Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M4 Y1 > Life Support > Flashcards

Life Support Flashcards

1
Q

What are the names of the two layers of pleura?

A

Visceral pleura - at the lungs
Parietal pleura - on chest wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does lung compliance describe?

A

How does the expansive force (transpulmonary pressure) translate to change in volume.

  • High compliance = less force required to induce a specific change in volume (↓stiffness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the effect of pulmonary surfactant on lungs

A

Reduces alveolar surface tension and therefore increases lung compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

A 31 year old man is stabbed in the back and suffers a traumatic pneuomothorax, causing atelectasis (collapse) of part of the lung. What changes would you expect to lung volume, pleural cavity
volume and intrapleural pressure in the affected tissue?

a) ↓Lung volume, ↓pleural cavity volume, ↓intrapleural pressure
b) ↓Lung volume, ↓pleural cavity volume, ↑intrapleural pressure
c) ↓Lung volume, ↑pleural cavity volume, ↓intrapleural pressure
d) ↓Lung volume, ↑pleural cavity volume, ↑ intrapleural pressure
e) ↑Lung volume, ↓pleural cavity volume, ↑intrapleural pressure

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

A 68 year old female patient is attending the clinic to receive the results from a recent respiratory function tests. The doctor interpreting the results observes that the patient’s lung compliance values are very high (the values are also increasing as time goes on).
What respiratory condition would information indicate?
a) Asthma
b) Chronic bronchitis
c) Emphysema
d) Neonatal respiratory distress syndrome
e) Pulmonary fibrosis

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A newborn baby develops neonatal respiratory distress syndrome
due to insufficient levels of pulmonary surfactant within the lungs.
What causes the decreased lung compliance observed in such a
patient?
a) Degradation of elastin fibres
b) Deposition of collagen
c) Reduced alveolar surface area
d) Increased surface tension at the air-liquid interface
e) Airway smooth muscle contraction

A

D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is spirometry used for?

A

Measures the volume and flow during maximal expiratory effort after
maximal inhalation

Useful in differentiating between obstructive & restrictive lung disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are peak flowmeters used for?

A

Diagnosis of variable airway obstruction & monitoring of treatment success

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

A spirometer shows a patient has a reduced FEV1 & FVC. The FEV1/FVC is normal. What kind of lung disorder?

A

Restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A spirometer shows a patient has a reduced FEV1 & normal FVC. The FEV1/FVC is lowered. What kind of lung disorder?

A

Airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What may a reduction in transfer factor result show? (respiratory)

A
  • Severe reduction in ventilation or perfusion
    • Severe emphysema (reduced surface area)
    • Heart failure (reduced ventilation
    • Pneumonia (reduced ventilation)
    • Pulmonary emboli (reduced perfusion)
  • Thickening of alveolar-capillary membrane
    • Intersitial lung disease e.g. pulmonary fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List some risk factors for asthma

A

Parental asthma; susceptibility genes; infant respiratory virus infection; caesarean; urban dwelling & pollution exposure; poor diet; obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Show how allergic sensitisation occurs (cellular level) for asthma

A
  1. Allergen is encountered & processed by adaptive immune system
    • Antigen presenting cell** (APC) (e.g. dendritic cell) engulfs & processes allergen - presents antigen to naive Th cell
    • (now mature) Th2 cell interacts with B cell, displaying antigen
      Interleukins produced by mature Th2 cell also activate eosinophils which proliferate
  2. IgE antibodies are generated by B cells, immune system ‘primed’
    IgE antibodies bind to IgE receptors on mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain what happens in asthma upon re-exposure to an allergen.

A

1) Allergen binds IgE on mast cells, inducing degranulation
- Inflammatory mediators released - PGs, LTs, chemokines

2) Allergen stimulates further T cell activation, which produce ILs that stimulate eosinophils, which are recruited to airways and degranulate
- Releasing inflammatory mediators - ROS, enzymes, leukotrienes
- Mast cells also induce this

3) Overall resulting in airway inflammation, contraction of smooth muscle, excess mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the roles of Th2 cells, B cells, mast cells & eosinophils in asthma pathophysiology

A

Th2 - sensitisation - induces B cells to produce allergen-specific IgE.
Inflammation - coordination of immune response by cytokine release (IL4,5,13)

B-cells - allergen-specific IgE production

Mast cells - allergen induced degranulation = release of inflammatory mediators (leukotrienes & prostaglandis)

Eosinophils - cytokine induced degranulation = release of inflammatory mediators (ROS, proteolytic enzymes, leukotrienes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What changes occur to the airways after long-term asthmatic airway remodelling?

A
  • ECM deposition & fibrosis
  • Epithelium disruption
  • Smooth muscle hypertrophy
  • Basement membrane thickening
  • Excess mucus & goblet cells
  • Immune cell infiltration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What controls, and which nerves innervate, respiration?

A

Respiratory cenre - ill defined group of neurons in reticular substance of brainstem

Motor discharges travel down the phrenic & intercostal nerves to respiratory musculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What gives input for chemical & neurogenic control of ventilation?

A

PERIPHERAL chemoceptors - aortic arch & carotid bodies

CENTRAL chemoceptors - brain

  • Hypothalamus - pain & emotional stimuli
  • Limb receptors during exercise
  • Juxtapulmonary receptors stimulated by pulmonary congestion
  • Stretch receptors in muscles & joints of chest wall
  • Consciously induced changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What gives specific substances affect chemical control of ventilation?

