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MD3001 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Define congenital heart disease?

A

Heart disease that patient is born with

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2
Q

Name 6 causes for congenital heart disease?

A
  1. Genetic defects
  2. Chromosomal abnormalities (Downs, Turners etc)
  3. Intrauterine infection (Rubella)
  4. Drugs
  5. Maternal alcohol
  6. Maternal diabetes
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3
Q

What are the 2 main great vessels that are derived from the 4th pharyngeal arch?

A
  1. Arch of Aorta (four rhymes with aOR)

2. Right subclavian artery (fouRS= Right Subclavian)

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4
Q

For the following stages in heart formation from the cardiac tube, name the day on occurrence and the milestones associated with stage:

  1. Cardiac crescent
  2. Linear heart tube
  3. Looping heart
  4. Chamber formation
A
  1. Cardiac crescent
    - Day 15
    - Cardiac differentiation
    - Migration to midline
  2. Linear heart tube
    - Day 20
    - Heart tube formation
    - First heartbeat
    - Anterior-posterior and dorsal-ventral patterning
  3. Looping heart
    - Day 28
    - Early chamber formation (FHF = ventricles, SHF = atria)
    - Looping to the right
  4. Chamber formation
    - Day 32
    - Chamber formation
    - Trabeculation
    - Cushion formation
    - Outflow tract septation
    - Early conduction system formation
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5
Q

What are the sources of congenital cardiovascular diseases? (5)

A
  1. Failure of septation
  2. Failure of development
  3. Failure of/or incorrect rotation
  4. Abnormalities of the great vessels
  5. Failure of closure
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6
Q

How does oxygenated blood from umbilical vein by pass the lungs (uninflated, high resistance)?

A
  1. Crossing the fossa ovalis
  2. Passing from PT to aorta via ductus arteriosus.

Ductus arteriosus opening is maintained by prostaglandins

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7
Q

What conditions are caused by the following:

  1. Failure of septation
  2. Failure of development
  3. Failure of/or incorrect rotation
  4. Abnormalities of the great vessels
  5. Failure of closure
A
  1. Failure of septation: VSD, ASD
  2. Failure of development:
    Obstruction= Tricuspid/pulmonary atresia, pulmonary stenosis, coarctation of the aorta
    Hypoplasia= Hypoplastic left heart
  3. Failure of/or incorrect rotation =TGA, congenitally corrected transposition of the great vessels, dextrocardia
  4. Abnormalities of the great vessels= Wrong connections/embryology
  5. Failure of closure=Persistent ductus arteriosus
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8
Q 
What do the following abbreviations for congenital heart diseases mean:
ASV
VSD
TGA
PDA
PAH
A 
ASD= Atrial septal defect
VSD= Venticular septal defect
TGA= transposition of great arteries
PDA= Patent ductus arteriosus
PAH= Pulmonary arterial hypertension
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9
Q

What are 4 issues of congenital cardiovascular disease and how do they present?
Hint: CHIP

A
  1. Incidental: Murmur, echo finding
  2. Heart failure: Pulmonary pressure (Qp) > Systemic pressure (Qs)
  3. Central cyanosis: Result of venous mixing with systemic blood
  4. Pulmonary hypertension: Increased pulmonary pressure (Qp)
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10
Q

Name 6 presenting problems for congenital cardiovascular disease?

A
  1. Heart failure: Difficulty feeding, failure to thrive, tachypnea, cyanosis
  2. Cyanosis
  3. Clubbing
  4. Murmur
  5. Squatting (Fallot’s)
  6. Syncope
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11
Q

Name 3 acyanotic congenital CV diseases that are:

a) with shunts
b) without shunts

A

WITH SHUNTS

  • ASD
  • VSD
  • PDA

WITHOUT SHUNTS

  • Pulmonary stenosis
  • Coarctation of the aorta
  • Aortic/left heart obstruction
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12
Q

Name 3 cyanotic congenital CV diseases that are:

a) with shunts
b) without shunts

A

WITH SHUNTS

  • Transposition of great vessels
  • Fallots tetralogy

WITHOUT SHUNTS

  • Hypoplastic left heart
  • V severe pulmonary stenosis
  • Pulmonary/tricuspid atresia
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13
Q

Discuss the management of congenital CV diseases?

Prevention and palliative

A

Prevention: Foetal ECG
Palliative:
1.To allow growth for definitive treatment
2. As long term treatment: Creation of systemic to pulmonary shunt
3. Definitive treatment: Correction of TGA, closure devices for septal defects
4.Transplantion

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14
Q

What are the 7 complications of congenital CV diseases?

A
  1. Failure to thrive
  2. Paradoxical embolus
  3. Endocarditis
  4. Pulmonary hypertension
  5. Polycythaemia
  6. Haemoptysis
  7. Artythmias
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15
Q

What is a paradoxical embolus?

