Cardiovascular Flashcards

(56 cards)

1
Q

Enzyme that statins inhibit?

A

HMG Co A reductase

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2
Q

Changes to the ECG in an exercise street test when the patient has angina?

A

ST segment depression

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3
Q

What do you do if a GP diagnoses a patient with unstable angina

A

Send to A&E it is a medical emergency (acute coronary syndrome)

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4
Q

Main difference in STEMI and NSTEMI?

A

STEMI - lumen is completely blocked

NSTEMI - the lumen is partially blocked

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5
Q

Treatments for STEMI and NSTEMI?

A

STEMI - Thrombolysis or PCI

NSTEMI - no thrombolysis but PCI could be useful

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6
Q

Features of cardiac pain?

A

Triggered by exercise and relieved at rest

Heavy, pressing or tight

Breathless, nausea

Radiates to arms

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7
Q

In a normal ECG are leads I, II and III positive or negative?

A

Leads I, II and III should be positive

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8
Q

What interval on an ECG do you use to assess heart rate?

A

RR interval

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9
Q

Possible causes of chest pain?

A
MI
Angina
GORD
Aortic Dissection
PE
Pericarditis
Musculoskeletal costochondritis
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10
Q

Types of heart block?

A

1st degree - enlarged PR interval

2nd degree:

Mobitz type I - PR interval gradually enlarges then skips a beat

Mobitz type II - Intermittent non-conducting p waves, some do some don’t

3rd degree - bundle branch block, no communication between SAN and AVN at all, random p waves

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11
Q

Signs of ventricular tachycardia?

A

Widened QRS

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12
Q

What is the ECG sign in ischaemia and in a previous infarction?

A

Ischaemia - ST elevation

Infarction - ST depression

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13
Q

What is a vulnerable plaque?

A

A plaque with a large risk of rupture

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14
Q

Initial pharmacological treatment for a STEMI?

A

Aspirin, Clopidogrel, B-blocker, atorvastatin, LMW heparin, ACE inhibitor

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15
Q

Other treatment for STEMI?

A

PCI

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16
Q

What is classified as an acute coronary syndrome?

A

STEMI, NSTEMI, unstable angina

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17
Q

Three physiological buffers, which has the biggest buffering capabilities?

A

Bicarbonate (is regulated to produce acid-base changes)

Proteins (mostly haemoglobin) carry a negative charge and will accept H+, has the most capacity but is not regulated

Phosphate buffer

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18
Q

What enzyme catalyses the reaction forming carbonic acid and bicarbonate?

A

Carbonic anhydrase

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19
Q

Where is bicarbonate formed, how?

A

In the red blood cell, the reaction is catalysed by carbonic acid, CO2 reacts with O2 to form H2CO3, which bissociates to form bicarbonate (HCO3) and H+ (which is buffered by haemoglobin).

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20
Q

How is acid secreted?

A

CO2 is blown off in the lungs and metabolic acids are excreted in the kidney

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21
Q

What primarily drives the impulse to breathe?

A

Acid/base balance driven by CO2 in the medulla

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22
Q

What substances are detected in the peripheral and in the central chemoreceptors?

A

Central - CO2

Peripheral - H+

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23
Q

What’s the Haldane effect?

A

The fact that during the passage of blood through the lungs O2 is taken up by red blood cells (makes them a stronger acid) This promotes the excretion of CO2

24
Q

What two measurements of blood gas data show metabolic acidosis/alkalosis and what two show respiratory acidosis/alkalosis