A

Rise in CO2 is strongest stimulant (central & peripheral chemoceptors detect this)

Peripheral chemoceptors (aortic arch & carotid bodies)
- Rise in H ions increases ventilation
- Reduced pO2 increases ventilation (peripheral chemoreceptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Comment on these ABG taken on air:

pH – 7.4 (7.35 - 7.45)
pO2 – 20 kPa (11-13.3kPa)
pCO2 – 5 kPa (4.9-6.1)
HCO3- - 25 mmol/l (22-30)

A

This is impossibe on room air. Must be on O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

21yr. Old man - acutely short of breath

pH  -  7.49 	(7.35 - 7.45)
pO2  -  7.0 kPa     (11-13.3kPa)
pCO2   - 3.0 kPa     (4.9-6.1)
HCO3-  - 24 mmol/l  (22-28)

How do you interpret these blood gases?
How would you treat this patient?

A

Type I respiratory failure, respiratory alkalosis. Treat with high flow Oxygen

Potential causes include acute asthma, PE, COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

73 year old woman admitted with increased confusion:

pH - 7.25 (7.35 - 7.45)
PaO2 - 7.1 kPa (11-13.3kPa)
PaCO2 - 9.2 kPa (4.9-6.1)
HCO3- - 29 mmol/l (22-28)

How do you interpret these blood gases?

A

Respiratory acidosis - Type II resp failure.
Partial metabolic compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

21 year old woman admitted with breathlessness:

pH - 7.15 (7.35 - 7.45)
PaO2 - 14.0 kPa (11-13.3kPa)
PaCO2 - 2.9 kPa (4.9-6.1)
HCO3- - 14 mmol/l (22-28)

How do you interpret these results?
Why is she breathless?

A

Metabolic acidosis with attempted respiratory compensation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the main differences between type I & II respiratory failure?

A

Type I:
- Hypoxic; pCO2 < 6.5kPa
- Increased resp rate leads to fall in CO2
- VQ mismatch

Type II:
- Hypercapnic; pCO2 > 6.5kPa
- Ventilatory failure, insufficient to excrete CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What characterises asthma?

A

Classical symptoms (more than one of wheeze, chest
tightness, breathlessness or cough) and variable airflow obstruction.

Airway hyper-responsiveness and airway inflammation are components of the disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the clinical features of asthma?

A
  • Cough; wheeze; chest tightness; sputum production; dyspnoea; reduction in exercise tolerance
  • Variability, particularly diurnal
    • Throughout day if severe
  • Associated with triggers i.e. exerxise, allergen exposure
  • May see no symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give two specific examples of how asthma can be diagnosed.

A

Spirometry - FEV1 pre & post bronchodilator - Dx if 12% improvement & 200ml vol increase

PEFR - Dx if mean variability >20%, or >15% dirunal variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a challenge test (asthma)

A

Challenge test for bronchial hyper-responsiveness - done if spirometry & peak flow charts normal.

Histamine (or other allergen inducer) challenge. The PC20 is calculated - dose of agent provoking 20% fall in FEV1

If PC20 is <8mg/ml, asthma can be diagnosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the aims for chronic asthma management?

A
  • No daytime symptoms
  • No night-time awakening due to asthma
  • No need for rescue medication
  • No asthma attacks
  • No limitations on activity including exercise
  • Normal lung function (in practical terms FEV1 and/or PEF>80% predicted or best)
  • Minimal side effects from medication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some signs that acute asthma is life-threatening?

A

PaCO2 normal or raised. Altered conscious level, exhaustion, cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How should acute asthma be managed? First things.

A
  • Oxygen to maintain spO2 94%+
  • Bronchodilator (salbutamol, SABA)
  • Ipratropium bromide via nebs
  • Prednisolone tablets
  • No sedatives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

A patient with high blood pressure is prescribed the Ca channel blocker
amlodipine. What best describes how this drug produces a reduction in
blood pressure?

a) Increases parasympathetic activity
b) Increases vasodilatation
c) Reduces blood volume
d) Reduces contractility
e) Reduces heart rate

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What best describes the process increased by stimulation of B1
adrenoceptors to enhance contractility?

a) Action potential duration
b) Ca-ATPase
c) Ca-induced Ca release
d) K channel activity
e) If channel activity

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the main ways in which cardiac output is affected by sympathetic activity? (no mechanisms)

A

HR increase (chronotropic effect)
Contractility increase (inotropic effect)
Venoconstriction (Starling’s law)
TPR increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Outline the chronotropic effect of sympathetic activity on the heart

A

SA node! increases HR.
https://www.notion.so/Physiology-pharmacology-of-ANS-on-heart-blood-vessels-fb242dffd419468fbc58a0c21dec4211#3a96915ef89146d9b98e1a55dec42b23

NA stimulates B1 adrenoceptor to produce cAMP from ATP, which increases activity of the If channel, generating Na influx.

Na influx means more fequent depolarisations can occur, increasing heart rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the main receptors of ANS control in the heart & blood vessels? Parasymp or symp, and their specific locations.

A

M2 (para) & B1 (symp) - SA & AV node
B1 (symp) - ventricles
a1 (symp) - blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What directly maintains blood pressure?

A

Contraction of the left ventricle, resistance of small blood vessels, arterial walls, and volume & viscosity of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give the BP ranges for optimal, normal, high, & grade 1-3 hypertension

A

(Systolic, diastolic)
Optimal = <120, <80
Normal = <130, 85
High = 130-9, 85-9

Grade 1 (mild) = 140-159, 90-99
2 (moderate) = 160-179, 100-9
3 (severe) = >180, >110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do changes in the following affect BP:
SV, TPR, & HR

A

Lowers BP:
Low SV
Slow or very fast HR
Reduced TPR

Raises BP:
High SV
High TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is a normal blood volume, distribution, & circulation capacity.

