Cardiovascular Flashcards

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
Q

Causes of metabolic acidosis?

A

Uraemia/renal disease

Lactic acidosis

Ketoacidosis

Poisoning

Diarrhoea

26
Q

What is the Base excess?

A

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
Q

What is standard bicarbonate?

A

the plasma bicarbonate concentration at a paCo2 of 5.3 (by pumping 5.3 pco2 through a blood sample) and full O2 sats

28
Q

Three layers of the vascular endothelium?

A

Tunica intima (inner)

Tunica media

Tunica adventitia

29
Q

Some roles of the vascular endothelium?

A

Interface between blood body tissues

Control of blood coagulation

Mediates inflammatory response

Regulates vascular tone

30
Q

Two key endothelial factors?

A

NO

Endothelins

31
Q

Three types of NO synthase and where they are located, and whether they are constituently produced?

A

eNOS - endothelium (constituently)

nNOS - neurones (constituently)

iNOS - smooth muscle + macrophages (cytokine activated)

32
Q

Action of NO?

A

Vasodilator

anti-thrombogenic/anti-atherogenic

Inhibits: cell growth, cell adhesion, platelet aggregation

33
Q

How does NO reduce blood pressure?

A

Increase veno/vaso-dilatation (less preload)

Increasing Na+ and H2O excretion in the kidney (less blood volume)

Decreasing vascular remodelling

34
Q

What happens when superoxide ions (O2-) react with NO, what causes superoxide anions to be formed?

A

Forms peroxinitrite (ONOO-)

This stops NO’s vasodilatory properties

Smoking forms superoxide anions

35
Q

Two main drugs that act in the NO pathway?

A

Nitrates - e.g. GTN, acts as NO

Phosphodiesterase inhibitors (type V) e.g. sildenafil, Prevents the breakdoen of cGMP

36
Q

Endothelin production pathway?

A

Stimulation of endothelin gene

preproendothelin

proendothelin

endothelins - by endothelin converting enzyme

37
Q

The two endothelin receptors and their actions?

A

ETa - mediates vasoconstriction

ATb - mediates vasodilatation via NO

38
Q

Actions of endothelin?

A

Vasoconstriction through ET receptors

Constriction of renal afferent arteriole

Prothrombogenic

Mitotic (promotes cell growth)

39
Q

Role of enothelins in the kidney?

A

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
Q

What can ET antagonists be used for?

A

Pulmonary hypertension

41
Q

Definitions of compliance, concordance and adherence?

A

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
Q

What’s self-efficacy?

A

Personal confidence in ability to successfully perform a behaviour

43
Q

What’s creative/intelligent non-adherance?

A

Deliberate decisions to stop/change treatments taken

44
Q

What is blood pressure determined by?

A

CO (cardiac output)

Total peripheral resistance (TPR)

CO x TPR

45
Q

Factors determining Cardiac Output?

A

Contractility, Afterload and Heart rate

46
Q

Factors determining Peripheral resistance?

A

Vagal tone, Viscosity, Vessel length

47
Q

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

A fibres, C fibres

PNS output will increase

SNS output will decrease

48
Q

What is the definition of hypertension?

A

Rise in BP without an increase in CO

49
Q

Two categories of hypertension?

A

Primary - 95%

Secondary - 5%

50
Q

What are some causes of secondary hypertension?

A

Renal hypertension: issues with the RAAS pathway

Endocrine tumour

Pre-acclampsia in pregnancy

51
Q

Common environmental causes of essential hypertension?

A

High salt intake

Obesity, high calorie diet

High alcohol intake

52
Q

Normal osmotic pressure?

A

290 mosmol/l

53
Q

Two types of fluids to give to patients?

A

Crystalloids - salt/glucose and water

Colloids - suspesion (water and protein) and salts

54
Q

What fluid space do colloids and crystalloids stay in?

A

Crystalloids - to the interstitial

colloids - the intravascular (vascular system) due to proteins

55
Q

Valves of the heart?

A

Tricuspid (left AV valve)

Pulmonary

Bicuspid (mitral valve)

Aortic valve

56
Q

Warfarin mechanism of action?

A

Vit. K inhibitor