LO Related (Part 2) Flashcards

(75 cards)

1
Q

Cardiac arrest would present with which acid-base abnormality

A

Cardiac arrest

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2
Q

Pink puffer

Are they likely to be in type I or type II resp failure

A

Type 1

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3
Q

Where should an ET tube sit normally?

A

Just above the carina

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4
Q

Where is the centre that controls the RESPIRATORY DRIVE found?

A

In the medulla

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5
Q

Max oxygen that can be given with nasal canulae

RATE

PERCENTAGE

A

4l/min

34%

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6
Q

What is the treatment for type 2 respiratory failure

A

Controlled O2 therapy

Treat the underlying cause

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7
Q

What is the DEFINITION of respiratory failure

A

Failure of the lungs to oxygenate the arterieal blood and/or failure to eliminate CO2

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8
Q

TWO roles of Tregs

A

Peripheral tolerance

Dampening down of immune responses

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9
Q

What is a thymocyte

A

Immature T cell found in the thymus

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10
Q

Mutations in FOXP3 (Treg marker) can lead to which syndrome

A

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

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11
Q

Cancer is only MALIGNANT when

A

The basement membrane has NOT been breached

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12
Q

Describe the stigma associated with lung cancer

Why is this an issue

A

Often seen as a disease brought on by smoking “brought on themselves by smoking”

This stigma can delay people seeking help

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13
Q

What is the single cause of preventable illness

A

Smoking - lung cancer

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14
Q

Example of a benign tumour that despite being benign can have SERIOUS COMPLICATIONS

A

Meningioma

Benign slow growing tumour in the arachnoid mater

Can lead to increased intercranial pressure

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15
Q

Describe the 5 steps of CENTRAL TOLERANCE

A

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

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16
Q

Markers of Treg cells

A

CD4 and CD25

ALSO FOXP3 (this is the key transcription factor in Treg development)

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17
Q

Cytokine produced by Th cells to activate B cells and CT cells

A

IL-2

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18
Q

What are the three different types of stigma

A

Physical

Moral

Tribal

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19
Q

What is a LEIOMYOSARCOMA

A

Malignant tumour of the smooth muscle

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20
Q

Symptoms of Horners syndrome

A

Miosis - constriction of the pupil

Ptosis - drooping of the upper eyelid

Anhidrosis - lack of sweating

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21
Q

What is nuclear pleomorphism

A

Abnormalities in the size/shape of the nucleus

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22
Q

What are the FIVE As of PATIENT CENTRED COUNSELLING

A

Ask

Assess

Advise

Agree

Assist/arrange

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23
Q

SCLC arise from which cells

A

NEuroendocrine

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24
Q

What is a leimyoma

A

Benign tumour of the smooth muscle

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25
What does release of IFN-gamma from Th cells promote
The activation of MACROPHAGES and NK cells
26
Describe how DENDRITIC cells are SUPER ANTIGEN PRESENTING CELLS
Exogenous antigen can be presented on MHC1 by dendritic cells
27
What is the theory of SELF-AFFIRMATION
People respons to situations in a certain way to protect their self-identity
28
What is the gap between the FIRST and SECOND heart sound
SYSTOLE
29
Vircows triad for blood clot formation
Stasis Hypercoagulation Endothelial damage
30
Secondary pacemaker of the heart and its rate
Av node - 50 bpm
31
ST depression is the reuslt of
Myocardial ischaemia
32
What is a PHAEOCHROMOCYTOMA
Tumour of the adrenal medulla - catecholamine secreting
33
Define postural hypertension
Sudden decrease in blood pressure upon standing Systolic BP drops by OVER 20mmHG
34
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
35
6Ps of CIRITICAl LIMB ISCHAMEIA
``` Pallor Pain Pulseless Paresthesia Paralysis Perishingly cold ```
36
What is a FUSIFORM aneurysm
Dilation of the ENTIRE CIRCUMFERENCE of the artery
37
Gp1b/Ix binds
vWF
38
What are the VITAMIN K DEPENDENT CLOTTING factors
7 10 and prothrombin
39
What are GARTANS
Direct thrombin inhibitors
40
What are XABANS
Direct factor X inhibitors
41
GpIIb/IIIa binds
Fibrinogen and vWF inducing platelet aggregation`
42
What type of clots would anti-platelets be most useufl against
Arterial
43
MOA abciximab and tirofiban
Inhibition of gpIIb/IIIa
44
When post infarct would you see yellow discolouration and neutrophil infiltrate
24-72 hours
45
When post infarct will you see HYPERAEMIA around yellow dead muscle (macroscopic) and visible granulation tissue (micro)
3-10 days
46
How is the extrisnic pathway of the coagulation cascade activated
TISSUE INJURY Causing the release of tissue factor or phospholipid exposure
47
What is the most common HEPARIN used now and why
LMWH COmpared to unfractionated LONGER DURATION with a MORE PREDICTABLE EFFECT
48
What is a saccular aneurysm
Aneurysm with a sac-like bulge on the one side
49
At what time after an infarct will white fibrotic scar tissue appear
Weeks to months
50
GpIa/IIa binds...
Collagen
51
At what time after an infarct will you see pale discolouration and intracellular oedema
12-24 hours
52
When do troponins rise post-MI
Within 3 hours
53
Function of type II pneumocytes
Production of surfactant
54
Side effects of GTN sprays
Reflex tachy Postural hypotension Headache
55
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
56
What type of Ca channel do CCBS block
L-type
57
Describe the acute (WITHIN HOURS) changes as a reuslt of MI
ST elevation Abnormal Q wave T wave inversion Tachycardia
58
What is KARYOREXXIS
Nuclear fragmentation
59
Risk calculatory for CVD
QRISK3
60
Where in the body to dihyrdropyrdines work
They work on the ARTERIOLAR SMOOTH MUSCLE They DO NOT work on the heart
61
How do Na, Adre and Ang II contribute to cardiac remodelling
Increased production of TGF-B
62
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
63
Normal level of what peptide excludes HF
BNP
64
Causes of ACUTE heart failure
MI PE Valve rupture
65
How does aldosterone lead to cardiac remodelling
Increased levels of EGF
66
Treatment for chronic HF
``` Diuretic ACEi/ARB Beta blockers Digoxin Pacemaker if arrhythmia ```
67
2 potential causes of right heart failure
Shunt (left to right) Cor pulmonale
68
Why do K sparing diuretics INCREASE PROGNOSIS of HF
Inhibtiion of aldosterone - thus also inhibits the effects aldosterone has on cardiac remodelling
69
3 main causes of HF
Ischaemic heart disease Dilated cardiomyopathy Long standing HTN
70
Which drugs releive symptoms in HF
Loop and thiazide diuretics Inotropic drugs (e.g. digoxin)
71
RSR in V1 =
RBBB
72
M shaped QRS in lead 5/6 ==>
LBBB
73
Limits of an RCt
Sometimes unethical Expensive Poor design is common Can take time MUST BE CRITICALLY APPRAISED
74
Treatment of ACUTE HF
``` Sit up High flow O2 IV loop diuretic Morphine Nitrate CPAP ```
75
What are three threats to the reliability of evidence
BIAS CHANCE CONFOUNDERS