Year 3 Lectures
Terms in this set (512)
what are the commonest causes of airway compromise?
reduced level of consciousness
management of airway compromise
head tilt/chin lift
removal of obstruction
assessment of breathing (ABCDE)
Types of shock
what normally drives respiration
what is hypoxic drive and who does it occur in?
COPD patients breathe in response to hypoxia instead of high CO2 levels (removal of hypoxia = removal of respiratory drive)
factors affecting heart rate
factors affecting stroke volume
duration of contraction
what is the definition of hypotension?
systolic BP < 90
or 20mmHg below patient's norm
assessment of circulation (ABCDE)
end organ perfusion
what is the definition of shock?
inadequate tissue perfusion
clinical signs of shock
tachypnoea (often secondary to metabolic acidosis)
What is the definition of anaphylaxis?
sever life threatening generalised or systemic hypersensitivity reaction
what is a fluid challenge?
administer 250-500mls fluid through a 16g cannula
measure pulse and BP before and after
if improved, patient is hypovolaemic
elements of SOFA score?
mean arterial pressure
Glasgow Coma Scale
elements of qSOFA (HAT) score
hypotension (sBP <100)
altered mental state
What is the definition of shock?
inadequate tissue perfusion
Symptoms of anaphylaxis
Treatment for anaphylaxis
(0.5mls of 1 in 1000)
What is sepsis?
life threatening organ dysfunction caused by a disregulated host response to infection- A clinical syndrome caused by the body's immune and coagulation systems being switched on by the presence of infection (bacteria or viruses) in the blood
What is severe sepsis?
End organ dysfunction or tissue hypoperfusion (decreased blood flow) in addition to sepsis
What is septic shock?
Life-threatening condition that is characterised by low blood pressure despite adequate fluid replacement in addition to organ dysfunction and sepsis
What are the sepsis 6?
What immune cells are responsible for mediating anaphylaxis?
What is anaphylactic shock?
systemic reaction characterised by acute circulatory failure (systolic BP <70) with a faint rapid or unobtainable pulse and respiratory failure
Mediators of type 1 hypersensitivity
IgE antibodies and mast cells
Examples of type 1 hypersensitivity
Mediators of type 2 hypersensitivity
antibodies binding to cell surface antigens (+/- complement)
Examples of type 2 hypersensitivity
Rhesus factor incompatibility
Mediators of type 3 hypersensitivity
circulating immune complexes and IgG
Examples of type 3 hypersensitivity
Mediators of type 4 hypersensitivity
CD4+ T cells
Examples of type 4 hypersensitivity
type 1 diabetes
What are the products of mast cell degranulation?
when does type 4 hypersensitivity develop?
2-3 days after antigen exposure
what is a granuloma?
macrophages + lymphocytes
What receptors does histamine act through?
What are the effects of histamine?
smooth muscle contraction
What are the effects of mast cell mediators?
smooth muscle contraction
In addition to adrenaline, what other drugs would be used in the management of anaphylaxis?
(H1 receptor antagonist)
200mg hydrocortisone (steroid)
What type of virus is HIV?
What are the AIDS defining illnesses?
Atypical mycobacterium Pneumocystis jiroveci
What is the primary pathophysiology of HIV?
Destruction of CD4+ T cells (impairment of cell mediated immunity)
how is HIV transmitted?
shared IV drug paraphernalia
mother-child transmission (birth or breastfeeding)
what is the viral set point of HIV?
the host immune response keeps the virus at a relatively stable level
what signs are suggestive of declining immune function (e.g. during HIV infection)
herpes zoster infection
how can HIV be diagnosed?
CD4+ cell count
HIV blood test
what are the problems with a absolute CD4+ cell count?
can vary with infection, time of day
why is a CD4+ cell percentage better for HIV diagnosis?
percentage of CD4+ cells relative to total lymphocytes should remain stable
what is the window period in HIV?
first 20 days of infection
difficult to pick up antigen and antibody during this period
What is the pathophysiology of type 1 hypersensitivity?
Allergen binds to IgE on mast cells or basophils- triggers release of mast cells mediators (mainly histamine)
what is the level of CD4+ cells that define AIDS
what tumours are associated with HIV?
Lymphoma (especially high grade B cell)
squamous epithelial tumours (especially cervical)
What is atopy?
inherited tendency to overproduction of IgE
What is the pathophysiology of type 2 hypersensitivity?
antibody binds to cell surface antigens
What is the pathophysiology of type 3 hypersensitivity?
Antigen-antibody complexes formed in circulation and deposited in various tissues and organs
when does Rhesus factor incompatibility occur?
Rh+ baby and Rh- mother
what is the pathophysiology behind Rhesus factor incompatibility?
1st Rh+ baby born to Rh- mother
(no reaction but antibodies form)
if mother becomes pregnant with a 2nd Rh+ baby, antibodies from the 1st pregnancy attack foetal RBCs
how can Rhesus factor incompatibility be treated?
treat mother with antibodies to rhesus antigen after 1st birth
What is a latent TB infection?