A

Respiratory - High CO2 suggests respiratory acidosis

Metabolic - negative BXS suggests metabolic acidosis

25
Causes of metabolic acidosis?
Uraemia/renal disease Lactic acidosis Ketoacidosis Poisoning Diarrhoea
26
What is the Base excess?
The amount of bicarbonate that must be added to the blood to return it to standard pH - so therefore indicates that the bicarbonate concentration is above or below the amount expected
27
What is standard bicarbonate?
the plasma bicarbonate concentration at a paCo2 of 5.3 (by pumping 5.3 pco2 through a blood sample) and full O2 sats
28
Three layers of the vascular endothelium?
Tunica intima (inner) Tunica media Tunica adventitia
29
Some roles of the vascular endothelium?
Interface between blood body tissues Control of blood coagulation Mediates inflammatory response Regulates vascular tone
30
Two key endothelial factors?
NO Endothelins
31
Three types of NO synthase and where they are located, and whether they are constituently produced?
eNOS - endothelium (constituently) nNOS - neurones (constituently) iNOS - smooth muscle + macrophages (cytokine activated)
32
Action of NO?
Vasodilator anti-thrombogenic/anti-atherogenic Inhibits: cell growth, cell adhesion, platelet aggregation
33
How does NO reduce blood pressure?
Increase veno/vaso-dilatation (less preload) Increasing Na+ and H2O excretion in the kidney (less blood volume) Decreasing vascular remodelling
34
What happens when superoxide ions (O2-) react with NO, what causes superoxide anions to be formed?
Forms peroxinitrite (ONOO-) This stops NO's vasodilatory properties Smoking forms superoxide anions
35
Two main drugs that act in the NO pathway?
Nitrates - e.g. GTN, acts as NO Phosphodiesterase inhibitors (type V) e.g. sildenafil, Prevents the breakdoen of cGMP
36
Endothelin production pathway?
Stimulation of endothelin gene preproendothelin proendothelin endothelins - by endothelin converting enzyme
37
The two endothelin receptors and their actions?
ETa - mediates vasoconstriction ATb - mediates vasodilatation via NO
38
Actions of endothelin?
Vasoconstriction through ET receptors Constriction of renal afferent arteriole Prothrombogenic Mitotic (promotes cell growth)
39
Role of enothelins in the kidney?
Decrease GFR (constriction of afferent arteriole) Natriuresis: - decrease proximal tube reabsorption - inhibition of aldosterone - promotes synthesis of ANP and BNP Diuresis: - opposes ADH action
40
What can ET antagonists be used for?
Pulmonary hypertension
41
Definitions of compliance, concordance and adherence?
Compliance: degree to which the patient obeys instructions of doctor Concordance: Patient and doctor working together towards treatment aims Adherence: The extent to which the patients behaviour corresponds to the AGREED recommendations of the doctor
42
What's self-efficacy?
Personal confidence in ability to successfully perform a behaviour
43
What's creative/intelligent non-adherance?
Deliberate decisions to stop/change treatments taken
44
What is blood pressure determined by?
CO (cardiac output) Total peripheral resistance (TPR) CO x TPR
45
Factors determining Cardiac Output?
Contractility, Afterload and Heart rate
46
Factors determining Peripheral resistance?
Vagal tone, Viscosity, Vessel length
47
Two types of fibre that respond to stretch of arteries in carotid body and aortic arch (baroreceptors)? What will firing of the fibres then increase and decrease?
A fibres, C fibres PNS output will increase SNS output will decrease
48
What is the definition of hypertension?
Rise in BP without an increase in CO
49
Two categories of hypertension?
Primary - 95% Secondary - 5%
50
What are some causes of secondary hypertension?
Renal hypertension: issues with the RAAS pathway Endocrine tumour Pre-acclampsia in pregnancy
51
Common environmental causes of essential hypertension?
High salt intake Obesity, high calorie diet High alcohol intake
52
Normal osmotic pressure?
290 mosmol/l
53
Two types of fluids to give to patients?
Crystalloids - salt/glucose and water Colloids - suspesion (water and protein) and salts
54
What fluid space do colloids and crystalloids stay in?
Crystalloids - to the interstitial colloids - the intravascular (vascular system) due to proteins
55
Valves of the heart?
Tricuspid (left AV valve) Pulmonary Bicuspid (mitral valve) Aortic valve
56
Warfarin mechanism of action?
Vit. K inhibitor