A

When a venous thrombi enters the systemic circulation via an atrial septal defect

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16
Q

Pulmonary hypertension:
Cause:
Consequences:
Investigations:

A

Cause:Arises as a result of “high flow” through the pulmonary bed

Consequences:
Left to right shunts reverse to become right to left = cyanosis
Very high maternal mortality usually means that pregnancy is best avoided

Investigations:

  1. ECG and Doppler
  2. Cardiac catheterization
  3. Genetic
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17
Q 
ASD:
If uncomplicated, presents as?
Heart sound abnormality?
Secundum vs primum?
Management?
A

If uncomplicated, presents as: Heart failure, failure to thrive or incidental finding

Heart sound abnormality: Fixed splitting of the second heart sound

Secundum vs primum: Secundum is isolated, primum often complicated by other lesions

Management: Nothing/ percutaneous closure (dependent on size of shunt)

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18
Q

What are the clinical differences between small and large VSDs?

A

Small VSDs:

  • Restrict shunt to trivial levels (termed as a restrictive VSD)
  • Safe ie never causes PAH
  • Loud murmur

Large VSD:

  • High Qp:Qs present in early infancy
  • Palliated until definitive treatment
  • Loud holosystolic murmur
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19
Q

What is PDA and how does it present itself clinically with large and small?

A

Patent ductus arteriosus

Larger PDA: will present as heart failure with continuous murmur and wide pulse pressure
Can cause PAH but this will only show lower body cyanosis

Smaller PDA: Continuous murmur, normal pulse pressure. In infancy, prostaglandin inhibition may close duct

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20
Q 
Coarctation:
Define?
Men/women?
Leads to..
Associations?
Indications?
Treatment?
A 
Definition: Narrowing of the aorta: from complete interruption to small low gradient stenosis
More common in men
Causes: Systemic hypertension in adults
Associations: with intracranial aneurysms
Indications:
- Absent/delayed femoral pulses
-Lower bp in legs
-Scapula collaterals 
-Rib notching on CXR
Treatment:
-Balloon dilatations
-Surgery
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21
Q

What difference does the septum being intact make to the presentation of the TGA?

A

If the septum is intact, TGA presents rapidly as a blue and failing baby. This is because there is no mixing of oxy and de oxy blood, hence there is complete incorrect supply to the pulmonary artery and aortic.

The symptoms appear later is septum is not intact

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22
Q

Name 4 palliative approaching to TGA?

A
  1. Pharmacologic maintenance of arterial duct
  2. Atrial septostomy
  3. Radical switch procedure
  4. Pallative surgery- mustard procedure
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23
Q

Tetralogy of Fallot involves four heart defects, name them.

A
  1. A large ventricular septal defect (VSD)
  2. Pulmonary stenosis
  3. Right ventricular hypertrophy
  4. An overriding aorta
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24
Q

Tetralogy of Fallot:
Definite cause of?
Characteristic behavior?

A

Cyanosis
BUT one which is reversible as they never have PAH

Characteristic: Squatting as it raise systemic resistance

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25
Q

What are the 7 stages of a cardiovascular examination?

A
  1. Introduction and explanation
  2. Inspection
  3. Palpation
  4. Percussion
  5. Auscultation
  6. Other areas
  7. Conclusion
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26
Q

What must be covered in the introduction in CVS exam? (7)

A
  1. Adequate hygiene of hands and stethoscope
  2. Introduce self
  3. Confirm patient’s name and DOB
  4. Ask if patient is in any discomfort
  5. Explain the procedure
  6. Seek permission to examine
  7. Position patient at 45 degrees with chest adequately exposed
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27
Q

What 4 steps are covered in a general inspection of the CVS?

A
  1. Stand at the end of the bed
  2. Look around the patient
  3. Look at the patient (discomfort, pain, breathlessness, pallor)
  4. Any pathological signs
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28
Q

What additional steps are covered in a close inspection that aren’t done in a general inspection in CVS exam?

A
  1. Inspection of hands: Warmth, capillary refill time, pathology signs
  2. Inspect face, eyes and mouth: Pallor, sweating, specific signs of pathology
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29
Q 
For each of the following, name abnormal conditions that can be identified during a CVS examination:
Hands: 7
Lips: 1
Cheeks: 1
Eyes: 1
A

Hands: Peripheral cyanosis, tar staining, nail clubbing, Splinter haemorrhage, koilonychias (Fe deficient anaemia), oslers nodes, janeway lesions
Lips: Central cyanosis
Cheeks: Malar flush
Eyes: Conjunctivae (appears yellow/pale), Xanthelasma (high cholesterol), Corneal arcus (high cholest)

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30
Q

Describe the pulses section of a CVS exam?

