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resit part 2c > cardiovascular intro > Flashcards

cardiovascular intro Flashcards

1
Q

what are the risk factors of CVD?

modifiable and non-modifiable?

A

modifiable:

High blood pressure (hypertension)
Physical inactivity
Smoking
Diet and weight
Diabetes
Cholesterol
Stress(?)

non-modifiable
Age/Sex
Family history
Race/ethnic background

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2
Q

what are non-pharmacological preventions of CVD?

A

Prevention is better than treatment!

Regular exercise
Recommended 30 min moderate exercise 5 days per week

Well balanced diet
E.g. the eat well plate, 5-a-day etc

Other lifestyle choices e.g.
Give up smoking
Moderate alcohol
Sleep

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3
Q

what are the risk assessments which takes place for CVD

A

Should be assessed + reviewed on an ongoing basis after age 40

If estimate a 10 year risk factor >10% full formal risk assessment should be considered
For formal risk assessment use a standardised risk tool e.g. Qrisk2 not all risk tools are appropriate for all patients

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4
Q

what are the types of cardiovascular diseases?

A

Cardiovascular disease is caused by disorders of the heart and blood vessels

Coronary Heart Disease (CHD) - disease of the blood vessels supplying the heart muscle

Cerebrovascular disease - disease of the blood vessels supplying the brain

Peripheral arterial disease - disease of blood vessels supplying the arms and legs

Rheumatic heart disease damage to the heart muscle and heart valves from rheumatic fever, caused by streptococcal bacteria

Congenital heart disease malformations of heart structure existing at birth

Deep vein thrombosis and pulmonary embolism- blood clots in the leg veins, which can dislodge and move to the heart and lungs.

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5
Q

what is coronary heart disease?

A

Coronary Heart Disease (CHD) - disease of the blood vessels supplying the heart muscle

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6
Q

what is Cerebrovascular disease

A

Cerebrovascular disease - disease of the blood vessels supplying the brain

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7
Q

what is Peripheral arterial disease

A

Peripheral arterial disease - disease of blood vessels supplying the arms and legs

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8
Q

what is Rheumatic heart disease

A

Rheumatic heart disease damage to the heart muscle and heart valves from rheumatic fever, caused by streptococcal bacteria

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9
Q

what is Congenital heart disease

A

Congenital heart disease malformations of heart structure existing at birth

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10
Q

what is Deep vein thrombosis and pulmonary embolism-

A

Deep vein thrombosis and pulmonary embolism- blood clots in the leg veins, which can dislodge and move to the heart and lungs.

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11
Q

how does a healthy heart work?

A
  • deoxygenated blood enters via the vena cava into the right atrium
  • passes through tricuspid valves into the right ventricle
  • pumped through pulmonary valve to the pulmonary artery
  • it takes deoxygenated blood to the lungs
  • the oxygenated blood enters via the pulmonary vein
  • into the left atrium through the mitral valve into the left ventricle
  • which pumps through the aortic valve into the aorta
  • into the body
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12
Q

what are the three types of blood vessles?

A
  • artery
  • vein
  • capillary
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13
Q

what are the differences between the three blood vessles

A 
ARTERY              VEIN.              
- lumen              - lumen 
-medial layer consisting
of smooth muscle cells 
-covered by adventitia
(connecting tissues and 
nerves) 
-Thicker            -Thinner 
walls                   walls 
-h Pressure      -low 
systems            pressure

capillary

  • single layer of endothelial cells
  • nucleus of endothelial cells
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14
Q

Age and progression of vascular disease

A

Plaque tends to grow with HBP and cholesterol
it can increase with age aswell
plaque restricts the blood flow to the heart/organs

Healthy - Normal
Fatty streak -Normal
plaque -High blood pressure and cholesterol
obstructive plaque with core - chest pain + above
ruptured plaque -angiogram/abnormal ECG - heart attack + above
thrombus - heart attack + above

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15
Q

what is hypertension

A

high blood pressure

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16
Q

what is primary hypertension?
causes
risk factor

A

Primary (essential) Hypertension 90-95%
Classed as an “asymptomatic” syndrome
High blood pressure with no apparent individual cause
Recent evidence suggest inflammatory/immune responses may be involved*

risk factors similar to those for CV disease N.B.:
Age
(35-50 in men; following menopause in women)
Race
1 in 3 African/Caribbean’s

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17
Q

what are the causes of secondary hypertension?

A

Secondary hypertension
Adrenal gland disorders

Cushing’s syndrome (see PM3A-inflammation), hyperaldosteronism (Chronn’s syndrome), pheochromocytoma (rare tumour)

Kidney diseases
polycystic kidney disease, kidney tumor, kidney failure

Drugs
anti-inflammatory corticosteroids (e.g. prednisone);
birth control pills (esp. containing estrogen);
cold medicines (e.g. containing pseudoephedrine, phenylephrine)

Pregnancy

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18
Q

what is clinical BP?

