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BM4 Year 1 - Quizlet Cards > LO Related (Part 2) > Flashcards

LO Related (Part 2) Flashcards

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
Q

What does release of IFN-gamma from Th cells promote

A

The activation of MACROPHAGES and NK cells

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26
Q

Describe how DENDRITIC cells are SUPER ANTIGEN PRESENTING CELLS

A

Exogenous antigen can be presented on MHC1 by dendritic cells

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27
Q

What is the theory of SELF-AFFIRMATION

A

People respons to situations in a certain way to protect their self-identity

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28
Q

What is the gap between the FIRST and SECOND heart sound

A

SYSTOLE

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29
Q

Vircows triad for blood clot formation

A

Stasis
Hypercoagulation
Endothelial damage

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30
Q

Secondary pacemaker of the heart and its rate

A

Av node - 50 bpm

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31
Q

ST depression is the reuslt of

A

Myocardial ischaemia

32
Q

What is a PHAEOCHROMOCYTOMA

A

Tumour of the adrenal medulla - catecholamine secreting

33
Q

Define postural hypertension

A

Sudden decrease in blood pressure upon standing

Systolic BP drops by OVER 20mmHG

34
Q

What is the primary pacemaker of the heart

What is its INHERENT ryhthm

Why is the actual HR usually less

A

SA node

100 bpm

PSNS tonic inhibiton via CNX

35
Q

6Ps of CIRITICAl LIMB ISCHAMEIA

A 
Pallor
Pain 
Pulseless
Paresthesia
Paralysis 
Perishingly cold
36
Q

What is a FUSIFORM aneurysm

A

Dilation of the ENTIRE CIRCUMFERENCE of the artery

37
Q

Gp1b/Ix binds

A

vWF

38
Q

What are the VITAMIN K DEPENDENT CLOTTING factors

A

7 10 and prothrombin

39
Q

What are GARTANS

A

Direct thrombin inhibitors

40
Q

What are XABANS

A

Direct factor X inhibitors

41
Q

GpIIb/IIIa binds

A

Fibrinogen and vWF inducing platelet aggregation`

42
Q

What type of clots would anti-platelets be most useufl against

A

Arterial

43
Q

MOA abciximab and tirofiban

A

Inhibition of gpIIb/IIIa

44
Q

When post infarct would you see yellow discolouration and neutrophil infiltrate

A

24-72 hours

45
Q

When post infarct will you see HYPERAEMIA around yellow dead muscle (macroscopic) and visible granulation tissue (micro)

A

3-10 days

46
Q

How is the extrisnic pathway of the coagulation cascade activated

A

TISSUE INJURY

Causing the release of tissue factor or phospholipid exposure

47
Q

What is the most common HEPARIN used now and why

A

LMWH

COmpared to unfractionated

LONGER DURATION with a MORE PREDICTABLE EFFECT

48
Q

What is a saccular aneurysm

A

Aneurysm with a sac-like bulge on the one side

49
Q

At what time after an infarct will white fibrotic scar tissue appear

A

Weeks to months

50
Q

GpIa/IIa binds…

A

Collagen

51
Q

At what time after an infarct will you see pale discolouration and intracellular oedema

A

12-24 hours

52
Q

When do troponins rise post-MI

A

Within 3 hours

53
Q

Function of type II pneumocytes

A

Production of surfactant

54
Q

Side effects of GTN sprays

A

Reflex tachy

Postural hypotension

Headache

55
Q

Describe UNSTABLE ANGINA

A

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
Q

What type of Ca channel do CCBS block

A

L-type

57
Q

Describe the acute (WITHIN HOURS) changes as a reuslt of MI

A

ST elevation

Abnormal Q wave

T wave inversion

Tachycardia

58
Q

What is KARYOREXXIS

A

Nuclear fragmentation

59
Q

Risk calculatory for CVD

A

QRISK3

60
Q

Where in the body to dihyrdropyrdines work

A

They work on the ARTERIOLAR SMOOTH MUSCLE

They DO NOT work on the heart

61
Q

How do Na, Adre and Ang II contribute to cardiac remodelling

A

Increased production of TGF-B

62
Q

How does the NYHA classify the stages of heart failure

A

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
Q

Normal level of what peptide excludes HF

A

BNP

64
Q

Causes of ACUTE heart failure

A

MI

PE

Valve rupture

65
Q

How does aldosterone lead to cardiac remodelling

A

Increased levels of EGF

66
Q

Treatment for chronic HF

A 
Diuretic
ACEi/ARB
Beta blockers
Digoxin 
Pacemaker if arrhythmia
67
Q

2 potential causes of right heart failure

A

Shunt (left to right)

Cor pulmonale

68
Q

Why do K sparing diuretics INCREASE PROGNOSIS of HF

A

Inhibtiion of aldosterone - thus also inhibits the effects aldosterone has on cardiac remodelling

69
Q

3 main causes of HF

A

Ischaemic heart disease

Dilated cardiomyopathy

Long standing HTN

70
Q

Which drugs releive symptoms in HF

A

Loop and thiazide diuretics

Inotropic drugs (e.g. digoxin)

71
Q

RSR in V1 =

A

RBBB

72
Q

M shaped QRS in lead 5/6 ==>

A

LBBB

73
Q

Limits of an RCt

A

Sometimes unethical
Expensive
Poor design is common
Can take time

MUST BE CRITICALLY APPRAISED

74
Q

Treatment of ACUTE HF

A 
Sit up 
High flow O2
IV loop diuretic 
Morphine 
Nitrate 
CPAP
75
Q

What are three threats to the reliability of evidence

A

BIAS

CHANCE

CONFOUNDERS

BM4 Year 1 - Quizlet Cards (3 decks)

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