme disease caused by and who spreads it

Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.

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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

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Later features of lyme disease (after 30 days)

cardiovascular
heart block
peri/myocarditis
neurological
facial nerve palsy
radicular pain
meningitis

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Investigations for lyme disease

-Diagnosed clinically if erythema migrans is present
-Enzyme linked immunosorbent assay antibodies to Borrelia Burgdorferi first line test

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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)

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Shockable rhythms

Ventricular fibrillation
Pulseless ventricular tachycardia

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Non shockable rhythms

Asystole
Pulseless electrical activity

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What drug do you give in non-shockable rhythms

Adrenaline 1mg and repeated every 3-5 minutes

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What should be given to patients who are in VF/ pulseless VT after 3 shocks

Amiodarone

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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

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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

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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

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Features of aortic dissection

Sharp chest/ back pain
Pulse deficit
-Aortic regurgitation
Hypertension
Non specific ECG changes

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What is Boerhaaves syndrome

Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.

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Causes of myocarditis

viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin

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Presentation of myocarditis

usually young patient with an acute history
chest pain
dyspnoea
arrhythmias

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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

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Complications of pericarditis

heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication

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Cyanotic congenital heart disease

tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia

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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

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4 Characteristics of TOF

ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

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Features of transposition of the great arteries

cyanosis
tachypnoea
loud single S2
prominent right ventricular impulse
‘egg-on-side’ appearance on chest x-ray

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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.

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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.

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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

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Features of hypoglycaemia

Sweating
Shaking
Hunger
Anxiety
NauseaWeakness
Vision changes
Confusion
Dizziness Convulsion
Coma

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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

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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

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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

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Investigation of subarachnoid haemorrhage

Non contract CT head
If normal and ofter 6 hours of symptom onset do a lumbar puncture- xanthochromia

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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

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Complications of subarachnoid haemorrhage

Re-bleeding
Hydrocephalus
Vasospasm
Hyponatraemia
Seizures

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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

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

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Acute and Emergency Flashcards

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