A

Feel for radial pulses:

  • Palpate both
  • Rate
  • Rhythm
  • Collapsing pulse

Carotid pulse:

  • Only one at a time
  • Volume
  • Character

BP

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31
Q

What are the 5 different abnormal pulses in terms of rate/rhythm and name one condition for each?

A
  1. Fast and regulation: Anxiety
  2. Regularly irregular: Ectopic beat
  3. Irregularly irregular: Atrial fibrillation
  4. Slow and regular: Athletic training
  5. Slow and irregular: Complete heart block
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32
Q

What are the conditions that cause high/low volume pulses?

A

Low volume: Hypovolaemia, left ventricular failure

Increased volume: Anaemia, fever, thyrotoxicosis

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33
Q

What are the 2 abnormal pulses that reveal character?

A

Slow rising pulse: Aortic stenosis

Collapsing pulse: Aortic regurgitation

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34
Q 
Jugular Venous Pulse (JVP):
What vessel?
Patient position when palpating?
Position?
How can the pressure in vein be increased?
A

Vessel: Right internal jugular vein
Patient position: Lying at 45 degreees, with head turned to left
Position: Between the clavicular and sternal heads of sternocleidmastoid muscle
Technique for increasing venous pressure: Abdomino-jugular reflex ie pressing on liver as this has no effect on carotid artery

Note: The pulsation does not arise from vein but reflects changes in pressure within the right atrium

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35
Q

What is the praecordium?

A

The area of the anterior chest wall over the heart.

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36
Q

What are the 4 steps in examining the praecordium in a CV exam?

A
  1. Look: Shape, respiratory rate, scars, visible apex beat, pacemaker
  2. Apex beat: Find it, then check position
  3. Heaves: Left sternal edge for right ventricular enlargement
  4. Thrills: Palpable murmur
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37
Q

What are the 4 stages in auscultation during a CV exam?

A
  1. Palpate carotid pulse initially: Distinguish between 1st and 2nd heart sounds
  2. Listen for: Heart sounds, added sounds, murmurs
  3. Use bell + diaphragm and listen in all 4 key areas
  4. Manoeuvres to accentuate murmurs and remember carotids
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38
Q

What are the manoeuvres to accentuate murmurs at the following positions:

  1. Apex in the left lateral position
  2. At left axilla
  3. At lower left sternal edge with patient sat forwards
  4. Over carotids
A
  1. Apex in the left lateral position
    - Bell at apex
    - In expiration
    - Accentuation of mitral stenosis
  2. At left axilla:
    - With diaphragm
    - Radiation of systolic murmur of mitral regurgitation
  3. At lower left sternal edge with patient sat forwards
    - With diaphragm
    - In expiration
    - Accentuation of aortic regurgitation
  4. Over carotids
    - With diaphragm
    - In held inspiration
    - For aortic radiation/carotid bruits
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39
Q

What is the grading system for murmurs?

A 
1/6 = V quiet = Absent thrill
2/6 = Quiet = Absent thrill
3/6 = Easy audible = Absent thrill
4/6 = Loud= Present thrill
5/6 = V loud = Present thrill
6/6 = Audible without stethoscope= Present thrill
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40
Q

What are the “other areas” to be covered in a CV exam?

A
  1. Auscultate lung bases
  2. Sacral oedema
  3. Offer abdominal exam
  4. Peripheral vascular examination: Femoral, popliteal, dorsalis pedis, posterior malleolus
  5. Ankle oedema
  6. BP
  7. Fundoscopy
  8. Urinalysis
  9. Observation chart
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41
Q

Define health promotion

A

Health promotion is the process of enabling people to increase control over, or to improve, their health

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42
Q

Describe health promotion programes in the context of cardiovascular disease

A

Primary prevention: HEBS campaign to encourage walking groups
Secondary prevention: Blood pressure and cholesterol checks
Tertiary prevention: Personality

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43
Q

What are the 3 types of prevention in health promotions?

A

Primary prevention: Preventing onset of poor health (i.e. seatbelts)
Secondary prevention: Identfy and treating potential illness early
Tertiary prevention: Focus on people who already have health problem, aims to reduce symptoms

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44
Q

How is personality assessed to predict CVD?

A

Type A and Type B personalities that link to coronary heart disease
Type A= competitive, high time urgency, high hostility
Type B= Low competitiveness, low time urgency, low hostility

Type A = higher risk

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45
Q

List the order of the “stage model of behavioural change” starting with pre-compemplation..

A
  1. Pre-contemplation
  2. Contemplation
  3. Preparation
  4. Action
  5. Maintenance
  6. Replapse —> 1.
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46
Q

List the order of the “stage model of behavioural change” starting with pre-compemplation..