Patients infected with M. tuberculosis who have no clinical, bacteriological, or radiographic evidence of active TB
what pathogen causes tuberculosis?
What is active TB?
Active tuberculosis may occur from re-activation of previously latent infection or from progression of primary infection
How is TB spread?
What 3 situations can occur after exposure to M. tuberculosis?
physical clearance by mucus
immune clearance by macrophages
persistent latent infection
who is most at risk of acquiring tuberculosis?
HIV infected individuals
IV drug users
risk factors for active tuberculosis
chronic renal failure
solid organ transplantation with immunosuppression
How many individuals with latent TB will progress to active disease?
What pathogens are cleared by neutrophils?
bacteria and fungi
What pathogens are cleared by T cells?
viruses, certain bacteria and fungi
signs and symptoms of tuberculosis
investigations for TB
pleural fluid analysis and biopsy
what are the diagnostic tests/findings for TB
granulomas on transbronchial biopsy
management of TB (RIPE)
method of prevention of TB
what features may be present on chest X-Ray in tuberculosis?
what pathogens are cleared by antibodies?
Examples of gram-positive bacteria
Anaerobes (e.g. Clostridium)
Examples of gram-negative bacteria
Enterobacteriae (E. coli, salmonella)
What colour is a Gram-positive stain?
What colour is a Gram-negative stain?
Rod shaped bacteria
Round shaped bacteria
Round shaped bacteria arranged in clumps
Round shaped bacteria arranged in strands
Where is E. coli normally found?
What is E.coli commonly associated with?
Where is S. aureus normally found?
interior of nose, skin
What is S. aureus commonly associated with?
skin/soft tissue infections
What are most S. aureus strains resistant to and why?
Penicillin (except flucloxacillin)
Produce beta-lactamase enzymes
Where is group A streptococcus normally found?
upper respiratory tract
What is group A streptococcus commonly associated with?
Where is group B streptococcus usually found?
female genital tract (passed on to neonate)
What is group B streptococcus commonly associated with?
neonatal meningitis and sepsis
Where is pseudomonas aeruginosa usually found?
What is pseudomonas aeruginosa associated with?
chest infections in patients with lung disease (e.g. CF)
infections from indwelling devices
infections in the immunocompromised
What antibiotics can be used to treat Pseudomonas?
What antibiotic is the only oral agent effective against Pseudomonas?
What antibiotics are Streptococci sensitive to?
What antibiotics are Staphylococci and Gram-positive bacilli sensitive to?
What antibiotics are Gram-negative bacilli sensitive to?
extended spectrum penicillins
What antibiotics are Gram-negative cocci sensitive to?
What drug is used to tackle MRSA?
What is type 1 respiratory failure?
hypoxia without hypercapnia
What is type 2 respiratory failure?
hypoxia with hypercapnia
Possible causes of type 1 respiratory failure
low ambient oxygen
asthma or COPD
Possible causes of type 2 respiratory failure
asthma or COPD
GBS/motor neuron disease
What is the recommended target oxygen saturations for a patient not at risk of type 2 respiratory failure
What is the recommended target oxygen saturations for a patient at risk of type 2 respiratory failure
At what oxygen saturation does loss of consciousness occur?
At what oxygen saturation does impaired mental function occur?
With what patients would you use a high concentration reservoir mask?
critical illness/trauma patients
What % O2 concentration does a high concentration reservoir mask deliver?
60-80% and above
With what patients would you use a simple face mask?
patients with type 1 respiratory failure
What % O2 concentration does a simple face mask deliver?
What % O2 concentration does a Venturi mask deliver
What features indicate heart failure with reduced ejection fraction?
LV systolic dysfunction
What features indicate heart failure with preserved ejection fraction?
What ejection fraction would be defined as HF-REF?
What ejection fraction would be defined as HF-PEF?
what are the 3 main aetiologies for heart failure?
abnormal loading conditions
Causes of diseased myocardium
ischaemic heart disease
Causes of abnormal loading conditions
chronic pressure overload
chronic volume overload
impaired ventricular filling
pulmonary heart disease
high output states
Signs of left sided heart failure
chest crepitations (pulmonary oedema)
increasing S3 (gallop rhythm)
displaced apex beat
Signs of right sided heart failure
NYHA heart failure class I
No limitation, ordinary physical exercise does not cause dyspnoea
NYHA heart failure class II(s)
Slight limitation of physical activity; dyspnoea on walking more than 200 yards or on stairs
NYHA heart failure class II(m)
Moderate limitation of physical activity; dyspnoea walking less than 200 yards
NYHA heart failure class III
Marked limitation of physical activity; comfortable at rest but dyspnoea washing and dressing, or walking from room to room
NYHA heart failure class IV
Severe limitation of physical activity; dyspnoea at reat with increased symptoms with any level of physical activity
Mechanism of action of ACE inhibitors
block the conversion of angiotensin I to angiotensin II
Effects of ACE inhibitors
relaxation of blood vessels
decrease in heart volume
decreased myocardial oxygen demand
Contraindications of ACE inhibitors
impaired renal function
aortic valve stenosis
Mechanism of action of aldosterone antagonists
inhibit sodium reabsorption in the collecting duct of the nephron
Effects of aldosterone antagonists
reduce urine K+ excretion
increase water excretion
reduce cardiac workload
At what K+ level would you stop an aldosterone antagonist?