A

in a clinical setting (for example, an outpatient clinic), blood pressure is measured by the auscultation method using a mercury or aneroid sphygmomanometer, or using an automatic sphygmomanometer that has been calibrated by the auscultation method, and maintaining the arm-cuff position at the heart level.

19
Q

what is ABPM?

A

Ambulatory monitoring of blood pressure (AMBP) is a non-invasive exam (i.e., it does not require opening the patient) that records blood pressure over a period of 24 hours

20
Q

what is HBPM?

A

The main difference between ABPM and HBPM is that ABPM assesses daytime and nighttime blood pressure during routine daily activities typically during one 24-hour period, whereas HBPM assesses blood pressure at specific times during the day and night over a longer period of time while the patient is seated and resting.

21
Q

what is the normal BP?

A

<120/80
The 1st value is Systolic BP
The 2nd is Diastolic BP

22
Q

what is the clinical BP?

A

Hypertension is defined as a clinic BP >140/90

23
Q

explain the classification of hypertension

A

(clinical) under 140/90 - check BP at least every 5 years
(ABPM + HBPM)- under 135/85

140/90 - 179/119 - offer ABPM/HBPM

  • investigate for target organ damage
  • assess cardiovascular risk

180/120 +
assess organ damage ASAP
consider drug treatment without ABPM/ HBPM is there is a target organ damage
repeat clinical BP in 7 days if there is no target organ damage
refer to same day specialist review - if there is any life threatening symptoms, or hemorrhage

24
Q

what is hypertensions treatment strategy ( NICE guideline)

A

HYPERTENSION WITH TYPE 2 DIABETIES + AGEE <55 AND NOT BLACK AFRICAN OR AFRICAN CARABEIAN FAMILY WITHOUT DIABETIES TYPE 2

1) ACEi or ARB
2) ACEi or ARB and CCB or thiazide like diruetics
3) ACEi or ARB + CCB + thiazide like diruetics
4) seek experts advice

HYPERTENSION WITHOUT TYPE 2 DIABETES , AGE 55 OR OVER , BLACK AFRICAN OR AFRICAN CARABIEAN FAMILY ORIGIN

1) CCB
2) CCB and ACEi or ARB or thiazide like diruetics
3) ACEi or ARB + CCB + thiazide like diruetics
4) seek experts advice

25
Q

regulation of blood pressure

A

Blood Volume
Blood viscosity
Cardiac output (CO)
Work performed by heart

Total peripheral resistance (TPR)
Resistance to blood flow

BP= CO x TPR
TPR largely dictated by arterial diameter particularly of small “resistance size” arteries

26
Q

what are resistance vessle

A

Consist of small arteries and arterioles
Largest pressure drop occurs here
Thus contractile state of these arteries has a massive impact on blood pressure

27
Q

Maintaining normal blood pressure

Stimulus: Rising blood pressure

A

1) Arterial blood pressure rises above normal range
2) Baroreceptors in carotid sinuses and aortic arch stimulated
3)Impulse traveling along afferent nerves from baroreceptors:
Stimulate cardio-inhibitory center (and inhibit cardio- acceleratory center)
4)decrease in Sympathetic impulses to heart ( decrease in HR and decrease in contractility)
5)decrease in cardiac output
6)decrease in CO and decrease in R return blood pressure to homeostatic range
7)Homeostasis: Blood pressure in normal range

2) also inhibit vasomotor center
3) decrease in Rate of vasomotor impulses allows vasodilation (increase vessel diameter)
4) decrease in pheripheral resistance
5) decrease in CO and decrease in R return blood pressure to homeostatic range
6) Homeostasis: Blood pressure in normal range

28
Q

Maintaining normal blood pressure

Stimulus: Declining blood pressure

A

1) Arterial blood pressure falls below normal range
2) Baroreceptors in carotid sinuses and aortic arch inhibited
3) Stimulate vasomotor center
4) Vasomotor Fibers stimulate vasoconstriction
5) increase Peripheral resistance (R)
6) increase in CO and increase in R return blood pressure to homeostatic range
7) Homeostasis: Blood pressure in normal range

2) Impulses from baroreceptors: Stimulate cardio- acceleratory center (and inhibit cardio-
inhibitory center)
3) increase in Sympathetic impulses to heart ( increase in HR and increase in contractility)
4) increase in Cardiac output (CO)
5) increase in CO and increase in R return blood pressure to homeostatic range
6)Homeostasis: Blood pressure in normal range

29
Q

how can blood pressure be calculated?

A

Blood pressure can be calculated as:
BP= CO x TPR

Total peripheral resistance is largely dictated by small arteries and arterioles called “resistance arteries” or “resistance vascular beds”

30
Q

what is the structure of resistance arteries?