A
  1. Pre-contemplation
  2. Contemplation
  3. Preparation
  4. Action
  5. Maintenance
  6. Replapse —> 1.
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47
Q

How is Type A personality assessed?

A

Structured interview

Questionnaries: Jenkins Activity Survey, Framingham Type A Scale

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48
Q

How can Type A personality behavior be reduced?

A
  1. Stress reduction strategies
  2. Relaxation techniques
  3. Anger management
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49
Q

What are the 3 different types of IVD (intravascular device)?

A
  1. Peripheral venous catheters
  2. Central venous catheters (CVCs): Either-
    - Peripherallly inserted CVCs
    - Skin-tunneled CVCs (e.g. Hickman and Broviac lines)
  3. Arterial catheters
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50
Q

What are the 3 different methods for administering intravenous medications?

A

Continuous infusion:

  • Stable drugs (don’t degrade)
  • Short half-life
  • Time dependent effects
  • Needs dedicated IV site

Intermittent infusion:

  • Unstable drugs
  • Long half-life
  • Concentration dependent effects
  • Less compatibility concerns

Bolus injection:

  • Rapid response required
  • Incompatibilities
  • Unstable srugs
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51
Q

7 Complications of IV drug administration?

A
  1. Fear/phobia/pain
  2. Infection / Sepsis
  3. Thrombophlebitis
  4. Extravasation / Infiltration
  5. Emboli
  6. Anaphylaxis / Hypersensitivity
  7. Overdose
  8. Insufficient mixed on bag between drug and diluting fluid
  9. Stability of medicines in solution
52
Q

What is red man syndrome?
Cause?
Incidence reduced by?

A

Hypersensitivity reaction due to histamine release
Symptoms:
– erythematous rash of face, neck, and upper torso
– diffuse burning, itching, generalised discomfort
– rare cases: hypotension, angioedema, chest pain, dyspnea
Cause: Fast infusion rate of vancomycin
Incidence reduced by: Slower infusion rate, more dilute drug solution

53
Q

What are the different factors which affect the stability of the medicines in solutions?

A

Light
Temperature
Concentration
pH

54
Q

Why does the graph of plasma concentration against time for infusions ben towards a plateau when rate in = rate out?

A

As the drug is being eliminated by the kidney on entry tot circulation
The amount of drug eliminated per unit time is related to the concentration of drug in the plasma (first order kinetics)
ie
Higher concentrations, more drug is removed per unit of time
Lower concentrations, less drug is removed per unit time

55
Q

What is clearance (CL)?

A

The volume of blood or plasma cleared of drug in a unit time

56
Q

In first order kinetics, whilst amount of drug eliminated per unit time varies, clearance…..

A 
is constant
(bath of glitter analogy)
57
Q

The time taken to reach the Css of a drug depends
on its _______

The Css reached depends on the ____ of drug in, and
the rate of _____ of the drug from the plasma

A

The time taken to reach the Css of a drug depends
on its HALF LIFE

The Css reached depends on the RATE of drug in, and
the rate of CLEARANCE of the drug from the plasma

58
Q

What are the 6 disadvantages of IV administration?

A
  1. Increased cost and time to administer the medicine
  2. Requires trained staff to administer (plus location)
  3. Rapid onset of action
  4. Volume of fluid needed to dilute the medicine
  5. Can cause discomfort/pain to the patient
  6. Health risks (e.g. infection)
59
Q

What are 8 reasons for administrating drugs via IV?

A
  1. 100% bioavailability
  2. Cannot swallow, only route option
  3. Fast acting
  4. Direct entry to vascular system
  5. Medicine only available via injection
  6. Need constant/high blood level of medicine needed
  7. Some medications are more effective via IV
  8. Rarely, to ensure compliance
60
Q

6 factors that affect drug distribution

A
  1. Cardiac output and blood flow: Large affect on initial blood flow
  2. Plasma protein binding
  3. Lipid solubility
  4. Degree of drug ionisation
  5. pH of compartments
  6. Capillary permeability
61
Q

Albumin binding, how do different drugs bind differently?

A
  • Lipid-soluble drugs bind non-specifically

* Weak acids bind to a specific, saturable site

62
Q

What is albumin?

A

Predominate plasma binding proteins

63
Q

What is the effect drug ionization on diffusion across cell membrane?

A

Ionised drugs have low lipid solubility hence ionized drugs will not diffuse across cell memebrane

64
Q

What is the blood brain barrier?

A

A physical and functional barrier between the blood plasma and the brain

65
Q

What conditions allows drugs to cross the blood brain barrier and how?

A

Meningitis
Due to:
- Inflammation of maninges that weakens barrier

66
Q

What are the 4 specialized drug barriers/compartments?