A

Normal volume - 5-6L
Normal capacity - 25-50L

81% of blood is in veins, 13% in arteries & 6% in capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Control of blood pressure involves which systems?

A

CV, renal, endocrine & sympathetic nervous systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do the kidneys regulate blood pressure?

A

Must retain 99.5% of filtered sodium to maintain BP.
- Proximal tubule Na/H exchanger - 60% absorption
- Ascending loop of Henle - Na-K-2Cl cotransporter - 30%
- DCT - Na-Cl co-transporter - 7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the RAAS? Give an overview.

A

RAAS is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance.

Angiotensinogen -> Angiotensin I (+Renin)
Angiotensin I -> Angiotensin II (+ACE Chymase)

Angiotensin II induces aldosterone release & vasoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is angiotensin II, & its function?

A

Most powerful vasoconstrictor, fomed by action of ACE on angiotensin I.
Also stimulates secretion of aldosterone, resulting in water & Na retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the effects of epinephrine on blood pressure, & how is it released?

A

Released by adrenal medulla in response to sympathetic activity

  • Increases mean arterial pressure
  • Acts on heart - Increases HR & SV
  • Acts on smooth muscle of arterioles & veins to increase TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the main effects of vasopressin? What stimulates its release?

A

Enhances water retention in collectinf duct.

Secretion from Pituitary increased by drop in blood volume and/or
Increase in osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the main effects of ANP? What stimulates its release?

A

Atrial natriuretic peptide - increases salt excretion via kidneys by reducing water reabsorption, relaxes renal arterioles & inhibits Na reabsorption.

Released in response to stimulation pf atrial receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Explain what would happen when blood pressure drops, with regards to baroreceptors.

A

Baroreceptors in aortic arch & carotid sinus detect drop in BP -> afferent signals in the CNS -> SNS activated -> HR, contractility rise & vascular smooth muscle contraction

Heart & pulmonary artery detect drops in volume -> activation of cardiopulmonary receptros -> SNS activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Outline the inotropic effect at myocytes upon B1 adrenoceptor stimulation

A

1) B adrenoceptor (GPCR - Gas) stimulated, which converts ATP to cAMP with adenylate cyclase

2) cAMP causes an increase in PKA, which:
a) stimulates VGCCs -> Ca influx
b) Ca release from SR by acting at RyR
c) further release from SR by CICR

3) Ca binds to troponin, increasing crossbridge formations, INCREASING CONTRACTILITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What controls total peripheral resistance? (ANS)

A
  • A & NA release from adrenal medulla via symp nerves, acting A1 adrenoceptors on VSMCs
  • NA& A also induce venoconstriction, increasing SV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Outline mechanism of A1 adrenoceptor stimulation at vascular smooth muscle cells

A

1) A adrenoceptor (GPCR - Gaq) stimulated, which converts PIP2 to IP3 & DAG using PLC

2) DAG stimulates Na channel, influx causes depolarisation
a) Depolarisation causes Ca influx by VGCC

3) IP3 stimulates Ca release from SR

4) Overall effect of [Ca] increase causes contraction by myosin light chain kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Briefly describe parasympathetic activity on the heart (blood pressure). NT release & effects.

A

Release of ACh from vagus nerve controls CO by acting at M2 receptors

-Decreased freq of pacemaker potentials at SA node
- Decreased conduction through AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe how baroreceptors detect and deal with changes in posture

A

Decreased cardiac output is detected by theshold detectors, which reduces stimulation of afferent fibres. This induces Sympathetic nerves, and inhibits vagus nerve (parasymp). This has the effects of increasing HR via SA node, increasing venoconstriction & TPR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is bioavailability? (Pharm)

A

Bioavailability:which refers to the proportion of the administered dose of a drug that reaches the systemic circulation (unaltered)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is ‘apparent volume of distribution? (Pharm)

A

A mathematical construct that describes the volume of fluid that would be required to contain the drug, if it were at the same concentration as measured in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Routes of administration: what is meant by Buccal, sublingual, subcut, intradermal & intrathecal?

A

Buccal - between gum & cheek
Sublingual - under tongue
Intradermal - in the skin
Subcutaneous - under the skin
Intrathecal - into cerebrospinal fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is meant by drug distribution? (ADME)

A

How drugs are distributed between body compartments, both in terms of the extent to which they penetrate different compartments, and the rate at which this occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does the apparent volume of distribution tell us?

A
  • How well distributed the drug is
  • How the drug is distributed (see table)
  • Calculation of loading dose to obtain a given plasma conc
  • Determines how quickly drugs will be eliminated (high = slow, e.g.concentrated in fat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the functions of the pericardium?

A
  • Restrict excessive movements of the heart
  • Serve as a lubricated contained in which different parts of the heart can contract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Show & describe membrane potential at the pacemaker

A

https://www.notion.so/The-Cardiac-Cycle-87e3ba3911264d9d9e5f628f3d43972a#44d443084a874de2add132e96d6b9916
Resting membrane potential is negative.

0) Depolarisation - VGCCs open, rapid influc of Ca causing rapid depolarisation

3) Repolarisation - VGCCs close, activation of V-gated K channels -> K efflux

4) Repolarisation - membrane repolarises below If threshold (-40mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What best describes the stage in the cardiac cycle that begins with the S1 heart sound?

a) Atrial contraction
b) Diastole
c) Ejection
d) Isovolumetric contraction
e) Ventricular refilling

A

D)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Which best describes the function of A-V node?

a) Coordinates ventricle filling
b) Contains gap junctions
c) Determines contractility
d) Generates pacemaker potentials
e) Speeds up conduction

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Outline the route of conduction through the heart, start to finish.