Mechanism of action of beta blockers
target beta-adrenergic receptors (inhibit sympathetic activity)
What effect do beta blockers have on renin secretion?
decrease renin secretion
- lower extracellular volume
- increase O2 carrying capacity of blood
Main contraindication for beta blockers
- can cause bronchospasm
In what situation would you use Sacubitril/Valsartan?
replacement of ACE-inhibitor/ARB in patients with HF-rEF
What is Valsartan?
angiotensin type 1 receptor blocker
What is Sacubitril?
What is the mechanism of action of Sacubitril
inhibits the enzyme neprilysin degrades vasoactive peptides
Effects of Sacubitril
blood vessel dilatation
reduction of ECF volume via sodium excretion
What is digoxin derived from?
Mechanism of action of digoxin
potent inhibition of Na/K pump
Effects of digoxin
increase in intracellular Na+ and Ca
Ca increases vagal efferent activity to the heart
- decreases HR
- increases BP
- increases tissue perfusion
Mechanism of action of loop diuretics
Block Na/K/Cl transporter in thick ascending limb of loop of Henle
What type of diuretic is more effective in patients with impaired kidney function?
Mechanism of action of thiazide/thiazide-like diuretics
Block Na/Cl cotransporter on DCT of kidney
Contraindications of thiazide/thiazide-like diuretics
Mechanism of action of Ivabradine
inhibition of funny channel in pacemaker cells
Contraindications of Ivabradine
sick sinus syndrome
verapamil or diltiazem use
WHO definition of a myocardial infarction
pain >20 mins
complete blockage of coronary artery causing ischaemia and full thickness cardiac muscle death
partial blockage of coronary artery, without full thickness muscle death
Up to what % occlusion from an atheromatous plaque is a patient asymptomatic?
Anterior ECG leads
Lateral ECG leads
I, aVL, V5-V6
Inferior ECG leads
II, III, aVF
Non-cardiac causes of troponin release
cardiac causes of troponin release
post cardiac surgery
Level of troponin rise for MI diagnosis
50% increase at 12hrs
20% increase if already elevated
oxygen (if sats<94%)
dual antiplatelet therapy (aspirin+clopidogrel/ticagrelor)
ECG changes in NSTEMI
T wave inversion
oxygen (if sats <94%)
dual antiplatelet therapy
definition of asthma
reversible airway obstruction
definition of COPD
partially reversible or irreversible airway obstruction
what mediators are responsible for airway inflammation
what type of receptors are present in the sympathetic nervous system
beta adrenergic receptors
example of a short acting beta agonist
class of drugs that block the action of the sympathetic nervous system (thus relax smooth muscle)
what type of receptors are present in the parasympathetic nervous system
example of a long acting beta agonist
class of drugs that block the action of parasympathetic nervous system (thus result in smooth muscle relaxation)
example of a short acting muscarinic antagonist
example of a long acting muscarinic antagonist
asthma management step 1
SABA as required
asthma management step 2
+ inhaled corticosteroid
asthma management step 3
+ LABA or corticosteroid/LABA combination inhaler
asthma management step 4
+ leukotriene receptor blocker, theophylline or increase inhaled steroid to 2000mcg/day
asthma management step 5
oral steroid tablets, referral to severe asthma service, ?IgE blockers
management of COPD (FEV1 <50%)
ICS/LAMA combination inhaler OR LAMA inhaler
management of COPD (FEV1 >50%)
LAMA or LABA inhaler
management of acute asthma
salbutamol 5mg (neb)
ipratropium 500mcg (neb)
40mg prednisolone PO or 200mg IV hydrocortisone
what other therapies can be used for acute asthma if initial treatment (SABA+SAMA+corticosteroid) has failed?
2g IV magnesium sulfate
what is the mechanism of action of aminophylline
acts as a sympathetic nervous system stimulant, therefore induced smooth muscle relaxation + bronchodilator
non-therapeutic treatment of COPD
vaccinations (influenza and pneumonia)
dysmorphic red cells
red cell casts
heavy proteinuria (>3.5g/day)
what is glomerulonephritis?
immune-mediated disorders that cause inflammation within the glomerulus
inherited forms of glomerulonephritis
thin basement membrane disease
definition of primary glomerulonephritis
disease starts in the glomerulus itself
examples of primary glomerulonephritis
definition of secondary glomerulonephritis
involvement of the glomeruli as part of a systemic disease
examples of secondary glomerulonephritis
pathophysiology of acute glomerulonephritis
antigen-antibody complexes become trapped within glomerulus
what antigen is usually responsible for acute glomerulonephritis?
clinical presentation of acute glomerulonephritis
sore throat, followed ~2 weeks later by oliguria, haematuria, hypertension and abnormal renal function
management of acute glomerulonephritis
reduced fluid+salt intake
antibiotics/diuretics if necessary
presentation of chronic glomerulonephritis
acute/chronic renal failure
what is minimal change glomerulonephritis?
