LO Related (Part 2) Flashcards
Cardiac arrest would present with which acid-base abnormality
Cardiac arrest
Pink puffer
Are they likely to be in type I or type II resp failure
Type 1
Where should an ET tube sit normally?
Just above the carina
Where is the centre that controls the RESPIRATORY DRIVE found?
In the medulla
Max oxygen that can be given with nasal canulae
RATE
PERCENTAGE
4l/min
34%
What is the treatment for type 2 respiratory failure
Controlled O2 therapy
Treat the underlying cause
What is the DEFINITION of respiratory failure
Failure of the lungs to oxygenate the arterieal blood and/or failure to eliminate CO2
TWO roles of Tregs
Peripheral tolerance
Dampening down of immune responses
What is a thymocyte
Immature T cell found in the thymus
Mutations in FOXP3 (Treg marker) can lead to which syndrome
IPEX
Condition in which Treg function is lost - thus individuals will mount inappropriate immune responses and the body will not be able to supress these
Cancer is only MALIGNANT when
The basement membrane has NOT been breached
Describe the stigma associated with lung cancer
Why is this an issue
Often seen as a disease brought on by smoking “brought on themselves by smoking”
This stigma can delay people seeking help
What is the single cause of preventable illness
Smoking - lung cancer
Example of a benign tumour that despite being benign can have SERIOUS COMPLICATIONS
Meningioma
Benign slow growing tumour in the arachnoid mater
Can lead to increased intercranial pressure
Describe the 5 steps of CENTRAL TOLERANCE
T cell progenitors enter the cortex of thymus
TCR a and B chains generated
Thymocytes exp TCR WEAKLY recongising SELF MHC allowed to survive (FIRST SELECTION IS POSITIVE)
Thymocytes exp a TCR STRONGLY binding SELFMHC with a SELF PEPTIDE are KILLED (SECOND SELECTION IS NEGATIVE)
REMAINING CELLS WEAKLY BIND TO SELF MHC IS THE PRESENCE OR ABSENCE OF SELF PEPTIDES
Markers of Treg cells
CD4 and CD25
ALSO FOXP3 (this is the key transcription factor in Treg development)
Cytokine produced by Th cells to activate B cells and CT cells
IL-2
What are the three different types of stigma
Physical
Moral
Tribal
What is a LEIOMYOSARCOMA
Malignant tumour of the smooth muscle
Symptoms of Horners syndrome
Miosis - constriction of the pupil
Ptosis - drooping of the upper eyelid
Anhidrosis - lack of sweating
What is nuclear pleomorphism
Abnormalities in the size/shape of the nucleus
What are the FIVE As of PATIENT CENTRED COUNSELLING
Ask
Assess
Advise
Agree
Assist/arrange
SCLC arise from which cells
NEuroendocrine
What is a leimyoma
Benign tumour of the smooth muscle
What does release of IFN-gamma from Th cells promote
The activation of MACROPHAGES and NK cells
Describe how DENDRITIC cells are SUPER ANTIGEN PRESENTING CELLS
Exogenous antigen can be presented on MHC1 by dendritic cells
What is the theory of SELF-AFFIRMATION
People respons to situations in a certain way to protect their self-identity
What is the gap between the FIRST and SECOND heart sound
SYSTOLE
Vircows triad for blood clot formation
Stasis
Hypercoagulation
Endothelial damage
Secondary pacemaker of the heart and its rate
Av node - 50 bpm
ST depression is the reuslt of
Myocardial ischaemia
What is a PHAEOCHROMOCYTOMA
Tumour of the adrenal medulla - catecholamine secreting
Define postural hypertension
Sudden decrease in blood pressure upon standing
Systolic BP drops by OVER 20mmHG
What is the primary pacemaker of the heart
What is its INHERENT ryhthm
Why is the actual HR usually less
SA node
100 bpm
PSNS tonic inhibiton via CNX
6Ps of CIRITICAl LIMB ISCHAMEIA
Pallor Pain Pulseless Paresthesia Paralysis Perishingly cold
What is a FUSIFORM aneurysm
Dilation of the ENTIRE CIRCUMFERENCE of the artery
Gp1b/Ix binds
vWF
What are the VITAMIN K DEPENDENT CLOTTING factors
7 10 and prothrombin
What are GARTANS
Direct thrombin inhibitors
What are XABANS
Direct factor X inhibitors
GpIIb/IIIa binds
Fibrinogen and vWF inducing platelet aggregation`
What type of clots would anti-platelets be most useufl against
Arterial
MOA abciximab and tirofiban
Inhibition of gpIIb/IIIa
When post infarct would you see yellow discolouration and neutrophil infiltrate
24-72 hours
When post infarct will you see HYPERAEMIA around yellow dead muscle (macroscopic) and visible granulation tissue (micro)
3-10 days
How is the extrisnic pathway of the coagulation cascade activated
TISSUE INJURY
Causing the release of tissue factor or phospholipid exposure
What is the most common HEPARIN used now and why
LMWH
COmpared to unfractionated
LONGER DURATION with a MORE PREDICTABLE EFFECT
What is a saccular aneurysm
Aneurysm with a sac-like bulge on the one side
At what time after an infarct will white fibrotic scar tissue appear
Weeks to months
GpIa/IIa binds…
Collagen
At what time after an infarct will you see pale discolouration and intracellular oedema
12-24 hours
When do troponins rise post-MI
Within 3 hours
Function of type II pneumocytes
Production of surfactant
Side effects of GTN sprays
Reflex tachy
Postural hypotension
Headache
Describe UNSTABLE ANGINA
Plaque that has a THIN FIBROUS cap so ruptures unpredictably causing CP that resolves in 20mins as the thrombus resolves
THERE IS NO LASTING DAMAGE
What type of Ca channel do CCBS block
L-type
Describe the acute (WITHIN HOURS) changes as a reuslt of MI
ST elevation
Abnormal Q wave
T wave inversion
Tachycardia
What is KARYOREXXIS
Nuclear fragmentation
Risk calculatory for CVD
QRISK3
Where in the body to dihyrdropyrdines work
They work on the ARTERIOLAR SMOOTH MUSCLE
They DO NOT work on the heart
How do Na, Adre and Ang II contribute to cardiac remodelling
Increased production of TGF-B
How does the NYHA classify the stages of heart failure
Symptoms are graded dependent on their ability to carry out physical activity
1 = no limitations
4 = inability to carry out activities of daily life
Normal level of what peptide excludes HF
BNP
Causes of ACUTE heart failure
MI
PE
Valve rupture
How does aldosterone lead to cardiac remodelling
Increased levels of EGF
Treatment for chronic HF
Diuretic ACEi/ARB Beta blockers Digoxin Pacemaker if arrhythmia
2 potential causes of right heart failure
Shunt (left to right)
Cor pulmonale
Why do K sparing diuretics INCREASE PROGNOSIS of HF
Inhibtiion of aldosterone - thus also inhibits the effects aldosterone has on cardiac remodelling
3 main causes of HF
Ischaemic heart disease
Dilated cardiomyopathy
Long standing HTN
Which drugs releive symptoms in HF
Loop and thiazide diuretics
Inotropic drugs (e.g. digoxin)
RSR in V1 =
RBBB
M shaped QRS in lead 5/6 ==>
LBBB
Limits of an RCt
Sometimes unethical
Expensive
Poor design is common
Can take time
MUST BE CRITICALLY APPRAISED
Treatment of ACUTE HF
Sit up High flow O2 IV loop diuretic Morphine Nitrate CPAP
What are three threats to the reliability of evidence
BIAS
CHANCE
CONFOUNDERS