A

SA node -> atria (via gap junctions) -> AVn -> Bundle of His (L&R bundle branches) -> Purkinje fibres through ventricles, beginning at apex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is meant by isovolumetric contraction?

A

Stage in cardiac cycle when pressure in ventricles > atria, valves open to arteries & ejection begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

List some causes of secondary hypertension

A
  • Coarctation of aorta
  • Renal & renal vascular disease
  • Adrenal disease
    • Cushings
    • Primary hyperaldosteronism
  • Pregnancy
  • Drugs
    • Oral contraceptive pill
    • HRT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are some causes of essential hypertension?

A

High: BMI; alcohol, salt, fat intake

Low: physical activity, fibre, potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the main drug classes used to treat hypertension?

A

A - ACE inhibitors

B - Beta blockers

C - Calcium channel blockers

D - Diuretic (thiazide)

Others:

  • Alpha blockers
  • Angiotensin II receptor blockers (antagonist) (ARBs)
  • Centrally acting (imidazoline I1 receptor antagonist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Outline the NICE guidelines for hypertension management

A

https://www.nice.org.uk/guidance/ng136/resources/visual-summary-pdf-6899919517

  • Under 140/90 = fine, check every 5 years
  • 140/90-179/119 - ABPM/HBPM, investigate for organ damage & assess CVD risk
    • 135/85-149/94
      • > 40 - lifestyle advice & discuss drug treatment
      • <40 - specialist evaluation of 2ndary causes
    • 150/95+ (stage 2)
      • Lifestyle & drug treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What treatment options would be considered in a pt with hypertension & high CVD risk?

A

BP lowering treatments (small doses of multiple Rx)
Cholesterol-lower treatment
‘Healthy heart’ diet
Smoking cessation

70
Q

ACE inhibitors - mechanism & indication?

A

First line against hypertension, in lower risk indivduals. Blocks the conversion of angiotensin I -> II, which is a vasoconstrictor and stimulates aldosterone secretion. Overall, reduces BP

71
Q

Draw out & label the ECG waveform, and what each section represents (basic)

A
  • P wave- atrial depolarisation
  • PR segment- AV node delay
  • QRS complex- ventricular depolarisation (atria repolarising simultaneously)
  • ST segment- time during which ventricles are contracting & emptying
  • T wave- ventricular repolarisation
  • TP interval- time in which ventricles are relaxing & filling
72
Q

Draw out the LV pressure changes. Include valve opening/closing points, aortic, LV & atrium pressure.

A

https://www.notion.so/The-Cardiac-Cycle-87e3ba3911264d9d9e5f628f3d43972a#17b051c51c9d45d18bbfb5a86e809099

73
Q

What causes an increase in jugular venous pressure?

A

Raised pressure in r atrium (e.g. from R-sided HF), less blood is ejected from R ventricle, so higher afterload, atrium pumping against greater pressure.
Venous distension is increased as a result

74
Q

What are the four heart sounds, and what do they represent?

A

S1 “Lub” - closure of tricuspud/mitral valves at beggining of ventricular systole

S2 “dub” - closure of aortic/pulmondary valves at end of ventricular systole

S3 - occasional - turbulent blood flow into ventricles, detected near end of first 1/3 of diastole, especially in older people

S4 - pathological in adults - forceful atrial contracion against a stiff ventricle

75
Q

What values denote respiratory failure, and its’ types?

A

Resp failure exists when paO2 <8kPa

Type I (hypoxic) - pCO2 < 6.5kPa
Type II (hypercapnic) - pCO2 > 6.5kPa

76
Q

What are the different types of hypoxia?

A

Hypoxic hypoxia - low O2 tension
Hypoxaemic hypoxia - low blood content
Circulatory hypoxia - low CO & delivery
Histotoxic hypoxia - poor usage of O2 by tissues (mitochondria)

77
Q

What are some causes of hypoxic hypoxia?

A

Lack of O2 in atmosphere; airway obstruction; hypoventilaion; VQ mismatches (shunt perfusion or alveolar pathology)

78
Q

What are some causes of hypoventilation?

A

Coma, COPD, obesity, neuromuscular diseases, brainstem & C-spine injuries

79
Q

List some causes of VQ mismatch

A

Shunt perfusion
- Pneumonia
- Pul oedema
- Pul fibrosis/ILD
- Airways disease

Deadspace ventilation:
- Pulmonary embolus
- Pneumothorax
- Right to left shunt

80
Q

What are some causes of hypoxaemic hypoxia?

A

Low Hb, abnormal Hb (SS, thal), other substances bound to Hb (CO, methemoglobinaemia)

81
Q

What is circulatory hypoxia? List some causes.

A

Blood content is fine, but cardiac output is low, & delivery inadequate as a result.

Causes:
- Shock states
- Cardiac failure
- L->R shunting
- Can be global or focal

82
Q

What is histotoxic hypoxia, and what are some causes?

A

Inability to use oxygen for tissue metabolism. Causes include sepsis, drugs, and cyanide poisoning

83
Q

What are the principles of treating respiratory failure?

A
  • Correcting hypoxaemia by increasing inspired O2 to maximum
  • Identifying & treating the precipitating cause
  • Instituting respiratory support if necessary
    • Invasive/non-invasive
84
Q

What are the indications for intubation?

A

Inability to protect airway; failure of ventilation; failure of oxygenation; anticipated need for ventilation

85
Q

What, on an ABG, indicates need for ventilatory support?

A

High paCO2

86
Q

A pt in respiratory failure is given O2 and their hypoxia resolves. What is the most likely cause?