A
  1. Blood brain barrier
  2. Placenta: Tight endothelial cell junctions in maternal and foetal capillaries.
  3. Chronic abscesses: Avascular tissue compartments
  4. Lung infection: Local low O2 and high CO2 causes vasoconstriction
67
Q

What drugs are able to pass through the placenta drug barrier?

A

Lipid soluble drugs

Unionised forms of weak acids and bases

68
Q

What is the equation for Css=

A

Css= (rate of drug administered)/CL

CL= Clearance

69
Q

What is the equation for the elimination half life (t1/2)

A

t1/2= (ln2 x Vd)/ CL

CL= Clearance

70
Q

What is “Volume of distribution”?

A

the volume of distribution (VD) is the theoretical volume that would be necessary to contain the total amount of an administered drug at the same concentration that it is observed in the blood plasma.

71
Q

What is the equation for “Appartent volume of distribution” (Vd)=

A

Vd= (total mass of drug in body)/ (blood plasma conc of drug)

Units: L or L/Kg of body weight

72
Q

What is the difference between the single and two compartment model of distribution?

A

Single:
-Assumes rapid mixing of drug in plasma.
-Assumes drug in plasma is in rapid equilibrium with drug in extravascular tissues
Twp:
-Two compartments
- Central compartment e.g. blood and well perfused tissues
-Peripheral compartment e.g. poorly perfused tissues

73
Q

What is the clinical relevance of Vd?

A

Vd can be used t determine a loading dose to achieve a desired plasma concentration of drug

74
Q

What are the varying factors of Vd?

A
  • Height
  • Weight
  • Age
  • Fluid accumulation e.g. oedema
  • Accumulation of ffat
75
Q

What are 4 common CV defects in Down syndrome?

What gene causes the problems?

A
  1. Atrial septal defect
  2. Ventricular septal defect
  3. Atrioventricular canal defect
  4. Patent ductus arteriosus

In the derived Chr 21, the genes are in the incorrect position

Overexpression of transgenics (DSCAM and COL6A2) leads to heart defects similar to those seen in DS. These genes only affect hear

76
Q

What are the 5 features of 22q11.2 deletion syndrome (DiGeorge syndrome)?
(Hint: CATCH-22)

A 
Cardiac abnormalities (e.g. Interruption of aortic arch, Tetralogy of Fallot, Ventricular septal defect)
Abnormal Facies
Thymic aplasia
Cleft palate
Hypothyroidism
77
Q

What is TBX-1?

A

Transcription factor crucial for normal development of large arteries that carry blood out of the heart.
E.g. 4th pharyngeal arch arteries

78
Q

What dosage of TBX-1 is necessary for transcription?

A

A normal level

Too much or too little both result in no transcription

79
Q

What is the difference between hypertrophic cardiomyopathy and physiological hypertrophy?

A

Physiological hypertrophy: Controlled and organized

Hypertrophic cardiomyopathy: Thickening of ventricle wall and septum is disorganized

80
Q

Hypertrophic cardiomyopathy:
Phenotype?
Genotype?
Gene defects?

A 
Phenotype: 
-Increased muscle thickness
-Disorganised myocytes
-Fibrosis 
Genotype: Autosomal dominant 
Gene defects: Defects in more than one gene can cause phenotype (i.e. locus heterogeneity)
81
Q

Long QT:
Delay in?
Channelopathy?

A

Delay in repolarisation

Channelopathy: Na and K channel genes are altered

82
Q

What is allelic heterogeneity and what is a cardiology example of it?

A

Allelic heterogeneity: Different mutations in the same genes can cause the same disease
Examples:
1. Mutations in potassium transmembrane channel leading to LOSS of function
2. Mutations in Na channel leads to GAIN of function

83
Q

What is penetrance?

A

If we compare the phenotype and the clinical diagnosis, to what we’ve learned from genetic mapping. They do not match, there are more genetically predicted patients

84
Q

What is Familial Hypercholesterolemia?

Name two symptoms?

A

High concentration of serum LDL cholesterol (total cholesterol > 7.5mM)
Symptoms:
- Xanthoma
-Atherosclerosis

85
Q

Give examples of disorders arising from changes in gene dosage

A

Examples:

  • Down syndrome
  • DiGeorge deletation syndrome
86
Q

Population screening vs cascade testing

A

Cascade testing: The identification of close relatives of an individual with a disorder to determine whether the relatives are also affected or are carriers of the same disorder.
Population screening: A strategy used to identify the possible presence of an as-yet-undiagnosed disease in individuals without signs or symptoms

87
Q

In the treatment of angina what are the drug groups used to:

  • Reduce chest pain symptoms?
  • Prolong survival?
A

REDUCE CHEST PAIN SYMPTOMS

  1. Beta-blockers
  2. Nitrates
  3. Calcium channel antagonists
  4. Nirocandil
  5. Ivabradine
  6. Ranolazine

PROLONG SURVIVAL

  1. Beta-blockers
  2. Aspirin
  3. Statins
  4. ACE inhibitors
  5. Angiotensin II receptor blockers
88
Q

What does ACE inhibitor stand for?

