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LAST MINUTE REVISION Flashcards

1
Q

What is the new treatment for adenocarcinomas if patient has EGFR mutation

A

Tryosine kinase inhibitors

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2
Q

What onconogene is induced by smoking in lung cancer

A

KRAS

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3
Q

What is an example of a immunotherapy drug in the treatment of lung cancer

A

Nivolumab BMS -

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4
Q

What is a chemotherapy drug in lung cancer

A

cisplatin

{adeocarinoma - pemetrexed
SCLC - etoposide}

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5
Q

What is the treatment plan for TB

A 
4months:
Rifampicin 
Isonazid
Pyrazinamide 
Ethambutol

2months
rifampicin
isonazid

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6
Q

what tests are used to screen for TB

A

Heaf

Mantoux

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7
Q

What is the morphology of TB and what causes it

A

Central caseating necrosis and Laghan Granuloma- due to activated macrophages

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8
Q

What is the signs of ADV TB

A

finger clubbing
Bronchial breathing
Crackles
Erythema nodosum

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9
Q

What is the signs of TB

A 
weight loss 
fever 
malaise 
cough 
sputum 
heamoptysis
pleuritic chest pain
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10
Q

What is the investigation for TB

A 
CXT 
Sputum - culture, microbiology, PCR 
Bronchoscopy 
Pleural aspiration/ biopsy 
CT thorax
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11
Q

What is the treatment in CF

A

ANTIBIOTICS
Large dose of two antibiotics: Blactams & Aminoglycosides on a 2 week course

REDUCE INFLAMMATION
Ibuprofen
Azithromycin
Prednisolone

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12
Q

What drug directly treats CF and how does it work

A

Ivacaftor

binds to CFTR, improves the transport of chloride ions

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13
Q

What are the microbiology present in CF

A

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

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14
Q

Symptoms of CF

A

Chronic purulent sputum production

Recurrent chest infection
(pneumonitis / bronchiectasis / scarring / abscesses)

Weight loss

Fever

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15
Q

Symptoms and signs of CF

A 
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

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16
Q

What is the screening process for neonatal babies in the detection of CF

A

Guthrie test (heel-pin test) for day 5 babies;

  1. Initial - immunoreactive trypsinogen
  2. If positive - mutation analysis performed
  3. Screen positive referred sweat test
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17
Q

What is the management of pancreatic insufficiency

A

Enteric coates enzyme pellets (deal with fat)
H2 antagonists
Proton pump inhibitors
Good nutrition
- high energy diet
Fat soluble vitamin + mineral supplements
Active life

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18
Q

How do you treat Pseudomonas aeruginosa (60% CF microorganism)

A 
nebulised colomycin 
with antibiotics - 
oral ciprofloxacin 
or 
i.v. ceftazidime (if the other fails)
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19
Q

Blood flow rate is controlled by what two mechanisms

DARCYS LAW Flow = Pressure difference/ resistance

A

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

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20
Q

The increase in metabolites in active hyperaemia and pressure flow regulation creates a negative feedback effect by triggering the release of what

A

EDFR

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21
Q

What is the difference in pulmonary circulation compared to everywhere else

A

a decrease in oxygen causes arterial constriction

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22
Q

what is the result of stimulated RAAS

A

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

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23
Q

What is the best tool is diagnosing high blood pressure

A

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
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24
Q

What is the aetiologies of secondary (5-10%) hypertension

and what also increases the risk

A

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
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25
Q

What is the hypertension treatment plan over the age of 55, african-caribean race, pre pregnant

A
  1. CBB
    • Thiazide type diuretic
    • ACEI
      For resistant Hypertension
  4. spirolactotone/ higher dose thiazide
    Have to take into account potassium levels
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26
Q

What is the hypertension treatment plan for those under the age of 55

A
  1. ACEI/ARB
    • Thiazide type diuretics
    • CBB
      For resistant Hypertension
  4. spirolactotone/ higher dose thiazide
    Have to take into account potassium levels
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27
Q

When should CBBs not be used

A

when there is a risk or heart failure is present

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28
Q

What drugs are recommended pre pregnancy and during pregnancy

A 
Pre - 
CBB(Nifedipine MR) 
Centrally acting agents (Methyl dopa) 
Beta Blockers (Atenolol, Labetalol) 
Pregnant - add thiazide diuretic and/or amlodipine
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29
Q 
Example of 
ACEI 
CCB
ARB
BB
A

RAMIPRIL

VERAMIPRIL/ AMPLODIPINE

LOSARTAN

ATNEOLOL

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30
Q

What is the pathophysiology of IE

what organism is most likely the cause

A

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

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31
Q

what is the signs and symptoms of IE

A

Murmur
Muscoskeletal pain

splinter haemorrhages 
vasculitic rash 
Roth Spots 
Osler’s nodes 
Janeway lesions 
nephritis 
anemia
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32
Q

what is the signs and symptoms of IE

A 
F - fever 
R - roths spots 
O - oslers nodules 
M - Murmur 
J - Janeway leison 
A - anemia 
N - Nail splinter heamorhages 
E -  Emboli
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33
Q