A

VQ mismatch

87
Q

Describe the three phases of haemeostasis

A

Primary haemostasis (platelet plug)
- Vasoconstriction (immediate)
- Platelet adhesion (seconds)
- Platelet aggregation & contraction (minutes)

Secondary haemostasis (coagulation)
- Activation of coagulation factors (seconds)
- Formation of fibrin (minutes) to stabilise plug

Fibrinolysis
- Activation of fibrinolysis (minutes)
- Lysis of the plug (hours)

88
Q

Describe the function of endothelium in haemostasis in RESTING state and the mediators involved.

A

Antithrombotic (resting state):

Prostacylin/NO/ADPase - inhibit platelet activation
TPa - modulation of fibrinolysis
TFPi/thrombomodulin/heparin sulfate - inhibition of coagulation

89
Q

Describe the function of endothelium in haemostasis in ACTIVE state and the mediators involved.

A

Prothrombotic (active state)
- Tissue factor - released following endothelial damage
- VW factor - Platelet adhesion & aggregation
- PAi-1 - inhibits fibrinolysis

90
Q

Describe the activation of platelets:
- Platelet activators
- Surface changes

A

Platelet activators: thrombin, TXA2, ADP, collagen

Surface changes - activates glycoprotein IIb-IIIa
- Secretes ATP, ADP & Ca
- Thrombin generation
- Alpha-granule secretion - coagulation factors & proinflammatory factors
- Shape - change spreads out

90
Q

Describe the activation of platelets:
- Platelet activators
- Surface changes

A

Platelet activators: thrombin, TXA2, ADP, collagen

Surface changes - activates glycoprotein IIb-IIIa
- Secretes ATP, ADP & Ca
- Thrombin generation
- Alpha-granule secretion - coagulation factors & proinflammatory factors
- Shape - change spreads out

90
Q

Describe the activation of platelets:
- Platelet activators
- Surface changes

A

Platelet activators: thrombin, TXA2, ADP, collagen

Surface changes - activates glycoprotein IIb-IIIa
- Secretes ATP, ADP & Ca
- Thrombin generation
- Alpha-granule secretion - coagulation factors & proinflammatory factors
- Shape - change spreads out

91
Q

Where are platelets destroyed?

A

RE system in spleen

92
Q

What is Von Willebrand factor & its functions?

A

Glue-like factor required for platelet plug formation.

Serves as a bridge between platelets & injury sites (binds to collagen). Prevents excessive blood loss.
VWf binds to glycoprotein complex IbVIX on platelet surface.

Carries factor VIII which is vital for development of fibrin strands, which strengthen platelet plug.

Also involved in angiogenesis

93
Q

What allows platelet aggregation to occur?

A

GPIIb-IIa - receptor ligand that when becomes active is able to bind ligands (from other platelets)

94
Q

What is Petechiae?

A

Pinpoint, round spots that appear on skin as a result of bleeding from platelet disfunction or thrombocytopenia

95
Q

Outline how a platelet plug is formed

A
  1. VWf binds to collagen on surface of endothelium
  2. VWF binds GPIb on platelet, anchoring to endo-wall. GPIIb-IIIa also activates, linking platelets together
96
Q

What is Glanzmann thrombashenia?

A

Defect in GPIIb/IIIa complex arising from genetic mutations can impair both platelet recruitment & adhesion.

GT is a bleeding disorder caused by dysfunction of GPIIb/IIIa protein. Ability to form effective platelet plug is poor

97
Q

Where are most anticoagulant factors synthesised? List the bodies main ones.

A

Liver. Dysfunction therefore can cause bleeding issues.

TFPI, , APC, antithrombin (IXa, Xa & thrombin)

98
Q

Outline the extrinsic pathway of coagulation

A
  • Damage to the blood vessel means that factor VII exits the circulation into surrounding tissues
  • Tissue factor (factor III) is released by damaged cells outside the circulation
  • Factor VII and factor III/TF form a complex, known as the TF-VIIa complex.
  • TF-VIIa then activates factor X into its active form, factor Xa
  • In conjunction with factor Va, this triggers the formation of thrombin from prothrombin
    • Common pathway next
99
Q

Outline the intrinsic pathway of coagulation

A
  • Factor XIIis activated once it comes into contact with negatively charged collagen on the damaged endothelium, triggering the cascade
  • Along with clotting factors,plateletsform a cellular ‘plug’ at the site of injury. These platelets also release mediators thatfaciliatate further clotting, including Factor VIII.
  • Factor IX combines with Factor VIII to form an enzyme complex that activates factor X, which along with factor Va, stimulates the production of thrombin
100
Q

Outline the common pathway of coagulation

A
  • activated factor X causes a set of reactions resulting in the inactive enzyme prothrombin (also called factor II) being converted to its active form thrombin (factor IIa) by Prothrombinase.
  • The thrombin then converts soluble fibrinogen (also refereed to as factor I) into insoluble fibrin strands. The fibrin strands which comprise the clot are stabilised by factor XIII.
101
Q

Outline the process of fibrinolysis

A
  • The endothelial cells of the blood vessel wall secrete tissue plasminogen activators (tPAs) which convert the precursor plasminogen into plasmin.
    • Plasmin subsequently cleaves the fibrin within the thrombus, leading to its degradation
      • Including d-dimer
    • Fibrin degradation products (FDPs) are generated if non-cross linked fibrin or fibrinogen is broken down
102
Q

What are some signs of clotting disorders?

A

Ecchymosis (easy bruising) - increased fibrinolytic factors & decreased coagulation

Haemarthrosis - deformed joints, hallmark of haemophilia

103
Q

What is PT?

A

Prothrombin time - sensitive to factor VII (short half life) in extrinsic pathway.