T cell mediated glomerulonephritis
clinical presentation of minimal change glomerulonephritis
management of minimal change glomerulonephritis
ciclosporin (if steroids unsuccessful)
clinical presentation of IgA nephropathy
non-specific URTI followed by:
(1-2 days later)
purpuric rash (HSP)
clinical presentation of rapidly progressive glomerulonephritis
systemic symptoms (weight loss, malaise, arthralgia, fever)
vasculitis affecting other organs
clinical presentation of Goodpasture's disease
rapidly progressive glomerulonephritis +
pathophysiology of Goodpasture's disease
IgG antibodies against alpha 3 chain of type 4 collagen (anti-GBM antibodies)
what would you be looking for to confirm diagnosis of Goodpasture's disease?
anti-GBM antibodies (kidney biopsy)
management of Goodpasture's disease
management of IgA nephropathy
prognosis of IgA nephropathy
20% of patients will develop end stage renal failure at 20 years
what would you be looking for to confirm diagnosis of Wegener's granulomatosis?
cytoplasmic anti-neutrophil antibodies (cANCA)
investigations for suspected glomerulonephritis
FBC, U&Es, CRP/ESR
supportive management of glomerulonephritis
salt and water restriction
treatment of infection
manage electrolytes and acid-base balance
renal replacement therapy (dialysis)
definitive management of glomerulonephritis
high dose steroids (short treatment time)
Smoking cessation pharmacotherapy options
nicotine receptor antagonists (e.g. Champix)
dopamine releasing agents (e.g. Zyban)
management of acute exacerbation of COPD
5mg salbutamol (neb)
500 mcg ipratropium (neb)
30mg prednisolone PO or 200mg IV hydrocortisone
further options for management of acute exacerbations of COPD if previous treatment (SABA+SAMA+steroids) has failed?
pathophysiology of type 1 diabetes
autoimmune destruction of beta cells of the pancreas (T cell mediated)
peak age of onset of type 1 diabetes
what gene is linked to type 1 diabetes?
proposed environmental triggers for T1DM
bovine serum albumin
islet cell autoantibodies
clinical presentation of T1DM
consider type 1 diabetes in these cases
rapid weight loss
personal/family history of autoimmune disease
diagnosis of diabetes (HbA1c)
diagnosis of diabetes (fasting plasma glucose)
diagnosis of diabetes (2hr glucose at GTT)
in addition to hyperglycaemia, other features that support diagnosis of T1DM
rapid weight loss
personal/family history of autoimmune disease
1st line therapy for T1DM
basal-bolus insulin regimens
2x/daily Detemir as basal agent
Macrovascular complications of diabetes
peripheral arterial disease
Microvascular complications of diabetes
nephropathy and renal failure
definition of hypoglycaemia
blood glucose <4mmol/L
adrenergic symptoms of hypoglycaemia
neurological symptoms of hypoglycaemia
change in mood
lack of concentration
possible triggers for new onset hypoglycaemia
if hypoglycaemia is recurrent or severe, review the following
meal and activity patterns
injection site problems
changes in insulin sensitivity
lack of knowledge
management of hypoglycaemia in a patient who is able to swallow
15-20g of glucose
200ml orange juice
oral dextrose gel
management of hypoglycaemia in a patient who is unable to swallow
150mls IV 10% dextrose
oral carbohydrate (when safe)
how are ketones produced?
metabolism of fatty acids
why can illness precipitate DKA?
Patients lose appetite, reduce levels of insulin. Body actually needs 25% more insulin to help fight infection. Therefore, hyperglycaemia occurs.
key features of DKA
additional symptoms of DKA
confusion/altered mental state
low body temperature
fruity/pear drop breath
why does ketoacidosis occur?
when the number of free ketones in the blood exceeds those that can be metabolised
effects of ketone bodies in blood
what happens to potassium in DKA?
When acidosis occurs, H+ ions move into cells and K+ leaves cells. This causes initial hyperkalaemia. Extracellular K+ then causes vomiting or is lost in urine, eventually causing hypokalaemia.
name given to hyperventilation that occurs as a result of attempted respiratory compensation
Blood ketones > 6 mmol/L
Bicarb < 5 mmol/L
pH < 7.0
K+ < 3.5 (hypokalaemia)
GCS < 12
O2 sats < 92% (room air)
Systolic BP <90
HR <60 or >100
Raised anion gap
management of DKA
guide for potassium replacement
> 5.5 - don't replace
3.5-5.5 - 40mmol/L solution
< 3.5 - seek senior help
definition of resolved DKA
blood ketones <0.6
venous pH >7.3
which type of diabetes does hyperosmolar hyperglycaemic state occur in?