A

Angiotensin Converting Enzyme Inhibitor

89
Q

What 3 factors can potentially shrink the window for coronary flow?

A
  1. Shortening diastole e.g. increase heart rate
  2. Increased ventricular end diastolic pressure e.g. aortic valve stenosis as blood cannot exit ventricle as easily
  3. Reduced diastolic arterial pressure e.g. mitral or aortic valve incompetence (i.e. blood flowing back into ventricle), heart failure
90
Q

What is the relationship between coronary ischemia and infarction?

A
  1. Coronary ischaemia usually is the result of atherosclerosis, which causes angina
  2. Sudden ischaemia is usually cause by thrombosis, may result in MI
  3. Coronary spasms can cause variant angina
  4. Cellular calcium overload results from ischaemia. May cause cell death and dysrhythmias
91
Q 
Angina pectoris:
Define?
Symptoms?
Characteristic distribution of pain?
Association with heart attack?
A

Definition: Chest pain due to inadequate supply of oxygen to the heart.
Symptoms: Pressure and suffocation sensation behind breastbone
Characteristic distribution of pain:
- Chest, arm, neck, jaw
-Brought on by exertion/ cold/ excitement
Angina can accompany or be a precursor for a heart attack

92
Q

What are the three different classes of angina?

A
  1. Printzmetal’s variant angina: Predictable chest pair on exertion. Result of vasospasm. Causes supply ischemia (reduces O2 supply)
  2. Chronic stable angina: Result of fixed stenosis, atherosclerosis of coronary arteries. Causes demand ischemia (because oxygen demand has increases)
  3. Unstable angina: Result of thrombosis within coronary artery, not complete occlusion. Cause supply ischemia as when the clot forms, coronary flow is reduced, leading to a reduction in the oxygen supply/demand ratio (“supply ischemia”).
93
Q

What is the main aim of antianginal drugs?

Name 2 different classes?

A

Aim: Decrease the metabolic demand of the muscle

  1. Vasodilators
    - E.g. Organic nitrates, nicorandil, calcium antagonists
    - Decrease preload and afterload
  2. Slow down heart rate
    - E.g. B-blockers, ivabradine
    - Decreases metabolic demands of the muscle
94
Q

What is the difference between preload and afterload?

A 
Preload= Dictates how much blood that is returned to heart
Afterload= Pressure that the heart is pumping against
95
Q

What is the staged introduction of drugs for patients aged above and less 55yrs?``

A

Under 55yrs: ACE inhibitor or low-cost ARB
Over 55yrs: Calcium-channel blocker

If hypertension persists, try above drugs together. Then add thiazide-like diuretic.

Staged introduction of drugs starts with those with least side effects

96
Q

Major drug classes for treating hypertension and examples?

3 core
2 additional

A

Renin-angiotensin system inhibitors:

  • Angiotensin converting enzyme inhibitors e.g. Ramipril, Lisinopril
  • Angiotensin AT1 receptor antagonists (ARBs) e.g. losartan
  • Renin inhibitors e.g. aliskiren

Calcium channel blockers e.g. amlodipine, lercanidipine

Diuretics:
-Thiazide-like diuretics e.g. Indapamide, bendroflumethiazide

ADDITIONAL….
Sympathetic nervous system antagonists:
- Beta-blockers e.g. bisoprolol, atenolol
-Alpha-adrenoreceptor blocker e.g. doxazosin

Kidney function modifiers
-Potassium sparing diuretics and aldosterone antagonists e.g. spironolactone

97
Q

In kidney modifying drugs in hypertension, where do the different drugs act on the tubule?

A

Thiazide-like diuretics: Distal tubule Na/Cl channel inhibitor
Aldosterone antagonists: Collecting tubule Na/Cl channel inhibitor

98
Q

What are the common side effects of the following hypertensive drugs:

  1. Renin-angiotensin system inhibitors
  2. Calcium channel blockers
  3. Diuretics
A
  1. Renin-angiotensin system inhibitors
    - ACE inhibitors: Persistent dry cough, dizziness, tiredness, headaches
    - ARBs: Dizziness, headaches, leg/back pain
  2. Calcium channel blockers: Flushes, headaches, ankle oedema, dizziness
  3. Thiazide-like diuretics: Increase in K and blood sugar levels
99
Q

What is the action of beta blockers in treatment of angina?