Driven by tissue factor - stimulates clotting pathway, time taken measured

104
Q

What is APTT?

A

Activated partial thromboplastin time. Sensitive to intrinsic pathway. Contact activated. Main conditions resulting in abnormal APTT include haemophilias & VWf disease

105
Q

What is TT?

A

Thrombin time - sensitive to defects in conversion of fibrinogen to fibrin (common pathway)

106
Q

What are the three main indications of anticoagulants?

A

Stroke prevention (70%)
VTE treatment & prophylaxis (20%)
Arterial thrombotic disease (10%)

107
Q

What is the mechanism of action of heparin?

A

Binds to & activates antithrombin, which inhibits factor Xa & thrombin

108
Q

List some DOACs

A

Direct Xa inhibitors - Rivaroxaban, apixaban, fondaparinux

Thrombin inhibitor - dabigatran

109
Q

List the main clinical differences between unfractionated heparin & low molecular weight heparin

A

UFH - half life 1.5 hours (so must give more often). APTT ratio must be done to monitor anticoagulant. IV infusion.

LMWH - Half life 12 hours, no monitoring requied & more stable bioavailability. Renal clearance. No full reversal agent (Is for UFH)

110
Q

What is the mechanism of Warfarin?

A

Blocks recycling of vitamin K by inhibiting vitamin-k-epoxide reductase

Vitamin K is required for carboxylating proteins to become active: Factors VII, IX, X & II, and proteins C&S

111
Q

Describe the initial procoagulative effect of warfarin

A

Anticoagulative factors affected (protein C&S) have a shorter half life than some of the other factors, so initially heparin is used alongside to ensure anticoagulant effect

112
Q

Describe the pharmacokinetics of warfarin

A

Good bioavailability - rapidly absorbed, oral.
Half life 36-42 hours. Once stabilised, monitoring required every few weeks (& initially)
Eliminated by the liver.
Dose varies widely between individuals - sensitive to diet, other drugs, ethnicity, and age

113
Q

What is INR?

A

International normalised ratio.

Prothrombin time ratio, corrected by international sensitivity index (ISI). Higher INR = higher risk of bleeding.
Usually want ~ 2 (2x as long to clot)

114
Q

How is Warfarin reversed, and why would this be done?

A

Reversal needed due to major bleed.

Vitamin K Koniakon, prothrombin complex concentrate.
Fresh frozen plasma, & Omit further anticoagulation

115
Q

What are some side effects & contraindications of Warfarin?

A
  • Bleeding (RFs >70yo, INR >4.9, first 3/12 of Rx, comorbid disease)
  • Skin necrosis due to protein C deficiency (if not given alongside heparin)

Contraindication:
- Pregnancy - passes placenta, can cause bleeding in baby

116
Q

What are some advantages of DOACs?

A

Oral, rapid onset/offset of action.
Little to no food or drug interactions.
Predictable anticoagulant effect, so no routine monitoring required.

117
Q

What are some considerations and contraindications of DOACs?

A

Contraindication - obesity >40BMI or >120kg

Hair loss is a common side effect, and has renal excretion

118
Q

PE - Describe the changes that occur to the R side of the heart

A

1) Raised pulmonary pressure (acute cor pulmonale) ->

2) increased pressure in right ventricle at end-diastole, which dilates & leads to tricuspid incompetence.

3) This causes increased atrial pressure which leads to elevated JVP

119
Q

PE - Describe the changes that occur to the L side of the heart

A

Due to the raised pulmonary artery pressure, there is less blood getting to the left atrium from the RV via the lungs

  • This leads to a **reduced LV stroke volume & tachycardia
  • If the RV pressure is very high, the interventricular septum may impinge on the LV cavity leading to further compromise on LV function
120
Q

What are the potential causes of a third heart sound?

A

reverberation of blood rapidly filling the ventricles from the atria (volume overload) or increased transvalvular flow (tricuspid regurgitation)

121
Q

What changes can be seen in a PE ECG?

A

Often no change. Sinus tachycardia common.

Sometimes SI QIII TIII
Lead I - deep S wave
Lead III - pathological Q wave & T wave inversion

122
Q

What are the main causes of VTE?

A

Virchow’s triad
1) Reduced rate of blood flow
- Immobility, HF

2)Increased coagulability of blood
- Severe injury, cancer treatment, pregnancy, COCP, HRT, dhydration, hereditary thrombophilias

3) Damage to venous endothelium
- Trauma. obesity

122
Q

What are the glucose requirements for a near-term foetus?

A

~5g glucose/kg/day

122
Q

List the actions of insulin in an adult and foetus

A

In adults:
- Increased glucose uptake in muscle, fat & liver
- Decreased lipolysis, glucogenogenesis, & ketogenesis

In foetus insulin acts as a growth factor & increases adipose tissue stores

123
Q

What are catecholamines?

A

Hormones made by your adrenal glands. Released into the body in response to physical or emotional stress. The main types of catecholamines are dopamine, norepinephrine, and epinephrine

124
Q

At birth, what induces the start of catabolic processes?

A

Catabolic processes here are gluconeogenesis & glycogenolysis.

Abrupt cessation of transplacental flow of nutrients, and stress from birth induces huge surge in catacholamines, which switch on the mentioned processes

125
Q

Where do babies get their energy from in the 24 hours after birth, and why?

A

Newborns must initially meet metabolic demands from body stores. (gluconeogenesis, lipolysis & beta oxidation)

This is because the average intake of colostrum is only ~7mls per feed in first 24 hours.

126
Q

How do babies protect themselves from hypoglycaemia?

