Cardio Flashcards
1
Q
What can Atherogenesis cause?
A
Heart attack
Stroke
Gangrene of the extremeties
2
Q
What are the risk factors for atherogenesis?
A
Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history
3
Q
Where are atherosclerotic plaques commonly found?
A
Within peripheral and coronary arteries
4
Q
What can the distribution of atherosclerotic plaques be effected by?
A
By haemodynamic factors -
Changes in blood flow/turbulence at bifurcations cause the artery to adjust its wall thickness ∴ develop neointima (new growth)
5
Q
What can occur if an atherosclerosis plaque occludes the vessel lumen?
A
A restriction of blood flow (angina) OR a rupture
6
Q
What are some negative outcomes of inflammation?
A
Artherosclerosis
Rheumatoid arthritis
Ischaemic Heart Disease
Excessive wound healing
7
Q
What are some positive outcomes of inflammation?
A
Deals with : Pathogens, Parasites, Tumours
Wound Healing
8
Q
How are leukocytes guided to the arterial wall?
A
Chemoattractants are released from the endothelium and send signals to leukocytes. They are released from the site of injury, and a concentration-gradient is produced -> ∴ leukocytes move toward arterial wall
9
Q
How do leukocytes transmigrate into the vessel?
A
Selectins on the vessel wall capture the leukocyte and roll it along the vessel wall. Integrins and chemoattractants are responsible for firm adhesion of the leukocytes, and the transmigration into the vessel.
10
Q
What are the 4 stages of the progression of atherosclerosis?
A
- Fatty streaks
- Intermediate lesions
- Fibrous plaques of advanced lesions
- Plaque rupture
11
Q
Describe stage 1 of the progression of atherosclerosis
A
- Fatty streaks
- Appears at a v early age (<10 years)
- Consists of aggregations of lipid-laden macrophages within intimal layer of vessel wall
12
Q
Describe stage 2 of the progression of atherosclerosis
A
- Intermediate lesions
- Composed layers of vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall, isolated pools of extracellular lipid
13
Q
Describe stage 3 of the progression of atherosclerosis
A
- Fibrous plaques OR advanced lesions
- Impedes blood flow
- Prone to rupture
- Covered by dense fibrous cap, made by ECM proteins incl. collagen and elastin
- Laid down by SMC that overlies lipid core and necrotic debris
- May be calcified
- Contains smooth muscle cells, macrophages and foam cells and and T lymphocytes
14
Q
Describe stage 4 of the progression of atherosclerosis
A
- Plaque rupture
- Fibrous cap has to be reabsorbed and redeposited for it to be maintained -> if balance shifts (e.g. in favour of inflammatory conditions), cap becomes weak and plaque ruptures
- Thrombus formation and vessel occlusion
15
Q
What’s another cause of coronary thrombosis?
A
Plaque erosion
16
Q
What are the differences between Plaque rupture and Plaque erosion?
A
Plaque erosion :
- Lesions tend to be small lesions
- Collagen triggers the thrombosis
- White thrombus
- Small lipid core
Plaque rupture :
- Big lesion (rupture)
- Tissue factor triggers the thrombosis
- Red thrombus
- Large lipid core
17
Q
When there’s inflammation in the arterial wall, what occurs?
A
LDLs can pass in and out of the wall in XS ∴ accumulation in arterial wall and undergoes oxidation and glycation
∴ Endothelial dysfunction (response to injury hypothesis**)
18
Q
What’s a method to treat coronary artery disease?
A
PCI - percutaneous coronary intervention
19
Q
Describe PCI
A
Percutaneous Coronary Intervention - a family of minimally invasive procedures used to open clogged coronary arteries e.g. stent
20
Q
What’s a major limitation of PCI?
A
Restenosis - when a previously clogged artery that was opened with a stent or angioplasty becomes narrowed again
21
Q
Name some drugs used to treat coronary artery disease and describe their function
A
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel / ticagrelor – inhibits of the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
PCSK9 inhibitors - monoclonal antibodies that inhibit PCSK9 protein in liver -> leads to improved clearance cholesterol from blood
22
Q
What are some major cell types involved in atherogenesis?
A
Endothelium
Macrophages
Smooth muscle cells
Platelets
23
Q
Name a method to improve the duration of stents
A
Drug-eluting stents - anti-proliferative and inhibits healing
24
Q
What is cyclo-oxygenase required for?
A
The synthesis of Thromboxane A2 (TxA2)
25
What does TxA2 stimulate?