type 2 diabetic emergency
risk factors for HHS
lack of sufficient insulin (but enough to prevent ketosis)
poor kidney function
older age (50-70 yrs)
possible triggers for HHS
MI or stroke
certain mediations (glucocorticoids, beta blockers, thiazide diuretics, CCBs, phenytoin)
pathophysiology of HHS
trigger causes a relative insulin deficiency and high serum osmolarity, leads to osmotic diuresis and haemoconcentration (causing further increase in blood glucose)
key features of HHS
hyperglycaemia (without ketonaemia)
gradual onset (few days)
management of HHS
definition of hospital acquired pneumonia
48 hours following admission
typical causative organisms of Community Acquired Pneumonia
atypical causative organisms of community acquired pneumonia
causative organisms of hospital acquired pneumonia
risk factors for pneumonia
viral infection (influenza)
symptoms of pneumonia
shortness of breath
productive cough (green)
pleuritic chest pain
confusion (elderly patients)
diagnosis of pneumonia
physical signs + radiological changes
what is the C in CURB 65?
what is the U in CURB 65?
what is the R in CURB 65?
respiratory rate ≥ 30
what is the B in CURB 65?
systolic <90 or <60 diastolic
what is the 65 in CURB 65?
what should you do if a patient has a CURB score of 0-1
treat as outpatient/at home
what should you do if a patient has a CURB65 score of 2
admit to hospital
what should you do if a patient has a CURB65 score of ≥3
admit to hospital
consider ITU care
Management of pneumonia in a patient with a CURB65 score of 0-1 (NKDA)
Management of pneumonia in a patient with a CURB65 score of 0-1 (penicillin allergy)
erythromycin or doxycycline
Management of pneumonia in a patient with a CURB65 score of 2 (NKDA)
amoxicillin + erythromycin
Management of pneumonia in a patient with a CURB65 score of 2 (penicillin allergy)
doxycycline (7-10 days)
Management of pneumonia in a patient with a CURB65 score of 3+ (NKDA)
IV Co-Amoxiclav + Clarithromycin
Management of pneumonia in a patient with a CURB65 score of 3+ (penicillin allergy)
vancomycin + clarithromycin
When should a pneumonia patient be followed up?
definition of respiratory failure
PaO2 <8 kPa
treatment of respiratory failure
short term complications of pneumonia
medium term complications of pneumonia
late complications of pneumonia
what is the significance of 'coffee ground' vomit
blood has been oxidised by gastric acid (blood likely originated from the stomach)
what is melaena?
black, tarry faeces
what is the significance of melaena
oxidised, digested blood from an upper GI bleed
causes of upper GI bleeds
oesophageal causes of upper GI bleeding
causes of oesophagitis
what are oesophageal varices?
dilation of submucosal veins in lower 1/3rd of oesophagus
what causes oesophageal varices?
portal hypertension (liver cirrhosis)
what is a Mallory-Weiss tear?
laceration in the mucosa at the junction between oesophagus and stomach, usually caused by severe retching/vomiting
gastric causes of upper GI bleeding
causes of gastritis
H. pylori infection
duodenal causes of upper GI bleeding
medications that could cause upper GI bleeding
Haemorrhage class 1
<15% of circulating volume lost
no change in vital signs
haemorrhage class 2
15-30% of circulating volume lost
pallor + cool peripheries
haemorrhage class 3
30-40% of circulating volume lost
haemorrhage class 4
40% of circulating volume lost
reduced level of consciousness
components of Glasgow-Blatchford score
when is the Glasgow-Blatchford score used?
components of Rockall score
evidence of bleeding
management of upper GI bleed
insert 2 large bore cannulas
Terlipressin (if varices suspected)
endoscopic management of peptic ulcers
causes of liver cirrhosis
alcoholic liver disease
chronic Hep B or C
primary biliary/sclerosing cholangitis
infiltrative disease (e.g. haemochromatosis, Wilson's)
pathophysiology of liver cirrhosis
inflammation and damage to hepatic parenchyma leads to fibrosis and obstruction of hepatic blood flow
what do stellate cells do?
release TGF-β1, which leads to proliferation of connective tissue
elements of Child-Pugh classification
Child-Pugh class A
Child-Pugh class B
Child-Pugh class C
prehepatic causes of portal hypertension
splenic vein thrombosis
portal vein thrombosis
extrinsic compression of portal vein
intrahepatic causes of portal hypertension
Hep B and C related cirrhosis
alpha-1 antitrypsin deficiency
post-hepatic causes of portal hypertension
veno-occlusive liver disease
what is Budd-Chiari syndrome?
rare condition causing occlusion of hepatic veins that drain the liver
why does portal hypertension result in oesophageal varices?
The lower 1/3rd of the oesophagus is drained into the superficial veins lining the oesophageal mucosa, which drain into the left gastric vein, which in turn drains directly into the portal vein
management of oesophageal varices (not bleeding)
acute management of bleeding oesophageal varices
IV PPI + metoclopramide
- IV vit K
- fresh frozen plasma
- PT concentrate
endoscopic management of oesophageal varices
surgical management of oesophageal varices
tranjugular intrahepatic portosystemic shunt (TIPS)
liver transplant (last resort)
genetic risk factors for pulmonary embolism
protein C/S deficiency
factor V Leiden
prothrombin gene mutation
disease risk factors for pulmonary embolism
sickle cell anaemia
environmental risk factors for pulmonary embolism
surgery or trauma
air travel (>3000ft/4 hrs)
symptoms of PE
pleuritic chest pain
signs of PE
what would you be looking for in an ABG to rule out a PE?