A

Management of supplies:
- Astrocyte glycogen stores
- Use of alternative cerebral fuels - ketone bodies

Managing demand:
- Brain is highest proportion of resting energy expenditure, but CMR is only 30% of adult value

127
Q

What are the main issues/considerations of a preterm/IUGR baby in terms of nutritional requirements?

A
  • High demands - especially brain
  • Small nutrient stores
  • Immature metabolism
  • Establishment of enteral feeding delayed (preterm)
  • Poor fat absorption (preterm)
128
Q

What is congenital hyperinsulinism? What effects does this have?

A

Diabetic mother with high maternal glucose -> high foetal glucose.

This causes fetal & neonatal hyperinsulinism.
Neonatal macrosomia & hypoglycaemia are common effects of this.
(macrosomia = larger than 4.45kg baby)

129
Q

List some causes of neonatal hypoglycaemia (inborn errors of metabolism)

A

Glycogen storage disease (type I)
MCADD (medium acetyle-CoA dehydrogenase deficiency)
Galactosaemia
Maple syrup urine disease

130
Q

What is glycogen storage disease (type I) in neonates, and what are the effects of this?

A
  • Deficiency of glucose-6-phosphatase (needed for conversion of G6P to glucose)
  • Hypoglycaemia & lactic acidosis in newborn
  • Hepatomegaly in older child
131
Q

What is MCADD?

A

Medium chain acetyl CoA dehydrogenase deficiency.

A disorder where the body is unable to break down medium chain fatty acids into acetyl-CoA (see beta oxidation of fatty acids)
- This means reduced ability to tolerate fasts
- Also part of newborn blood spot screening

132
Q

What is galactosaemia? (neonates)

A
  • Lactose in milk is broken down into glucose or galactose
  • Galactose is then converted into glucose
  • Absence of any key enzymes causes the disease
    • Usually GALT
133
Q

What is maple syrup urine disease (neonates)? What is the presentation?

A
  • Inability to metabolise branched chain amino acids
    • Leucine, isoleucine, valine
  • Leads to build up of these amino acids & their byproducts
  • Part of newborn blood spot screening
  • Presents with hypoglycaemia & acidosis within first few days of life
134
Q

What two main things affect O2 & CO2 requirements?

A

Physical activity - affects O2 demand & CO2 production

Infection, injury, or metabolic dysfunction - increases oxygen consumption

135
Q

How is breathing initiated? (neurogenic)

A

Breathing is initiated byneural activation of respiratory muscles, which provide the movement required for ventilation

  • Respiratory muscles consist of skeletal muscle, so they require neural inputs/stimulation to contract
  • Innervation from motor neurons synapsing from descending spinal tracts provide the contractile signal.
136
Q

List the muscles/mechanisms used in inspiration & expiration. Divide into quiet breathing, & increased ventilation.

Divide increased ventilation into respiratory & accessory muscles

A

INSPIRATION
Quiet - diaphragm
Respiratory (+vent) - external intercostals
Accessory - pectorals, sternomastoid & scalene

EXPIRATION
Quiet - elastic recoil
Respiratory (+) - elastic recoi & internal intercostals
Accessory - abdominals

137
Q

What are the key cell groups in the respiratory centre of the brainstem? What does each control?

A

PRG (pontine respiratory group) - higher control

DRG (dorsal resp group) - inspiratory output

VRG - (ventral resp group) - expiratory output

138
Q

How do central respiratory chemoreceptors (CRCs) work?

A

Predominant over peripheral chemoceptors, CRCs detect pH within cerebrospinal fluid as a way of indirectly monitoring arterial CO2 (H+ cannot cross blood-brain barrier due to being polar).

  1. CO2 diffuses from arterial blood across blood brain barrier into CSF
  2. Reacts with water in spinal fluid:
  3. Produces carbonic acid & hydrogen ions
  4. Activates CRCs
  5. Stimulates ventilation increase
139
Q

Describe the changes to ventilation that occur during sleep.

A

Lower metabolic rate = ↓respiratory demands
- Postural changes alter mechanics of breathing
- ↓SNS & ↑PNS tone = ↓HR, BP & CO.
- ↓tidal volume, ↓breathing frequency, ↓minute volume ↓SaO2 (≈96%), ↑PaCO2 (≈7kPa)
- ↓upper airway calibre

140
Q

What is central sleep apnoea? What characterises it, and how is it investigated?

A

Temporarycessation of breathing during sleep caused by dysfunction of the processes that initiates breathing.

Characterised by >5 episodes per hour lasting >10 seconds. Durations of apnoeas may be as long as 90 seconds and the frequency of episodes as high as 160 per hour. Investigated by polysomnography.

141
Q

What are some causes and effects on health of central sleep apnoea?

A

Health: tiredness (poor sleep quality), CV complications (stress & +SNS tone), metabolic dysfunction.

Causes: stroke, drugs (e.g. opioids), central hypoventilation syndrome (Ondines curse), neonates, altitude

142
Q

Describe the mechanism of Cheyne stokes respiration

A

Hypercapnia & hypoxaemia caused by altitude, HF, cardiorespiratory dysfunction.

Compensatory hyperventilation leads to hypocapnia & alkalosis, DECREASING respiratory drive, compensatory hypOventilation. This increases hypercapnia & hypoxaemia further - positive feedback

143
Q

What are the vitamin K-depenant clotting factors?

A

1972!

10, 9, 7 & 2

144
Q

What are the four types of MI that can occur?

A

Type I - plaque rupture event causing reduced coronary artery flow resulting in ischaemia

Type II - Imbalance between demand & supply (Common in sepsis)

Type III - Pts who suffer cardiac death, die before blood samples or biomarkers can be obtained etc

Type IV - in operations

145
Q

What are the RFs for CHD?