Platelet aggregation and vasoconstriction
26
What drug reduces TxA2?
Aspirin
27
What role does P2Y(12) ADP play?
Plays a central role in platelet activation
28
What can ECGs identify?
Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (hyper/hypokalaemia)
Drug toxicity
29
What's the dominant pacemaker of the body and what's its intrinsic rate?
Sinoatrial node (60-100bpm)
30
What are the backup pacemakers of the body and what are their intrinsic rates?
Atrioventricular node (40 - 60bpm)
Ventricular cells (20 - 45bpm)
31
What is the standard calibration of an ECG machine?
25mm/s
0.1mV/mm
32
Describe the route of impulse conduction through the heart
SAN
AVN
Bundle of His
Bundle branches
Pukinje fibres
33
Describe the sections of an ECG wave
**P wave** – atrial depolarisation
**QRS** – ventricular depolarisation
**T wave** – ventricular repolarisation
**The PR interval** – atrial depolarisation and delay in AV junction (delay allows time for the atria to contract before the ventricles contract)
34
What are the two types of leads used in ECGs?
Bipolar leads & Unipolar leads
35
Describe bipolar leads
Two different points of the body (pos & neg)
36
Describe the Unipolar leads
One point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart (only require a positive electrode for monitoring)
37
Name the two types of cardiac myocytes
1. Atrio-ventricular conduction system (slightly faster conduction)
2. General cardiac myocyte
38
What are some common ECG abnormalities related to the P wave?
**Right atrial enlargement** - talkk > 2.5mm - P pulmonale
**Left atrial enlargement** - notched (M-shaped) - P mitrale
**Long PR interval** - first degree heart block
39
What are some common ECG abnormalities related to the QRS complex?
Depth of the S wave should NOT exceed 30mm
Pathological Q wave
= >2mm deep and >1mm wide
= >25% amplitude of the subsequent R wave
QRS axis represents the overall direction of heart's electrical activity ∴ abnormalities of QRS axis are likely to be ventricular enlargement OR conduction blocks
40
Describe a regular ST segment
ST segment usually flat (isoelectric) ∴ elevation/depression by ≥1mm can be pathological
41
Describe a regular T wave
Should be at least 1/8 but less than 2/3 of amplitude of R
**Abnormal** T waves are symmetrical, tall, peaked, biphasic or inverted
T wave amplitude RARELY exceeds 10mm
42
Describe a regular QT interval
Regular interval = 0.35 - 0.45s
& interval decreases when heart rate increases
Should NOT be more than half of interval between adjacent R waves
43
Describe a regular U wave
Small, round, symmetrical and positive in lead II w/ amplitude <2mm
U wave should be same direction as T wave
44
How do you determine heart rate from an ECG?
Rule of 300/1500 – regular rhythms
Count the number of big/small boxes between two QRS complexes and divide this into 300/1500 for regular rhythms.
10 second rule – irregular rhythms
Count the number of beats present on the ECG and multiply by 6.
45
Describe the quadrant approach for the QRS axis
The quadrant approach for the QRS axis
QRS complex in leads I and aVF
Determine if they are predominantly positive or negative
The combination should place the axis into one of the 4 quadrants below
**Lead aVF**
POS | Normal axis | LAD
**Lead 1**|
NEG | RAD | Indeterminate Axis
LAD = left axis deviation
RAD = right axis deviation
46
finish
47
What is the normal systolic ejection fraction?
60 - 65%
48
Define cardiac failure
Failure to transport blood out of the heart
49
What is cardiogenic shock?
**Severe** failure to transport blood out of the heart
50
What is required for relaxation of the heart to occur?
Removal of calcium (energy dependent)
51
Myocardial hypertrophy can be ________
adaptive / physiological
e.g. athletes and pregnancy
52
What happens if you stretch capability of sarcomeres?
Cardiac contraction force diminishes
53
What triggers the hypertrophic response?
Angiotensin-2
ET-1 and insulin-like growth factor 1
TGF - beta
54
What does Left-sided cardiac failure cause?
**Pulmonary Congestion**
LV cannot pump efficiently ∴ blood backs up in veins that take blood to lungs
Pressure in these vessels ↑↑
∴ Fluid pushed into alveoli
**∴ Overload of RHS of heart**
55
What does Right Sided Cardiac Failure cause?
**Venous Hypertension**
High pressure in veins of legs - caused by venous insufficiency where blood leaks downwards due to effect of gravity through leaky valves
∴ Congestion
56
What does Diastolic Cardiac Failure cause?
**Stiffer heart (LV)**
This means LV cannot fill with blood fully during diastole ∴ ↓blood pumped to the body
57
Describe the heart structure up until the 5th week of gestation
Single chamber, divided by intra-ventricular and intra-atrial septa from endocardial cushions
58
How do the further chambers form in the heart after the 5th week of gestation?
Muscular intra-ventricular septum grows upwards from apex of the heart - also allows valve development to occur
59
Define congenital heart disease
A general term for a range of birth defects that affect the normal way the heart works
60
Name the 4 most common congenital heart disease and
Ventricular Septal Defect (VSD)
61
Name the 4 most common congenital heart disease and its % occurence
Ventricular Septal Defect (VSD) 25 - 30%
Atrial Septal Defect (ASD) 10 - 15%
Persistent/Patent Ductus Arteriosus (PDA) 10 - 20%
Fallots 4 - 10%
62
Define multifactorial inheritance
One child with the defect increases the probability of second child with another defect
63
Give some examples of single genes associated with multifactorial inheritance
Trisomy 21, Turner Syndrome (XO)
64
What is Turner Syndrome?
When woman only have 1 X chromosome
Results in short stature and underdeveloped ovaries
65
Give some examples of Homeobox genes associated with multifactorial inheritance
Infections e.g. rubella - causes congenital heart disease in baby if pregnant mother develops rubella
66
Define a cardiac shunt
A pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system
67
What are some causes of a Left-Right cardiac shunt
Ventricular septal defect
Atrial septal defect
Persistent ductus arteriosus
Truncus arteriosus (a single blood vessel comes out of the right and left ventricles)
68
What happens during anomalous pulmonary venous drainage?
Blood flow from some pulmonary veins flows into RA instead of LA ∴ some pulmonary venous flow enters into systemic venous circulation
69
What happens during hypoplastic left heart syndrome?
Left side of heart is not formed correctly
∴ underdeveloped LV
70
What causes a Right-Left cardiac shunt?
Tetralogy of Fallot
Tricuspid atresia - absence of tricuspid valve
71
What are some defects that result in NO shunt. Describe them.
**Complete transposition of great vessels** - an abnormal spatial arrangement of any of the great vessels
**Coarctation** - congenital narrowing of a short section of the aorta
**Pulmonary stenosis** - narrowing at a point from the right ventricle to the pulmonary artery causing obstruction of blood flow
**Aortic stenosis** - narrowing of the aortic valve opening restricting blood flow from the left ventricle to the aorta
**Coronary artery origin from pulmonary artery
Ebstein malformation/anomaly** - faulty tricuspid valve
**Endocardial fibroelastosis** - thickening within the muscular lining of the heart chambers due to an increase in the amount of supporting connective tissue, leading to cardiac hypertrophy
72
Initial Left-Right shunting is ___________
Inefficient
73
What happens if Left-Right shunting progresses and is not repaired?
If progresses to Eisenmenger's complex, this will involve right-left shunting
∴ right side cardiac failure AND right side cardiac hypertrophy
74
What is patent foramen ovale?
A condition that occurs when the foramen ovale present before birth fails to close
75
What does patent foramen ovale cause?
Cardiac Arrythmias
Pulmonary Hypertension
Right ventricular Hypertrophy
Cardiac Failure
Risk of infective endocarditis
76
What is the ductus arteriosus?
A blood vessel connecting the pulmonary artery to proximal descending aorta before birth. Should occlude once baby starts breathing
77
What does patent ductus arteriosus cause?
Left-right shunt overloads lung circulation w/ pulmonary hypertention ∴ right side cardiac failure
Causes risk of infecting endocarditis
78
How can patent ductus arteriosus be treated?
Can be closed surgically, by catheters OR by prostaglandin inhibitors
79
What are the main 4 features of Tetralogy of Fallot?
1. Pulmonary stenosis
2. Ventricular septal defect
3. Dextroposition / Over-riding aorta (aorta straddles the VSD)
4. Right ventricle hypertrophy
80
What is pulmonary stenosis?
Narrowing of the valve between RV and lungs
∴ reduced blood flow
81
What is ventricular septal defect?
Hole in the ventricular septum, causes increased blood pressure
∴ decreased blood flow
82
//
83
What is angina?
A symptom which occurs as a result of restricted coronary blood flow, almost exclusively secondary to atheroscelorisis.
84
What are the types of angina?