CO2 above 36mmHg
normal a-a gradient
what would you expect to see on ABG if a PE was present?
hypoxia with low PCO2
what is a D-dimer used for?
to rule out PE
what would a ventilation/perfusion scan show in the event of a PE?
areas of ventilation/perfusion mismatch
what would a chest X-Ray show in the event of a PE?
relative absence of pulmonary vessels
what would you see on ECG in the event of a PE?
S-waves in lead I
Q waves in lead III
inverted T waves in lead III
management of pulmonary embolism
high flow O2
thrombolysis (if massive)
LMWH (7 days)
warfarin (3 months)
what is an an aortic dissection?
a false channel between layers of the vessel wall
what is the pathophysiology of aortic dissection?
blood flow through tunica intima into tear/crack in wall forms aortic haematoma
as haematoma grows larger, walls start to dissect
symptoms of aortic dissection
severe chest pain (radiates to back, 'tearing' in nature)
risk factors for aortic dissection
bicuspid aortic valve
management of aortic dissection
risk factors for lung cancer
lymphoma or breast cancer survivors treated with radiotherapy
lung disease (COPD, fibrosis)
oesophageal/head and neck cancer
what types of lung cancer are defined as non-small cell?
squamous cell carcinoma
what types of lung cancer are more likely to originate in a central location?
squamous cell carcinoma
small cell carcinoma
which type of lung cancer is most associated with smoking?
squamous cell carcinoma
what is seen on histology of squamous cell carcinoma?
which is the most aggressive type of lung cancer?
small cell carcinoma
what is the treatment for small cell carcinoma?
what can be seen on histology of small cell carcinoma?
what ectopic hormones does small cell carcinoma generate?
ACTH and ADH
what is the name given to tumours of the lung apex?
what are the features of Horner's syndrome?
which type of lung cancer is least associated with smoking?
what is the main association of malignant mesothelioma?
lung symptoms of cancer
cough (>3 weeks)
systemic symptoms of lung cancer
loss of appetite
what is Pancoast's syndrome
wasting of the small muscles of the hand
why does Horner's syndrome occur?
involvement of cervical sympathetic ganglion
what causes diffuse chest pain in lung cancer?
displacement of mediastinal structures
why does Pancoast's syndrome occur
involvement of the brachial plexus
why can lung cancer present with a hoarse voice
recurrent laryngeal nerve involvement
what causes localised pain in lung cancer?
pleural or bony metastases
signs of lung cancer
where is lung cancer most likely to metastasise to?
what paraneplastic syndromes can occur in lung cancer?
parathyroid-related peptide production
what are the symptoms of SIADH?
what are the symptoms of parathyroid-related peptide production?
nausea and vomiting
what may a chest X-Ray show in lung cancer?
stages of small cell carcinoma
staging of non small cell carcinoma
TNM staging of lung cancer - T1
tumour ≤3cm in diameter
TNM staging of lung cancer - T2
tumour >3cm and >2cm distal to carina
TNM staging of lung cancer - T3
tumour of any size invading surrounding structures but not
- great vessels
- vertebral body
or within 2cm of (but not involving) carina
TNM staging of lung cancer - T4
tumour of any size invading any structure excluded in T3
presence of malignant pleural effusion
TNM staging of lung cancer - N1
metastases to peribronchial or ipsilateral perihilar lymph nodes
TNM staging of lung cancer - N2
metastases to ipsilateral mediastinal or subcarinal lymph nodes
TNM staging of lung cancer - N3
metastases to any of the following lymph nodes
- contralateral hilar
- ipsilateral or contralateral scalene
management of limited small cell carcinoma
management of extensive small cell carcinoma
consider prophylactic radiotherapy to brain
management of early non-small cell carcinoma
side effects of chemotherapy
nausea and vomiting
bone marrow suppression (infections, anaemia, bruising)
side effects of tyrosine kinase inhibitors
abnormal hair growth
side effects of radiotherapy
side effects of immunotherapy
pancreatic enzyme abnormalities
prevention of lung cancer
reduce occupational exposure
definition of peripheral arterial disease
narrowing of the arteries (other than coronary or cerebral)
what is the main cause of peripheral vascular disease
risk factors for peripheral vascular disease
what is intermittent claudication?
a cramp-like pain that occurs in a group of muscles upon exercise (relieved by rest)
what vessel is most commonly affected by peripheral vascular disease?
superficial femoral artery
what is the absolute claudication distance?
the distance a patient can walk before the pain starts
what is critical limb iscemia
rest pain, ulceration and/or gangrene present for ≥2 weeks
why is critical limb ischaemia pain worse at night?
lying flat distributes blood away from the legs as well as BP decreasing during sleep
what is the 1st line investigation for peripheral vascular disease?