A

Non-modifiable - age, gender, genes, ethnicity

Modifiable - High BP, smoking, DM, physical inactivity, obesity, high blood cholesterol

146
Q

Describe stable vs unstable angina

A

Stable - in early stages (of CHD) will hear of predictable pain on exertion
- Rest helps - shouldn’t persist for longer than 20 mins
- At this stage, modifying risk factors is treatment

Unstable - chest pain occurs randomly, inc at rest. Isn’t resloved by resting for 20m.
Now considered ACS & risk of mortality is higher (than stable)

147
Q

Describe the difference between angina and non-cardiac chest pain

A

Angina - squeezing chest, heaviness, pressure, burning, tightness. 3-15m
Radiation to shoulder, neck, jaw

Non-cardiac - pleuritic, sharp, knife like, choking. Positional. Random onset & duration

148
Q

STEMI indicates an MI has occured. STEMI in which leads = where on heart was the MI?

A

Lateral (circumflex & diagonal)- I, aVL, V5-6

Anterior (LAD) - V1-V4

Inferior - II, III & aVF

149
Q

STEMI - What are the immediate actions that should be taken?

A

Monitoring & defib
IV access & blood tests
O2 as required

Analgesia (morphine with anti-emetic)
Antiplatelet therapy (aspirin & ticragrelor)

Reperfusion (potentially)

150
Q

What is the mechanism of action for aspirin?

A

Aspirin is an NSAID, which Irreversiby inhibit COX

COX leads to formation of PGs which cause inflammation, swelling, pain & fever

Also required to make precursor of thromboxane in platelets - for platelet aggregation

151
Q

When is surgical intervention appropriate for a STEMI? What is the alternative?

A

If presenting within 12h of symptoms & PCI can be done within <2h. CABG if this fails

If cannot give PCI, do fibrinolysis

152
Q

What is given for post-MI medical therapy?

A

B-blockers
ACE inhibitors
Statins
Dual antiplatelet therapy

153
Q

What is troponin, and its types? When would it rise & fall following an MI?

A

Protein released from myocytes when irreversible damage occurs.

Troponin I is more specific to cardiac than toponin T (non-CV death)

Level depends on severity & size of infarct (good indicator of prognosis)

Doesnt rise above normal in first 6 hours, peaks 24-48h & normal after ~1 week

154
Q

What is CK-MB used for in MIs?

A

As a marker of repeat MIs, as peaks at 1 & normalises after 2-3 days

Tn can stay high for 1 week plus

155
Q

What is myoglobin used for in MIs?

A

Only as early indicator as rises after 1h but normalises after a day

156
Q

How is stable angina managed?

A

GTN spray
Long term - Beta blockers & calcium channel blockers
Secondary prevention - aspirin, ACE-i

157
Q

How is an NSTEMI managed?

A

Stabilise pt & ruptured plaque first, consider reperfusion later.

BATMAN
(BBs, aspirin, ticagrelor, morphine, ACE-i, Nitrates)

For reperfusion:
Risk stratification - grace score

If unstable (ongoing chest pain) may need urgent revascularisation (PCI)

158
Q

What lifestyle advice would you give to someone who has just suffered from an MI?

A

Alcohol (-)
Phys activity (30m/day to breathlessness)
Smoking cessation
Weight management

(Maybe only primary) cholesterol reduction

159
Q

Describe the histological effects on cardiac tissue up to a month following an MI.

A

0-24h - cell death & neutrophil recruitment -> lyse dead cells

1-3d - immune response continues breaking cells down

3-14d - macrophages phagocytose debris, granulation tissue begins to form, myocardium fragile

14d-1month - scar tissue, leaving myocardium akinetic

160
Q

What are the short term complications of an MI?

A

Arrhytmias, muscle rupture, mural thrombus, acute pericarditis

161
Q

What are the long term complications of an MI?

A

HF, recurrent MI, ventricular aneurysm, Dresslers syndrome (secondary pericarditis)

162
Q

MI risk factors - what specific age, genders and ethnicity indicate higher risk?

A

Gender - men (>45)
Family history of early CHD (<55-60)

CHD - S Asian
Hypertention & stroke - African-Caribbean

163
Q

What is familial hypercholesterolaemia? How is it diagnosed?

A

Inherited disease, mutations in 3 genes inc LDLR. Affects 1 in 250-500

Increases CHD risk by 50% (age 50 males)

Diagnosis - Total chol >7.5; LDL >4.9 & family history of premature CHD

164
Q

How do statins work? What are some alternatives, and their effectiveness?

A

Inhibits cholesterol synthesis in liver (by blocking HMG coA reductase) - 40-60% reduction in LDL-C

Ezetimibe blocks cholesterol absorption in bowel - 15-20% reduction LDL-C

Praulent - stimulates PCSK9 to degranulate LDLR - ?60% reduction

165
Q

How is risk of CHD determined?

A

QRISK - gives 10y risk
if >10% mortality chance, statins are prescribed

166
Q

What are the main principles of secondary CHD management?

A

Lower BP & cholesterol (primary prevention too)

Lifestyle:
Cigarette smoking cessation
Dietary change (Red. sat fat, kcal & salt, mediter. diet)
Increase physical activity

Medications:
Statins, Beta blockers, ACEis & antiplatelet (e.g. aspirin)

167
Q

What are the main causes of CHD?

A

High blood cholesterol (LDL particularly)
High BP (weakens arteries)
Cigarette smoking
Diabetes
Obesity

168
Q

Why does high LDL lead to CVD complications?

A

Plaques are laden with cholesterol - LDL is the form of chol that transports fat to peripheral tissues

HDL however carries fat to liver for breakdown

M4 Y1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions