LAST MINUTE REVISION Flashcards
What is the new treatment for adenocarcinomas if patient has EGFR mutation
Tryosine kinase inhibitors
What onconogene is induced by smoking in lung cancer
KRAS
What is an example of a immunotherapy drug in the treatment of lung cancer
Nivolumab BMS -
What is a chemotherapy drug in lung cancer
cisplatin
{adeocarinoma - pemetrexed
SCLC - etoposide}
What is the treatment plan for TB
4months: Rifampicin Isonazid Pyrazinamide Ethambutol
2months
rifampicin
isonazid
what tests are used to screen for TB
Heaf
Mantoux
What is the morphology of TB and what causes it
Central caseating necrosis and Laghan Granuloma- due to activated macrophages
What is the signs of ADV TB
finger clubbing
Bronchial breathing
Crackles
Erythema nodosum
What is the signs of TB
weight loss fever malaise cough sputum heamoptysis pleuritic chest pain
What is the investigation for TB
CXT Sputum - culture, microbiology, PCR Bronchoscopy Pleural aspiration/ biopsy CT thorax
What is the treatment in CF
ANTIBIOTICS
Large dose of two antibiotics: Blactams & Aminoglycosides on a 2 week course
REDUCE INFLAMMATION
Ibuprofen
Azithromycin
Prednisolone
What drug directly treats CF and how does it work
Ivacaftor
binds to CFTR, improves the transport of chloride ions
What are the microbiology present in CF
Early years:
Staphylococcus aureus - oral
Haemophilus influenzae - oral
Later years:
Pseudomonas aeruginosa - IV/ cepacia- bad lung
Burkholderia cepacia - IV/cepacia- bad lung Stenotrophomonas maltophilia - IV
Mycobacterium abscessus
(High resistance) - lung transplant
Symptoms of CF
Chronic purulent sputum production
Recurrent chest infection
(pneumonitis / bronchiectasis / scarring / abscesses)
Weight loss
Fever
Symptoms and signs of CF
SYMPTOMS Chronic purulent sputum production Recurrent chest infection Weight loss Fever
SIGNS
haemopytsis (infection)
pneumothroax (older males)
male infertility
nasal polyps
Onset of diabetes - pancreas issues
Failure to thrive due pancreatic insufficiency:
Abnormal oilly and offensive stools (steatorhea)
meconium delay in babies (first poop)
osteoporosis
vitamin D issue
What is the screening process for neonatal babies in the detection of CF
Guthrie test (heel-pin test) for day 5 babies;
- Initial - immunoreactive trypsinogen
- If positive - mutation analysis performed
- Screen positive referred sweat test
What is the management of pancreatic insufficiency
Enteric coates enzyme pellets (deal with fat)
H2 antagonists
Proton pump inhibitors
Good nutrition
- high energy diet
Fat soluble vitamin + mineral supplements
Active life
How do you treat Pseudomonas aeruginosa (60% CF microorganism)
nebulised colomycin with antibiotics - oral ciprofloxacin or i.v. ceftazidime (if the other fails)
Blood flow rate is controlled by what two mechanisms
DARCYS LAW Flow = Pressure difference/ resistance
EXTRINIC
sns (pns has no effect)
Hormones
- Epinephrine from medulla = constrict, increase MAP
- vasopressin/ angiotensin = increase BV/MAP
- BNP/ANP = Decrease BV/MAP
INTRINSIC
Active metabolic hypernanemia - exercise
Pressure auto regulation - Cerebral, Renal
Reactive hyperanemia - blood blockage
Injury response - release histamine
The increase in metabolites in active hyperaemia and pressure flow regulation creates a negative feedback effect by triggering the release of what
EDFR
What is the difference in pulmonary circulation compared to everywhere else
a decrease in oxygen causes arterial constriction
what is the result of stimulated RAAS
Renin released from juxtaglomerular apparatus
Renin converts angiotensinogen to angiotensin I
Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)
angiotensin II: Vasoconstrictor (potent hypertrophic agent), release aldosterone, anti-natriuretic peptide
What is the best tool is diagnosing high blood pressure
Ambulatory Blood Pressure Monitoring (ABPM)
when your blood pressure is measured as you move around, living your normal daily life - measured for up to 24 hours
- avoid white collar syndrome
Normal blood pressure = 120/80mmHg
What is the aetiologies of secondary (5-10%) hypertension
and what also increases the risk
Renal disease - renal stenosis
Drug induced - oral contra. / NSAIDS/steroids
pregnancy -
endocrine diseases - Conns/ Cushings disease
Vascular diseases - co-arctation of the aorta
sleep apnoea
Increases risk obesity Hyperlipideamia smoking LVH/MI/Stroke Diabetes mellitus
What is the hypertension treatment plan over the age of 55, african-caribean race, pre pregnant
- CBB
- Thiazide type diuretic
- ACEI
For resistant Hypertension
- ACEI
- spirolactotone/ higher dose thiazide
Have to take into account potassium levels
What is the hypertension treatment plan for those under the age of 55
- ACEI/ARB
- Thiazide type diuretics
- CBB
For resistant Hypertension
- CBB
- spirolactotone/ higher dose thiazide
Have to take into account potassium levels
When should CBBs not be used
when there is a risk or heart failure is present
What drugs are recommended pre pregnancy and during pregnancy
Pre - CBB(Nifedipine MR) Centrally acting agents (Methyl dopa) Beta Blockers (Atenolol, Labetalol) Pregnant - add thiazide diuretic and/or amlodipine
Example of ACEI CCB ARB BB
RAMIPRIL
VERAMIPRIL/ AMPLODIPINE
LOSARTAN
ATNEOLOL
What is the pathophysiology of IE
what organism is most likely the cause
damage to the endothelium with invasion and adherence of micro-organism to injured surface, proliferation then breaking of causing thrombotic endocarditis
= a sterile fibrin-platelet vegetation (abnormal mass)
acute - s. aureas
sub acute - s. viridian’s
what is the signs and symptoms of IE
Murmur
Muscoskeletal pain
splinter haemorrhages vasculitic rash Roth Spots Osler’s nodes Janeway lesions nephritis anemia
what is the signs and symptoms of IE
F - fever R - roths spots O - oslers nodules M - Murmur J - Janeway leison A - anemia N - Nail splinter heamorhages E - Emboli
What is the antibiotic treatment for IE
Native valve: Gentamicin+ amoxycillin
Prosthetic valve: gentamicin + vancomycin + rifampicin
Native valve and sepsis: Gentamicin and vancomycin
6 weeks IV
What is the complications of IE
heart failure
fistula formation
leaflet perforation
uncontrolled infection
abscess formation
atrioventricular heart block
embolism
prosthetic valve dysfunction /dehiscence
What is the two aetiologies of oedema
Trasudate oedema - alteration of the haemodynamic forces which act across the capillary wall
e.g. cardiac failure, fluid overload
Exudate oedema - part of the inflammatory price due to an increase in vascular permeability
- Higher protein
e. g. tumour, inflammation, allergy
What is the different aetiologies of oedema
Congestive heart failure: - TRANSUDATE
LH- Pulmonary oedema
RH -Peripheral oedema
Lymphatic blockage
hypoalbuminaemia
abnormal renal function
inflammation - EXUDATE
signs of RHF
Increased JVP
Hepatomegaly
Peripheral oedema
What is the signs and symptoms of cardiac heart failure
fatigue
breathlessness
reduced exercise capacity
Chest crepitations, oedema, tachycardia dyspnoea fatigue Increased JVP Third systolic heart sound S3 Displaced apex
raised BNP concentration
What is the drug therapy for heart failure
– Diuretics
–ACE inhibitors
– Betablockers
–Aldosterone receptor blockers
–In some pateints ACE I or ARDB now replaced by angiotensin receptor neprilysin inhibitor
Aetiology of heart failure
Valve heart disease
aortic stenosis - excessive afterload
Mitral/aortic regurgitation - excessive preload
Arial/ventrical septal defect/ tricuspid incompetence - excessive preload
Hypertension
Coronary heart disease
Stuctural abnormailites
Myocardial ischaemia
dilated cardiomyopathy
What is the screening test and investigations for heart failure
ECG
BNP
ECHO - severe LV ejection fraction < 30%
MUGA - Radionuclide to see the pumping of the heart
CXR
MRI
What will provide objective evidence of cardiac dysfunction in the diagnosis of heart failure than
abnormal ECHO
-cardiomegaly
Cardiac murmurs -S3
raised natriuretic peptide concentration
responds to diuretics
What is an example of a drug that prevents the break down of ANP and DNP therefore enhancing natural diuretics in the body
Neprolysin
What drugs are used in the treatment of heart failure
Furosemide ± thiazide - dehydration
Loop diuretic: Furosemide - Main symptomatic treatment
ACE Inhibitor: rampril
Angiotensin receptor blocker: losartan
Beta-blocker - stable state
Ivabradine - those above 70bpm
Aldosterone antagonist: spironolactone
- HF with resistant oedema
Digoxin - improve contractility (end of HF)
Nitrate vasodialtors - Increase preload/ decrease after load
Warfarin - prevent thromboembolic event
When should beta blockers be administered in heart failure patients
when they are stable - no fluid retention
What does a decreased CO in systolic disfunction activate
RAAS activation
Sympathetic activation
Increasing blood volume - causing further problems
Define systolic and diastolic heart failure
SYSTOLIC
Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure
DIASTOLIC
Involves a thickened and stiff heart muscle
so the heart does not FILL with blood properly
resulting in fluid backup in the lungs and heart failure
What is the symptoms of mitral stenosis
Dyspnoea: Haemoptisis - pressure cause bv rupture Chest pain Hoarseness - Left atrium pressing on laryngeal palpitations
What is the aetiology of mitral regurgitation
Rheumatic Heart Disease Mitral valve prolapse (MVP) - acute MR Infective endocarditis Degenerative - fibrosis LV and annular dilatation - e.g. previous heart attack
What is the signs of mitral regurgitation
Pulse – normal/reduced Brisk and hyperdynamic apex beat RV heave palpitations Right heart failure: Increased JVP, pulmonary oedema
Auscultation:
-loud systolic murmur
pansytolic inbetween s1 -s2
What is the signs of mitral stenosis
Mitral facies - discolouration of nose and cheeks Pulse – normal JVP – prominent a wave Tapping apex beat and diastolic thrill RV heave
Auscultation:
Diastole murmurs (blow)
S3
EASIER TO SPOT FOLLOWING TACHYCARDIA
Aetiology of mitral stenosis
IE
rheumatic heart disease
congenital
What can mitral valvular diseases cause
Back track of pressure into pulmonary circulation:
RHF/Pulmonary oedema /Pulmonary hypertension
This causes the signs of JVP and reduced pulse
Increased left atrial:
AFIB - which causes embolism
Pulmonary hypertension
Infective endocarditis
What medication is given to Mitral valve diseases
and what medication delays until surgery can happen in regurgitation valvular disease
Diuretics
vasodilator
Whats the aetiology in aortic stenosis
Degenerative - calcification = senile aortic stenosis
Rheumatic
Bicuspid stenosis
What is the aetiology of aortic regurgitation
DYSFUNCTIONAL LEAFELTS Bicuspid aortic valve Rheumatic heart disease Endocarditis Myxomatous degeneration
DILATION OF AORTA
Connective tissue disorders
due to a pathological process e.g. hypertension
What is the only valve disease that doesn’t develop heart failure
aortic regurgitation
How is aortic stenosis differentiated from aortic sclerosis
Loss of aortic secondary heart sound
What is the signs and symptoms of aortic stenosis
Chest pain (angina)
Syncope/Dizziness (exertional pre-syncope)
Breathlessness on exertion
Heart failure
Pulse – small volume and slowly rising JVP /low BP – prominent if RH failure present Vigurous and sustained apex beat RV heave Systolic murmur - Harsh ejection sound
What is the signs and symptoms of aortic regurgitation
asymptomatic
exertional breathlessness
Pulse – large volume and retracting/collapsing
Wide pulse pressure e.g. 170/40mmHg
Hyperdynamic, displaced apex beat
DIASTOLIC MURMUR – difficult to hear between S2-S1
Rheumatic heart disease
strep infections
aspirin and bed rest
measured with ASO titre
What is the aetiology of hypertrophic cardiomyopathy
Inherited Autosomal dominant sarcomere gene defect that changes the genes in the heart muscle protein
Thyroid problems and diabetes can also cause hypertrophic cardiomyopathy
When is Brain Natriuretic Peptide polypeptide secreted
by the ventricles of the heart in response to excessive stretching of heart muscle cells
What is the general measures that should be taken with cardiomyopathy
Avoid heavy exercise
Avoid dehydration
Explore FH and first degree relatives,
ECGs and echoes may be required
Consider genetic testing
Investigations for dilated cardiomyopathy - dilation of heart chambers impairing systolic function
Repeated ECG noting left bundle branch block if present CXR N termial pro Brain Natriuetic Peptide Basic bloods Full; Blood Count, urea and electrolytes Echo Cardiovascular MRI Coronary angiogram Sometimes biopsy
What investigations are carried out for restrictive and infiltrative cardiomyopathy
Repeated ECG CXR N termial pro Brain Natriuetic Peptide Basic bloods FBC, U+E, antibodies testing (for sclerotic CT diseases) Test for Fabry (low plasma alpha galactosidase A activity) Echo MRI, Biopsy (amyloid non cardiac)
What are the signs of dilated cardiomyopathy
Poor superficial perfusion, pulse - irreg if in AF, SOB at rest, narrow pulse pressure, JVP elevated+/- TR waves, displaced apex, S3 and S4, MR murmur often, pulmonary oedema, pleural effusions, ankle oedema, sacral oedema, acites, (the accumulation of fluid in the peritoneal cavity) hepatomegally (liver enlargement)
What is the signs for hypertrophy cardiomyopathy
Notched pulse pattern
Irreg pulse if in AF or ectopy
Double impulse over apex, thrills and murmurs, often dynamic
LVOT murmur will increase with valsalve and decrease with squatting
JVP can be raised in very restrictive filling
what is the aetiology of dilated cardiomyopathy
Ischaemia
Valvular disease
Genetics and familial DCM
muscular dystrophy
Inflammatory/infectious
toxic exposure (alcohol, drugs, endocrine)
Post child birth
tropical disease
Injury, cell loss, scar replacement (sarcoid)
What is centracinar and panacinar emphysema most likely linked to
Centracinar - Enviromental exposures e.g. smoking
Panacinar - alpha 1 trypsin deficiency
What is the pathology of emphysema
Loss of elastin by destruction or dilation of alveoli wall
Leading to thickening of airways by inflammation and fibrosis
Inflammation triggers neutrophils causing further damage, triggering elastase for further break down of elastin
Loss of alveolar attachment
aetiology of COPD
Smoking Occupation ageing atmospheric pollution chronic asthma (alpha 1 trypsin deficiency)
What is the affect of smoking on your lungs
accelerates the loss of lung function by preventing the action of alpha 1-antitrypsin increasing elastase production
and causes neutrophilic inflamation in the lungs further triggering elastase production
BOTH - destroy the alveoli walls
What increase in residual volume shows their is gas trapping with pulmonary function test CO
> 30%
What is alpha 1-antitrypsin
made in the liver neutralises neutrophil enzymes and regulates elastase
what is the signs of COPD
Hyperinflation of the chest
(loss of recoil due to emphysema, push out and diaphragm be pushed down)
Reduced chest expansion
cardiac dulness on percussion
NO crackles
Prolonged expiration wheeze
Respiratory distress
(pursued lip breathing and using accessory muscles)
What steroids are used for COPD exasperation
Prednisolone
What is the inhaler therapy for COPD
Short acing bronchiodilators - salbutamol, terbutaline
Long acting bronchiodilators
High dose inhaled corticosteroids (ICS) and LABA
treatment plan for asthma
Step 1: Short acting beta agonists (SABA)
Step 2: Regular preventer = low dose inhaled corticosteroids - MAX DOSE 800MG in kids
Step 3: Add on preventers (either LABA or LTRA) or increase ICS dose… LABA proven to work better in kids than LTRA
Step 4: Experimental medicine
How does adult asthma treatment and child asthma treatment differ
Max dose ICS 800 microg
No oral B2 tablet
LTRA first line preventer in <5s (only montelukst
LABA has to be administrated with ICS
dry powder inhalers - not to be given to under 8s (Licensed to over 5s)
SABA + ICS
Salbutamol
Beclomethasone
What is the treatment for stable angina
ease symptoms:
BB - first line
short acting Nitrates - GTN (rapid symptomatic relief)
CCB - used with BB if symptoms worsen
Ivabradine - if above 70bpm
K channel openers: nicorandil
long acting nitrates: prophylaxis X1day
Halt disease progression:
Aspirin/ clopidogrel
Statins
ACE inhibitors - secondary prevention of other morbidities
Revascularisation
- angioplasty and stenting
- coronary artery bypass grafting (CABG)
Investigations for stable angina
Bloods test
- Full blood count,
- lipid profile and fasting glucose;
- Electrolytes,
- liver and thyroid tests (hyperthyroidism increase myocardial demand)
CXR - show other causes of chest pain e.g. pulmonary oedema
Electrocardiogram
Exercise tolerance test/ETT
Myocardial perfusion imaging
Computed tomography (CT) coronary angiography
Cardiac catheterisation/coronary angiography
Aetiology of stable angina
reduction in coronary blood flow to the myocardium - coronary atheroma
Uncommon:
Reduced O2 transport
e.g. anaemia
increased myocardial O2 demand
e.g. HR and BP rise (exercise, anxiety/emotional stress, cold weather and after a large meal, cold)
LVH
Hyperthyroidism
When should you never use nifedipine CCB immediate release (rapid acting vasodilators)
why?
Post MI (with impaired LV function) or Unstable angina (increase infarction rate and + death)
may precipitate a stroke or MI
When do you not use beta blockers
Asthma
Peripheral Vascular Disease - Relative contraindication
Raynauds Syndrome
Heart failure
Those patients who are dependent on sympathetic drive
Bradycardia / Heart block
What is dual anti-platelet therapy that all ACS patients should receive one year after the event
both aspirin and a ADP receptor blocker
When would ACE inhibitors be used the treatment of unstable angina and NSTEMI
if left ventricular dysfunction is present
How can ACS result in sudden cardiac death
As an ACS, the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia
ventricular Fibrillation tends to rapidly deteriorate into asystole - heart ceases to beat
aetiologies of stroke
Infarction
- Large artery athlersclerosis
- cardioembolic stroke - due to AF
- Lucunar stroke - deep white matter
Haemorrhage (don’t treat with thrombolysis)
- aneurysms/hypertension
MRI differentiates
What are the symptoms of a stroke
rapid / depend on area of brain affected
loss of power; motor problems (clumsy / weak limb)
loss of sensation; loss of feeling
loss of speech; dysarthria / dysphagia
loss of vision; visuospatial problems (one eye / hemianopia / gaze palsy)
loss of coordination; ataxia / vertigo / incoordination / nystagmus
What is the treatments of stroke
Thromblysis - restore perfusion before cell death occurs
(NOT FOR HEAMORRHAGIC STROKE)
- Ateplase
- Surgical, clot retrieval with catheter
Aspirin
Hemicrainectomy - relieve pressure
{>60 years MCA ishaemic stroke with complications of
Cerebral oedema /surgical decompression}
Secondary management: Clopidogrel aspirin BP drugs Statin Carotid endarectomy
What is the aetiologies of aneurysm disease
= weakened blood vessel wall, which is pushed outwards due to blood pressure causing excessive localised swelling in the wall of an artery
Degenerative disease
Connective tissue disease (e.g. Marfan’s disease)
Infection (mycotic aneurysm)
What is the symptoms of an AAA impending a rupture, and rupture
How is it diagnosed
PRE-RUPTURE
Increasing back pain
Tender AAA
Inflammation
RUPTURE
abdominal, back, side pain;
painful pulsatile mass;
haemodynamic instability (unstable blood flow/pressure); hypoperfusion (shock)
DIAGNOSIS
Ultrasound/ CT/ MRI
What is a non pharmaceutical option for prophylaxis in a stroke
carotid endarectomy
incision is made to open the carotid artery, plaque is removed, then the repaired artery is closed
stenting
What is the investigations and treatment options for chronic Limb ischeamia
CT/ MRI Duplex - Ultrasound digital subtraction angiogram buergers test brachial ankle pressure index
Surgical bypass
angioplasty and stenting
amputation
Aetiology of chronic limb ischeamia
Atheosclerotic
vasculitis
buergers disease
Presentation of acute limb ischaemia
Pain Pallor Perishingly cold Paraesthesia Paralysis Pulseless (compared in both legs)
is irreversible after 6-8 hours
causes by thrombus or embolism
define varicose veins
Dilated superficial veins in the lower limbs due to failure of venous valves as they become leaky and lead to back flow of blood
what is the signs and symptoms of
Cosmesis - disfiguring
Localised or generalised discomfort in the leg
Nocturnal cramps
Swelling
Acute haemorrhage
Superficial thrombophlebitis (inflammation of the wall of a vein associated with thrombosis)
Pruritus - itching
Skin changes: discolouration and spider veins ,
Treatment for varicose veins
Compression
ablation
saphenous surgery
What is ambulatory venous pressure
and what does a high AVP indicate
The fall in pressure from standing motionless to active movements High = failure of muscle pump valves or outflow obstruction Venous hypertension
What is the characteristics signs of chronic venous insufficiency
Ankle oedema
Telangectasia - spider veins
Venous eczema
Haemosiderin pigmentation - orangey colour in the lower limbs
Hypopigmentation “atrophie blanche” - white patches
Lipodermatosclerosis - inflammation of subcutaneous fat in the legs
Venous ulceration
Signs of DVT
Unilateral limb swelling
Persisting discomfort
Calf tenderness
Warmth
Redness- erythema
May be clinically silent - asymptomatic
What blood test is performed for DVT
d- dimer
DVT and pulmoary embolism are both what
venous thromboelbolisms