Ankle-Brachial pressure index
normal reading for ABPI
ABPI reading for intermittent claudication
ABPI reading for critical limb ischaemia
conservative management of peripheral vascular disease
surgical management of peripheral vascular disease
what are the 6 Ps for acute limb ischaemia?
usual site of arterial ulcers
forefoot and toes (pressure areas)
usual site of venous ulcers
'gaiter area' (from just above the malleolus to below the knee), especially medial side
features of venous ulcers
small or large, shallow
features of arterial ulcers
'punched out' border
management of venous ulcers
management of arterial ulcers
revascularisation (bypass surgery or angioplasty)
what does a prothrombin time (PT) look at?
factor 7 (extrinsic pathway) and common pathway
what does activated partial thromboplastin time (APTT) look at?
factors 8, 9, 11 and 12
causes of a long PT
vitamin K deficiency
factor 7 deficiency
causes of a long APTT
Von Willebrand disease
factor inhibitors (autoantibodies)
what are the genetics of haemophilia?
X-linked recessive genetic disorder
what is haemophilia A?
factor 8 deficiency
what is haemophilia B?
factor 9 deficiency
how can you clinically distinguish between haemophilia A and B
what clotting results would you get from haemophilia?
what is haemarthrosis?
bleeding into joint space
what is haemophilic arthropathy?
joint deformation as a result of repeated haemarthrosis
management of haemophilia
hep B vaccination
clotting factor infusions
what is the purpose of desmopressin in bleeding disorders?
increases release of factor 8 from vascular endothelium
what is the mechanism of action of tranexamic acid
antifibrinolytic- inhibits conversion of plasminogen to plasmin thus prevents breakdown of blood clots
what is the most common hereditary coagulation disorder?
Von Willebrand disease
what is the pathophysiology of von Willebrand disease?
defect in Von Willebrand factor (required for platelet adhesion)
which types of von Willebrand disease are autosomal dominant?
types 1 and 2
which type of von Willebrand factor is autosomal recessive?
presentation of Von Willebrand disease
coagulation findings for Von Willebrand disease
prolonged APTT and PT
management of Von Willebrand disease
OCP for menorrhagia
desmopressin (not type 3)
types of quantitative platelet disorders
reduced production (e.g. marrow failure)
increased destruction (e.g. immune thrombocytopenia, DIC)
sequestration (e.g. hypersplenism)
hereditary thrombocytopenia (e.g. Bernard-Sulier syndrome)
types of qualitative platelet disorders
platelet granule abnormalities
what does a vitamin K deficiency result in?
decreased synthesis of factors 2, 7, 9 & 10 and proteins C & S
causes of vitamin K deficiency
coagulation findings for vitamin K deficiency
very prolonged PT
management of vitamin K deficiency
vitamin K rich diet
vitamin K supplementation
what is disseminated intravascular coagulation?
Condition where small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding.
causes of DIC
massive tissue injury
management of DIC
treat underlying cause
cryoprecipitate or fresh frozen plasma
what is acquired haemophilia?
spontaneous development of factor 8 inhibitor (usually IgG antibody)
causes of acquired haemophilia
diagnosis of acquired haemophilia
very long aPTT with no correction on mixing studies
management of acquired haemophilia
Factor 8 inhibitor bypassing activity
Novo-7 (recombinant factor 7a)
what does correction on mixing studies signify?
what does no correction on mixing studies signify?
what is Acute Kidney Injury?
a rapid reduction in kidney function resulting in failure to maintain fluid, electrolyte and acid-base homeostasis
definition of AKI
increase in Cr ≥26 μmol/l (48hrs)
increase in Cr ≥1.5x baseline (7 days)
urine volume <0.5ml/kg/hr (6 hrs)
creatinine criteria for stage 1 AKI
Increase ≥26 μmol/l within 48h
Increase ≥1.5-1.9x reference level
urine output criteria for stage 1 AKI
<0.5 ml/kg/hour for >6 consecutive hours
creatinine criteria for stage 2 AKI
Increase ≥2-2.9x reference level
urine output criteria for stage 2 AKI
<0.5ml/kg/hr for >12 consecutive hours
creatinine criteria for stage 3 AKI
Increase ≥3x reference level
Increase ≥354 μmol/l
Commenced on renal replacement therapy
urine output criteria for stage 3 AKI
<0.3 ml/kg/hour for >24 hours
Anuria for 12 hours
Prerenal causes of AKI
Renal causes of AKI
bilateral renal artery stenosis
haemolytic uraemia syndrome
acute tubular necrosis
acute interstitial nephritis
Postrenal causes of AKI
risk factors for AKI
history of AKI
indications for dialysis
severe metabolic acidosis
consequences of hyperkalaemia
management of pulmonary oedema
Cheshire and Merseyside guidelines for AKI (FLUID)
Low BP (correct)
Urine dip + microscopy
Drugs (stop nephrotoxins)
types of kidney cancer
renal cell carcinoma
urothelial (transitional cell) carcinoma
squamous cell carcinoma
types of renal cell carcinoma
papillary (type I and II)
renal medullary sickle cell disease
risk factors for kidney cancer
chronic renal failure/dialysis
thyroid cancer or previous radiotherapy
VHL gene mutation
what genes are implicated in the development of kidney cancer?
von hippel Lindau (VHL)
Mesenchymal epithelial transition factors (MET)
tuberosclerosis genes 1 and 2 (TSC)
fumarate hydrase (FH)
sorbitol dehydrogenase (SDH)
what type of kidney cancer is VHL gene associated with?
clear cell carcinoma
what type of kidney cancer is MET gene associated with?
papillary type I RCC
what type of kidney cancer is FH gene associated with?
papillary type II RCC
what type of kidney cancer is FLCN gene associated with?
clinical presentation of kidney cancer (classical triad)
why does haematuria occur in kidney cancer?
neovascularisation of tumour, new vessels don't have time to form proper walls so more delicate
investigations for suspected kidney cancer
urine dip (blood ++)
Bosniak classification of kidney cancer - Bosniak I
Bosniak classification of kidney cancer - Bosniak II
Bosniak classification of kidney cancer - Bosniak IIF
5% risk of malignancy
Bosniak classification of kidney cancer - Bosniak III
50-60% of malignancy
Bosniak classification of kidney cancer - Bosniak IV
90-100% risk of malignancy
Stage 1 of renal cancer
tumour within capsule
Stage 2 of renal cancer
invasion of perinephric fact (confined to Gerota fascia)
Stage 3 of renal cancer
involvement of regional lymph nodes +/- renal vein/vena cava
Stage 4 of renal cancer
tumour spread to adjacent organs or distant metastases
Kidney cancer TNM staging - T1
<7cm and confined to kidney
Kidney cancer TNM staging - T2
>7cm and confined to kidney
Kidney cancer TNM staging - T3
any size tumour, extends into (but not beyond) Gerota's fascia or renal vein
Kidney cancer TNM staging - T4
any size tumour, invading ipsilateral adrenal gland or adjacent organs beyond Gerota's fascia
medical management of kidney cancer
surgical management of kidney cancer
nephrectomy (total or partial)
diathermy (low grade/superficial)
Where is calcitonin released from?
parafollicular cells of thyroid
functions of calcitonin
inhibits osteoclastic activity
inhibits renal tubule absorption of Ca + phosphate
possible causes of hypercalcaemia
Familial hypocalciuric hypercalcemia (FHH)
Hormone-independent bone resorption
Osteolytic bone mets
excessive dietary intake
ectopic calcitriol production
what malignancies cause increased production of PTHrp?
symptoms of hypercalcaemia
psychiatric moans (depression, anxiety, confusion)
signs of hypercalcaemia
slow muscle contraction/ weakness
ECG changes in hypercalcaemia
treatment of hypercalcaemia
how do loop diuretics treat hypercalcaemia?
inhibit calcium reabsorption in loop of Henle, increased urinary calcium excretion
long term complications of hypercalcaemia
hyperparathyroid bone disease
causes of hypocalcaemia
post surgical (thyroid/parathyroidectomy)
hungry bone syndrome
infiltration (granulomatous, iron overload, metastases)
vit D deficiency
symptoms of hypocalcaemia
peri-oral & digital paraesthesia
muscle stiffness, spasms and cramps
shortness of breath (diaphragmatic spasms)
management of hypocalcaemia
vitamin D preparations
treat underlying cause
causes of primary adrenal insufficiency
infections (TB, CMV, HIV, histoplasmosis)
infiltration (neoplastic, haemochromatosis, amyloid)
adrenal haemorrhage (anticoagulants)
causes of secondary adrenal insufficiency
clinical features of adrenal insufficiency
dizziness and postural hypotension
why does postural hypotension occur in adrenal insufficiency?
loss of aldosterone and loss of effect of cortisol
diagnosis of adrenal insufficiency
hyponatraemia + hyperkalaemia
inappropariately low cortisol for stress (<500nmol/L)
short synacthen test (30 min cortisol <500)
management of adrenal insufficiency
management of chronic adrenal insufficiency
glucocorticoids (hydrocortisone, higher dose in morning)
fludrocortisone (primary insufficiency)
what is pheochromocytoma?
adrenal medullary catecholamine secreting tumor
presentation of pheochromocytoma
actions of catecholamines
mobilisation of glycogen reserves
breakdown of glycogen to glucose
breakdown of fats and fatty acids
increase heart rate
increase force of contraction
diagnosis of pheochromocytoma
24hr urine catecholamine excretion
management of pheochromocytoma
alpha blockade (phenocybenzamine)
(avoids precipitating hypertensive crisis due to unopposed alpha adrenergic stimulation)
possible causes of secondary hypertension
primary renal disease
coarctation of aorta
medication (NSAIDs, steroids, OCP)
clinical features of primary hyperaldosteronism
drug resistant hypertension (3 drugs)
FH of early onset hypertension or CVA
diagnosis of primary hyperaldosteronism
plasma aldosterone/renin ration (>20)
management of primary hyperaldosteronism
what is used to treat Pneumocystis Jiroveci Pneumonia?