What is the antibiotic treatment for IE

A

Native valve: Gentamicin+ amoxycillin
Prosthetic valve: gentamicin + vancomycin + rifampicin
Native valve and sepsis: Gentamicin and vancomycin

6 weeks IV

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34
Q

What is the complications of IE

A

heart failure

fistula formation

leaflet perforation

uncontrolled infection

abscess formation

atrioventricular heart block

embolism

prosthetic valve dysfunction /dehiscence

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35
Q

What is the two aetiologies of oedema

A

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
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36
Q

What is the different aetiologies of oedema

A

Congestive heart failure: - TRANSUDATE
LH- Pulmonary oedema
RH -Peripheral oedema

Lymphatic blockage

hypoalbuminaemia

abnormal renal function

inflammation - EXUDATE

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37
Q

signs of RHF

A

Increased JVP
Hepatomegaly
Peripheral oedema

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38
Q

What is the signs and symptoms of cardiac heart failure

A

fatigue
breathlessness
reduced exercise capacity

Chest crepitations,
oedema, 
tachycardia 
dyspnoea 
fatigue
Increased JVP 
Third systolic heart sound S3 
Displaced apex

raised BNP concentration

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39
Q

What is the drug therapy for heart failure

A

– Diuretics

–ACE inhibitors

– Betablockers

–Aldosterone receptor blockers

–In some pateints ACE I or ARDB now replaced by angiotensin receptor neprilysin inhibitor

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40
Q

Aetiology of heart failure

A

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

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41
Q

What is the screening test and investigations for heart failure

A

ECG
BNP

ECHO - severe LV ejection fraction < 30%
MUGA - Radionuclide to see the pumping of the heart
CXR
MRI

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42
Q

What will provide objective evidence of cardiac dysfunction in the diagnosis of heart failure than

A

abnormal ECHO
-cardiomegaly
Cardiac murmurs -S3
raised natriuretic peptide concentration

responds to diuretics

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43
Q

What is an example of a drug that prevents the break down of ANP and DNP therefore enhancing natural diuretics in the body

A

Neprolysin

44
Q

What drugs are used in the treatment of heart failure

A

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

45
Q

When should beta blockers be administered in heart failure patients

A

when they are stable - no fluid retention

46
Q

What does a decreased CO in systolic disfunction activate

A

RAAS activation

Sympathetic activation

Increasing blood volume - causing further problems

47
Q

Define systolic and diastolic heart failure

A

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

48
Q

What is the symptoms of mitral stenosis

A 
Dyspnoea: 
Haemoptisis - pressure cause bv rupture 
Chest pain 
Hoarseness - Left atrium pressing on laryngeal 
palpitations
49
Q

What is the aetiology of mitral regurgitation

A 
Rheumatic Heart Disease 
Mitral valve prolapse (MVP)  - acute MR
Infective endocarditis 
Degenerative - fibrosis 
LV and annular dilatation - e.g. previous heart attack
50
Q

What is the signs of mitral regurgitation

A 
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

51
Q

What is the signs of mitral stenosis

A 
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

52
Q

Aetiology of mitral stenosis

A

IE
rheumatic heart disease
congenital

53
Q

What can mitral valvular diseases cause

A

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

54
Q

What medication is given to Mitral valve diseases

and what medication delays until surgery can happen in regurgitation valvular disease

A

Diuretics

vasodilator

55
Q

Whats the aetiology in aortic stenosis

A

Degenerative - calcification = senile aortic stenosis
Rheumatic
Bicuspid stenosis

56
Q

What is the aetiology of aortic regurgitation

A 
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

57
Q

What is the only valve disease that doesn’t develop heart failure

A

aortic regurgitation

58
Q

How is aortic stenosis differentiated from aortic sclerosis

A

Loss of aortic secondary heart sound

59
Q

What is the signs and symptoms of aortic stenosis

A

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
60
Q

What is the signs and symptoms of aortic regurgitation

A

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

61
Q

Rheumatic heart disease

A

strep infections
aspirin and bed rest
measured with ASO titre

62
Q

What is the aetiology of hypertrophic cardiomyopathy

A

Inherited Autosomal dominant sarcomere gene defect that changes the genes in the heart muscle protein

Thyroid problems and diabetes can also cause hypertrophic cardiomyopathy

63
Q

When is Brain Natriuretic Peptide polypeptide secreted

A

by the ventricles of the heart in response to excessive stretching of heart muscle cells

64
Q

What is the general measures that should be taken with cardiomyopathy

A

Avoid heavy exercise

Avoid dehydration

Explore FH and first degree relatives,

ECGs and echoes may be required

Consider genetic testing

65
Q

Investigations for dilated cardiomyopathy - dilation of heart chambers impairing systolic function