A

1) Endothelium releases vasodilators

2) Innervated by sympathetic nerves: noradrenaline acts on 1-receptor, vsm contracts

31
Q

explain the contraction of smooth muscle cells

A

Thick Filaments contain myosin, Thin actin
Dense bodies are cytoplasmic anchorage points
Thick and thin filaments slide over each other during contraction
Process involves actin/myosin cross bridge cycling
Shortens muscle fibre and cell shortens and “balloons”

32
Q

Contraction Vascular smooth muscle

A

1) GPCR - agonist (noradrenaline) binds
2) release PIP2 and PLC
3) leads to be DAG and IP3
4) IP3 binds to receptors in sarcoplasmic reticulum within the smooth muscle cells
5) which releases calcium
6) which will bind to calmodulin (signalling molecule)
7) release of calcium which cause the plasma membrane to depolarise (more positive within the cytoplasm)

1) VGCCs Activated by depolarization/stretch
2) calcium binds to calmodulin
3) which activates myosin light chain kinase
4) which then gets converted into myosin light chain phosphoralted
5) which causes constriction

33
Q

explain endothelium dependent relaxation

A
  • agonist binds to endothelium
  • increases calcium in endothelium
  • produces nitric oxide
  • they diffuse into smooth muscle layer
  • decrease the calcium concentration in smooth muscle cell layer
  • decreases the initiating contraction
  • smooth muscle relaxes
  • vasodilations

Increases in EC [Ca2+] activate nitric oxide (NO) synthase, COX and EDHF
NO diffuses to SMC and activates soluble guanylate cyclase (sGC) generating cGMP
cGMP evokes relaxation by activating Protein Kinase G (PKG)
PKG prevents Ca2+ release and Ca2+ entry also regulates MLCK to evoke relaxation
COX derived PGI2 diffuses to SMC activates IP receptor
IP receptor coupled to AC- cAMP generated activates PKA
PKA regulates MLCK and activates some SMC K+ channels
EDHF more complex
hyperpolarization of endothelial cells transferred to smooth muscle cells
Hyperpolarization of SMC closes VGCC reducing [Ca2+] and thus constriction

34
Q

what does vasodilator drugs do?

example

A

Most vasodilator Drugs can directly relax smooth muscle, mechanisms vary e.g.
Nitrates generate NO (also see Aorta practical, CHD lecture)
Potassium channel activators hyperpolarize smooth muscle preventing calcium entry via VGCC (voltage gated calcium channels; see later)
Calcium channel blockers directly inhibit VGCC (later)

Some vasodilator drugs do not relax smooth muscle directly
Prevent the action of vasoconstrictors such as noradrenaline or angiotensin (next lecture)

35
Q

what are the classes of antihypertensive drugs acting on the blood vessle?

A 
ACE inhibitors 
AT-1 receptor antagonists
Calcium channel blockers
Potassium channel openers
𝛂-1 adrenoceptor blockers
D1 dopamine agonists
36
Q

explain the mechanism of action of calcium channel blockers?

A

Block SMC VGCC
First tier therapeutic agent in the elderly and African/Caribbean populations (ACD)
Used as a second line in people under 55
Not used in pregnancy

37
Q

explain the mechanism of action of calcium channel blockers?

A

Block SMC VGCC
First tier therapeutic agent in the elderly and African/Caribbean populations (ACD)
Used as a second line in people under 55
Not used in pregnancy

38
Q

what are the three categories of calcium channel blockers?

A

Dihydropyridines - vascular (most effective hypertensives)
Phenethylalkylamines - cardiac
Benzothiazepines - mixed

39
Q

what are examples of Dihydropyridines

A

nifedipine
amlodipine,
felopine,
lacidipine

40
Q

what are examples of Phenethylalkylamines

A

verapamil

41
Q

what are examples of Benzothiazepines

A

diltiazem

42
Q

what is the indication and mechanism of action of amlodipine?

A

Indication:
Hypertension
Prophylaxis of angina

Mechanism of action:
Inhibition of L-type Voltage gated calcium channels (VGCC) “vascular selective”
Relaxes vascular smooth muscle (vasodilatation) lowers blood pressure.
Dihydropyridine: the dihydropyridine class of CCBs all have
names ending in pine

43
Q

what are the side effects for calcium channel blockers?

A

Side effects include (also see lectures on arrhythmia, ischemic heart disease):

Ankle swelling, flushing, palpitations
Tremor
Constipation
hypotension (causes dizziness)
Cardiac effects (Particularly with Phenethylalkylamines and Benzothiazepines)
AV block
Weaken heart beat (negative inotropic effect)
Nifedipine increases mortality following myocardial infarction

44
Q

what is potassium channel activators

A

1) agonist binding
2) calcium release
3) calcium entry
4) binds to calmodulin etx —- causing constriction

resit part 2c (25 decks)

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