Name 2 examples

A

Decrease cardiac oxygen consumption by slowing the heart
Antidysrhythmic action: reduce death after MI

Examples: Bisoprolol

100
Q

Calcium antagonists in the treatment of angina:
2 actions?
Main subtypes and example?

A

Action:

  1. Prevents opening of voltage-gated L-type Ca channels. Main effect on heart and smooth muscle to inhibit calcium entry upon muscle cell depolarization
  2. Vasodilator effect on resistance vessels, which reduces afterload. Also dilate coronary vessels

Two main types:

  • Dihydopyridine derivatives e.g. amlodipine and lercanidipine
  • Rate limiting e.g. verapamil and diltiazem
101
Q

How do the clinical uses of different calcium antagonists in angina differ:

  • Amlodipine/lercanidipine?
  • Diltiazem/verapamil?
A

Amlodipine/lercanidipine: Safe in patients with heart failure, used instead of beta-blocker in Prinzmetal angina and alongside beta-blockers in most angina. Treats hypertension
Diltiazem/verapamil: Used but contraindicated in heart failure, bradycardia, AV block or in presence of beta-blocker. Acts as a antidysrhythmics

102
Q

Side effects of calcium antagonists used to treat angina?

A

Headache, constipation, ankle oedema

103
Q

How does verapamil acts as a antidysrhythmic?

A
  • Slows ventricular rate in rapid atrial fibrillation
  • Prevents recurrence of supraventricular tachycardia
  • No effect on ventricular arrhythmias
104
Q 
Organic nitrates in angina treatment:
Name of 2 drugs?
Mechanism?
Side effects?
Clinical uses? 4
A

Examples: Glycerol trinitrate, Isosorbide mononitrate

Mechanism:

  • Powerful vasodialtors
  • Are metabolised to NO and relax smooth muscle
  • Acts of veins to decrease cardiac preload. At higher concentrations, arteries affected, so decreases afterload
  • Dilation of collateral coronary vessels, improves distribution of coronary blood flow towards ischaemic areas

Side effects: Headaches, postural hypotension

Clinical uses:

  1. Stable angina: Prevention by sublingual glycerol trinitrate shortly before exertion or isosorbide mononitrate long before
  2. Unstable angina: intravenous gylercol trinitrate
  3. Acute heart failure: Intravenous GTN
  4. Chronic heart failure (CHF): Isosorbide mononitrate with hydralazine
105
Q 
Potassium channel activators in angina treatment:
Examples?
Mechanism?
Side effects?
Clinical uses?
A

Example: Nicorandil

Mechanism:

  • Combines activation of K+ATP channels with nitrovasodilator actions. Leads to hyperpolarisation of vascular smooth muscle
  • Both arterial and venous dilator

Side effects: Headaches, flushing, dizziness

Clinical uses: Used in patients who remain symptomatic despite optimal management with other drugs

106
Q

Name 4 differences between systemic and pulmonary hypertension?

A
  1. Systemic is more common
  2. Pulmonary artery pressure is hard to measure
  3. Pulmonary hypertension be idiopathic or associated with other disease
  4. Pulmonary only diagnosed when severe and symptomatic
107
Q

What does idiopathic mean?

A

Unknown origin

108
Q

Cause of pulmonary hypertension? (6)

A
  1. Hypoxia
  2. Endothelial dysfunction
  3. Reynaud’s
  4. Genetics
  5. Blockage/damage to pulmonary blood vessels (PE, sickle cell etc)
  6. Side effect of some drugs
109
Q

Difference between between primary and secondary systemic hypertension?

A

Primary hypertension: Idiopathic

Secondary hypertension: Known cause. e.g. renal disease, diabetes, Cushing’s, some drugs

110
Q

How is hypertension classified?

A

Stage 1 hypertension:
- Clinic bp is 140/90mmHg or higher
+ ABPM/HBPM daytime average id 135/85mmHg or higher

Stage 2 hypertension
-Clinic bp 160/100mmHg or higher
+ ABPM/ HPBM is 150/95mmHg or higher

Severe hypertension:
-Clinic systolic BP is 180mmHg or higher
or Clinic diastolic BP is 110mmHg or higher

111
Q

What do the following stand for in blood pressure measurement:

  • ABPM?
  • HPBM?
A

ABPM: Ambulatory Blood Pressure Monitoring
HBPM: Home Blood Pressure Monitoring

112
Q

Primary hypertension:

Causes?

