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MPharm 2 - PH2113 COPY > PH2113 - Cardiovascular 1 > Flashcards

PH2113 - Cardiovascular 1 Flashcards

1
Q

What is a cardiovascular disease?

A

Is a general term for conditions affecting the heart or blood vessels

Excludes diseases relating to formation of blood (haematological disease)

Includes disorders of blood coagulation (thrombotic disease)

Includes diseases of other organs resulting from abnormal blood supply esp. stroke, vascular dementia, renovascular disease

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2
Q

SCALE of CV diseases

A

-Is a general term for conditions affecting the heart or blood vessels.
-45% of CV deaths are due to coronary heart disease (same as ~ ischaemic heart disease)
-Nearly all deaths from CHD are due to acute
myocardial infarction (heart attack)

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3
Q

What does ischaemic mean?

A

Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism.

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4
Q

What does coronary mean?

A

relating to the arteries which surround and supply the heart

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5
Q

Define stenosis of blood vessels

A

Narrowing of blood vessels

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6
Q

What is Coronary heart disease (CHD) (also known as ischaemic heart disease)?

A

Is when your coronary arteries become narrowed by a gradual build-up of fatty material within their walls. These arteries supply your heart muscle with oxygen-rich blood. (see later for more info)

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7
Q

Why has CHD (coronary heart disease) mortality fallen steadily since 1970s

A

due mainly to better treatments and more of them.

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8
Q

what is happening to the SCALE OF CV DISEASE IN THE UK

A

CHD mortality is falling but morbidity is rising
I.E : less people dying from CV but more people are getting the disease.

-In over 65s, morbidity (including disability) due to CHD has increased by 20% since late 1980s.

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9
Q

what is happening to the GLOBAL SCALE OF CV DISEASE

A
  • CV disease is the leading cause of death

worldwide: 17.3 million deaths in 2008

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10
Q

CV diseases can be CONGENITAL/INHERITED or Acquired

A
  • Most cardiovascular diseases are acquired (gradually develop).
  • Risk factors, environment and genetics influence it.
  • mix of modifiable factors ± genetic (fixed) factors.

-Most CV disease develops as a result of life-style
(environmental, modifiable) factors

-Modifications of risk factors help to prevent CV- called primary prevention

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11
Q

What are modifiable CV risk factors?

A
  1. serum LDL-cholesterol
  2. smoking
  3. low physical activity
  4. diabetes
  5. hypertension
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12
Q

What are fixed CV risk factors?

A
  1. age
  2. male gender
  3. family history
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13
Q

APPROACHES TO PRIMARY PREVENTION (modifying the risk factors)

A

Primary prevention:
preventative measures in individuals with a high risk
of developing CV disease

  1. screening programmes
    Identify populations at risk Investigate risk to individuals
  2. intervention to reduce modifiable risk educate about risk life-style/behavioural alteration pharmacological intervention to reduce risk.
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14
Q

Approaches to SECONDARY PREVENTION

A

Secondary prevention :
comprehensive risk factor reducing interventions (including pharmacotherapies) and rehabilitation for patients who have had a heart attack or stroke

Target individuals with
established disease to reduce severity/mortality

  • Early disease detection increases opportunities for
    interventions to prevent progression and mortality
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15
Q

AIMS of secondary prevention:

A

extend survival
improve quality of life
decrease need for major interventions e.g PCI, CABG
reduce risk of subsequent major adverse CV event

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16
Q

What is SYSTEMIC ARTERIAL HYPERTENSION

A
  • High blood pressure in the systemic arteries - the vessels that carry blood from the heart to the body’s tissues
17
Q

Defining ‘normal’ and ‘abnormal’ blood pressure

A

Blood pressure determines tissue perfusion pressure

It is a physiologically regulated variable.

MAP ~ CO x TPR;
Cardiac Output = Heart Rate x Stroke Volume

18
Q

Cardiac output

A

Is the volume of blood pumped by the heart per minute.
= Heart rate x Stroke volume (Volume of blood ejected by the left ventricle in one contraction to the body.)

Resting cardiac output: 4-7 l/min (depends on body size)

19
Q

what is inotropy and chronotropy?

A
  1. Heart rate= chronotropy

2. Force of contraction = inotropy

20
Q

how does resistance occur in the blood vessel?

A

Friction between walls and blood flow generate RESISTANCE.

21
Q

how can friction in the blood vessels be measured ? (the equation)

A

Resistance to flow= (Viscosity of blood(Vf) X length(L))/ radius of vessel^4

-L - Longer the tube the greater the wall surface
R - Radius of vessel is inversely proportional to flow

-Noradrenaline angiotensin 2 and other circulating locally acting hormones also acting on smooth muscle tone (contraction of the muscle in the vessels)

22
Q

What is hypertension?

A
  • Abnormally high blood pressure.
  • That level of blood pressure associated with increased risk of some adverse effect at some time.
  • High bp associated WITH INCREASED CV RISK
23
Q

What are guideline BP values?

A

Ideal < 120/80
STAGE 1: >140/90
STAGE 2: 160/100
severe: >180/110

For diabetic subjects and/or in cases of renal insufficiency, high BP is defined as 130/80 mmHg.

24
Q

What are the Types of Hypertension ?

A
  1. Essential (primary, idiopathic) hypertension- no identifiable cause most common
  2. Secondary hypertension-
    is high blood pressure that’s caused by another medical condition
  3. borderline hypertension- blood pressures are above the upper boundary of “normal” (120/80 mm Hg) but have not yet crossed into hypertensive territory.
  4. The top/first number of a blood pressure measurement — greater than 140 mm Hg
  5. “white coat” (in US “office”) hypertension -raised blood pressure due to being stressed
  6. accelerated (“malignant”) hypertension- rapid and sudden increase in blood pressure over the baseline level
  7. uncomplicated/complicated hypertension
25
Q

SECONDARY HYPERTENSION

A

hypertension secondary to an identifiable
physiological, pharmacological or structural
cause

~ 5% of cases

assessment and management of all cases of
hypertension should exclude treatable causal
conditions as far as possible

long-list of diseases, conditions, factors

26
Q

CAUSES OF SECONDARY HYPERTENSION

A
  1. renal or renovascular disease e.g. polycystic disease, renal artery stenosis
  2. adrenal disease
    e. g. primary hyperaldosteronism (Conn’s disease) phaeocromocytoma
  3. pregnancy
    complex/unknown aetiology; several forms
    chronic; gestational; pre-eclampsia; transient
  4. idiopathic or iatrogenic Cushing’s syndrome (high levels of cortisol in the body.)
    (incl. chronic glucocorticoid therapy)
  5. sleep apnoea? (you have one or more pauses in breathing or shallow breaths while you sleep) related to obesity
  6. thyroid and parathyroid disease hyperthyroidism
  7. congenital structural abnormalities coarctation of the aorta
8. many drugs
NSAIDs, COX-2 inhibitors
cocaine, amphetamine, sympathomimetics
ketamine
oral contraceptive hormones
cyclosporin, tacrolimus
erythropoietin
liquorice and derivatives
27
Q

ESSENTIAL HYPERTENSION

A

hypertension of unknown cause (“idiopathic”)

the most common form of hypertension

> 90% of cases

-likely to be multifactorial and polygenic with gene/ environment interactions.

28
Q

PHYSIOLOGICAL BASIS OF HYPERTENSION

A

the majority of people with established hypertension
do not have ↑CO (actually, may be slightly ↓ CO)

  • in pre-hypertension or in hypertension associated
    with obesity and pregnancy, there may be evidence
    of ↑CO but this is limited

↑TPR is the major finding in most hypertensive patients

29
Q

WHAT INITIATES ↑TPR IN HYPERTENSION?

A
  • UKNOWN

several possibilities based on interactions between
“environmental” factors and heritable susceptibility
(genetic factors)

environmental factors may include responses to
stress, dietary Na+ in salt-sensitive individuals,
alcohol consumption, obesity

genetic factors are multiple (polygenic) and not fully-
defined but strong familial and racial tendencies

renal, neural, endocrine and structural factors
could all contribute to ↑TPR

? increased circulating vasoconstrictors,
e.g. angII, ET-1, NAd

? local sensitivity to Na+ in vascular smooth muscle

? vascular remodelling (smooth muscle hypertrophy)
especially in arterioles

↑TPR maintained by medial hypertrophy in arterioles

almost certainly multifactorial

MPharm 2 - PH2113 COPY (39 decks)

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