A 
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
66
Q

What investigations are carried out for restrictive and infiltrative cardiomyopathy

A 
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)
67
Q

What are the signs of dilated cardiomyopathy

A 
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)
68
Q

What is the signs for hypertrophy cardiomyopathy

A

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

69
Q

what is the aetiology of dilated cardiomyopathy

A

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)

70
Q

What is centracinar and panacinar emphysema most likely linked to

A

Centracinar - Enviromental exposures e.g. smoking

Panacinar - alpha 1 trypsin deficiency

71
Q

What is the pathology of emphysema

A

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

72
Q

aetiology of COPD

A 
Smoking 
Occupation 
ageing  
atmospheric pollution 
chronic asthma 
(alpha 1 trypsin deficiency)
73
Q

What is the affect of smoking on your lungs

A

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

74
Q

What increase in residual volume shows their is gas trapping with pulmonary function test CO

A

> 30%

75
Q

What is alpha 1-antitrypsin

A

made in the liver neutralises neutrophil enzymes and regulates elastase

76
Q

what is the signs of COPD

A

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)

77
Q

What steroids are used for COPD exasperation

A

Prednisolone

78
Q

What is the inhaler therapy for COPD

A

Short acing bronchiodilators - salbutamol, terbutaline
Long acting bronchiodilators
High dose inhaled corticosteroids (ICS) and LABA

79
Q

treatment plan for asthma

A

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

80
Q

How does adult asthma treatment and child asthma treatment differ

A

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)

81
Q

SABA + ICS

A

Salbutamol

Beclomethasone

82
Q

What is the treatment for stable angina

A

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)
83
Q

Investigations for stable angina

A

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

84
Q

Aetiology of stable angina

A

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

85
Q

When should you never use nifedipine CCB immediate release (rapid acting vasodilators)
why?

A 
Post MI (with impaired LV function) 
or 
Unstable angina (increase infarction rate and + death)

may precipitate a stroke or MI

86
Q

When do you not use beta blockers

A

Asthma
Peripheral Vascular Disease - Relative contraindication
Raynauds Syndrome
Heart failure
Those patients who are dependent on sympathetic drive
Bradycardia / Heart block

87
Q

What is dual anti-platelet therapy that all ACS patients should receive one year after the event

A

both aspirin and a ADP receptor blocker

88
Q

When would ACE inhibitors be used the treatment of unstable angina and NSTEMI

A

if left ventricular dysfunction is present

89
Q

How can ACS result in sudden cardiac death

A

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

90
Q

aetiologies of stroke

A

Infarction

  • Large artery athlersclerosis
  • cardioembolic stroke - due to AF
  • Lucunar stroke - deep white matter

Haemorrhage (don’t treat with thrombolysis)
- aneurysms/hypertension

MRI differentiates

91
Q

What are the symptoms of a stroke

A

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

92
Q

What is the treatments of stroke

A

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
93
Q

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

A

Degenerative disease
Connective tissue disease (e.g. Marfan’s disease)
Infection (mycotic aneurysm)

94
Q

What is the symptoms of an AAA impending a rupture, and rupture

How is it diagnosed

A

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

95
Q

What is a non pharmaceutical option for prophylaxis in a stroke

A

carotid endarectomy
incision is made to open the carotid artery, plaque is removed, then the repaired artery is closed

stenting

96
Q

What is the investigations and treatment options for chronic Limb ischeamia

A 
CT/ MRI
Duplex - Ultrasound 
digital subtraction angiogram
buergers test 
brachial ankle pressure index

Surgical bypass
angioplasty and stenting
amputation

97
Q

Aetiology of chronic limb ischeamia

A

Atheosclerotic
vasculitis
buergers disease

98
Q

Presentation of acute limb ischaemia

A 
Pain 
Pallor 
Perishingly cold 
Paraesthesia 
Paralysis 
Pulseless 
(compared in both legs)

is irreversible after 6-8 hours

causes by thrombus or embolism

99
Q

define varicose veins

A

Dilated superficial veins in the lower limbs due to failure of venous valves as they become leaky and lead to back flow of blood

100
Q

what is the signs and symptoms of

A

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 ,

101
Q

Treatment for varicose veins

A

Compression
ablation
saphenous surgery

102
Q

What is ambulatory venous pressure

and what does a high AVP indicate

A 
The fall in pressure from standing motionless to active movements
High = 
failure of muscle pump 
valves or outflow obstruction 
Venous hypertension
103
Q

What is the characteristics signs of chronic venous insufficiency

A

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

104
Q

Signs of DVT

A

Unilateral limb swelling

Persisting discomfort

Calf tenderness

Warmth

Redness- erythema

May be clinically silent - asymptomatic

105
Q

What blood test is performed for DVT

A

d- dimer

106
Q

DVT and pulmoary embolism are both what

A

venous thromboelbolisms

RSNOTES (53 decks)

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