A
  1. Increase in total peripheral resistance due to:
    - Balance between contraction/relaxation changes
    - Increased sympathetic nerve activity… increase in NA released
  2. Increased vascular reactivity
    - Increase [Na]ECF
    - pathological Na/K-ATPase inhibition
    - Damage to endothelium leads to decreased NO production
    - Altered blood vessel wall morphology leads to increase wall thickness to lumen ratio
113
Q

Secondary hypertension:

Cause? 6

A

Cause:

  1. Renal disease: Altered blood pressure control
  2. Diabetes: damaged endothelium
  3. Endocrine disorders: Cushing’s, Conn’s etc
  4. Coarctation of the aorta
  5. Drugs e.g. contraceptive pill, cocaine, NSAIDS
  6. Pregnancy: Eclampsia
114
Q

Secondary hypertension risk factors:

  • Non-modifiable
  • Modifiable
  • Genetic factors
  • Psychogenic factors

12 total

A 
Non-modifiable:
1. Age 
Modifiable:
2. Exercise
3. Diet
4. Obesity
5. Smoking
6. Alcohol intake
7. Stress
Genetic factors:
8. Abnormal inhibition of Na/K-ATPase
9. Family history
10. African/Caribbean origin
11. Male
Psychogenic factors:
12. Personality type
115
Q

What are the main effects of hypertension of the body?

A
  1. Heart
  2. Vasculature
  3. Renal failure
116
Q

What are the effects of hypertension on the heart?

A
  1. Heart failure
    - Pressure overload from the increase in TPR
    - Volume overload due to kidney failure
  2. LV hypertrophy is a major risk factor for coronary disease, dysrhythmias, sudden death and congestive heart failure
  3. Myocardial infarction
117
Q

What are the effects of hypertension of the vasculature? 3

A
  1. Accelerated atherosclerosis
  2. Stroke
    - Narrowing and sclerosis of small cerebral arteries
    - White matter changes
  3. Retinopathy
    - Retinal blood vessels damaged by high pressure
    - Arteries become narrowed and tortuous
    - Subsequently veins occluded and oedema and haemorrhage occurs
118
Q

How does hypertension cause renal failure? 4

A
  1. Autoregulation tries to protect the glomerulus
  2. Albuminuria
  3. Continued high pressure…
    - Arteriolar walls thicken and narrow
    - Kidney function declines irreversibly
  4. Urine formation falls
    - Volume overload
    - Decreased clearance of creatine, urea and waste products
119
Q

For a 35yr old male with the following bp, what is his life expectancy:

  • 120/80
  • 140/100
  • 150/120
A
  • 120/80 = 38-40yrs
  • 140/100 = 15-20yrs
  • 150/120 = 8-10yrs
120
Q

What 7 life style changes can be made to reduce hypertension?

A
  1. Decrease alcohol intake
  2. Stop smoking
  3. Increase intake of unrefined carbs
  4. Crease fat intake
  5. Crease Na intake
  6. Increase fruit and veg intake (K+)
  7. Increase aerobic exercise
121
Q

Phrenic nerves: Anterior or posterior to lung roots?

A

Anterior

122
Q 
Borders of the heart:
Anterior/sternocostal surface?
Posterior?
Right?
Inferior?
Superior?
A

Anterior/sternocostal surface: Right ventricle
Posterior: Left atrium
Right: Right auricle and atrium
Inferior: Right and left ventricle
Superior: Auricular appendages and great vessels

123
Q

What muscular features are present on the anterior part of the RA?

A

Ridged by MUSCULI PECTINATI extending from the CRISTA TERMINALIS

124
Q 
What are the names of the cusps in the:
Tricuspid valve?
Pulmonary?
Mitral?
Aortic?
A 
Tricuspid: Septal, Anterior, 
Posterior
Pulmonary: Anterior, right, left 
Mitral: Anterior, posterior
Aortic: Right, left, posterior
125
Q

What is a central line?

A

A central line is a large bore cannula or catheter into one of the larger veins in the body.
Insertion: Internal jugular vein, subclavian vein RHS*

126
Q

Name 5 reasons for inserting a central line

A
  1. Measurement of central venous pressure (CVP)
  2. Administration of drugs that would damage smaller caliber veins such as chemo
  3. Venous access when peripheral veins are shut down
  4. Administration of high flow fluids
  5. Ease of administration of products in a patient likely to need IV access for several days
127
Q

7 complications that can occur when inserting a central line

A
  1. Puncturing the apex of the lung leading to a
    pneumothorax
  2. Puncturing a major vessel leading to a haemothorax
  3. Accidentally cannulating a large artery
  4. Damage to the thoracic duct if placing a line on the left
  5. Introducing air into the circulation whilst inserting the line and causing an air
    embolism
  6. If inserted under un-sterile conditions then introducing infection to a major blood
    vessel and into the bloodstream
  7. Risk of damage to anomalous venous valves which may result in thrombus formation

MD3001 (12 decks)

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