Stable
Unstable
Prinzmetal's
Microvascular
Crescendo
85
What is Pouisuille's Law?
Very small reduction in blood vessel causes large difference to blood flow
86
Describe the causes of O2 supply demand mismatch
Impairment of blood flow by proximal arterial stenosis
Increased distal resistance e.g. LV hypertrophy
Reduced oxygen-carrying capability in blood vessel causes large difference to blood flow
87
What is the flow through the vascular system determined by in a healthy system? Why?
Resistance of microvascular vessels
Because the resistance of the epicardial artery is negligible
88
What is the total flow through the vascular system?
~ 3ml/s
89
During exercise, in a healthy system, what happens?
More flow required to meet metabolic demand
∴ Microvascular resistance ↓
∴ Flow can increase up to 5x (15ml/s)
90
What does epicardial disease due to the resistance of the epicardial vessel? How does the microvascular resistance respond?
**Increases**
∴ Microvascular resistance **reduces** so flow is maintained at 3ml/s
91
What happens during exercise in a person with epicardial disease?
Epicardial resistance is high (due to stenosis)
∴ Microvascular resistance ↓ to increase flow
BUT at a point, microvascular resistance cannot fall any further
∴ Flow CANNOT meet metabolic demand
∴ Myocardium becomes ischaemic & pain is experienced
The only way to reverse this is to rest and reduce the demand for flow.
92
Name the non-modifiable risk factors for stable angina
Gender
Family history
Personal history
Age
93
Name the modifiable risk factors for stable angina
Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Sedentary lifestyle
Stress
94
What is a precipitant of angina?
A precipitant reduces blood supply/ increases demand.
95
Name the precipitants of angina that affect supply
Anaemia
Hypoxemia
Hypothermia
Hypovolaemia
Hypervolaemia
96
Name the precipitants of angina that affect demand
Hypertension
Hyperthyroidism
Valvular heart disease
Tachyarrhythmia
Cold weather
97
/inherited cardiac conditions
98
What is cardiomyopathy?
A primary heart muscle disease, often genetic. ALL cardiomyopathies carry an arrhythmic risk.
99
What is Hypertrophic cardiomyopathy (HCM) caused by?
Sarcomeric protein gene mutations
100
List some signs and symptoms for HCM
Angine
Dyspnoea
Palpitations
Dizzy spells
Syncope
101
What could be a feature of HCM?
Left ventricular outflow tract (LVOT) obstruction
102
What is Dilated cardiomyopathy (DCM) caused by?
Cytoskeletal gene mutations
103
What symptoms are associted with DCM?
Heart failure symptoms
104
What occurs in DCM?
LV/RV OR 4 chamber dilation and dysfunction
105
What is Arrhythmia cardiomyopathy (ARVC/ALVC) caused by?
Desmosome gene mutations
106
What occurs with ARVC?
May be some structural change OR may diffusely involve RV and LV
107
What is the main feature of arrhythmogenic cardiomyopathy?
Arrhythmia cardiomyopathy
108
What causes Channelopathy?
It's an inherited arrhythmia caused by ion channel protein gene mutations
109
How is the structure effected in Channelopathy?
Structurally normal
110
What are signs of Channelopathy?
Long QT / short QT
Brugada (abnormal electrical activity of the heart)
111
What channels does channelopathy usually effect?*
Potassium, sodium or calcium channels
112
What symptoms does channelopathy present with?
Recurrent syncope
113
What can QT prolonging drugs do to people with long QT symdrome?
Kill them
114
What is sudden cardiac death most likely due to?
An inherited condition
e.g. cardiomyopathy or ion channelopathy
115
What do sudden arrhythmic death syndromes (SADs) usually refer to?*
Normal heart arrhythmia
116
What is Familial hypercholestrolaemia (FH)?
An inherited abnormality of cholesterol metabolism (abnormal LDL protein)
117
What can FH lead to?
Serious premature coronary and other vascular disease
118
Inherited cardiac conditions are usually _______________
Dominantly inherited - offspring have 50% risk of inheritance
∴ family evaluation is essential
119
Name some aortovascular syndromes
Marfan
Loeys - Dietz
Vascular Ehler Danlos (EDS)
120
Describe the anatomy of pericarditis
**2** layers which are continuous
1. **Serous visceral** (single cell layer adherent to epicardium)
2. **Fibrous parietal** (2mm thick layer, has fibrous attachments to fix heart in thorax)
121
What is the mechanical function of the pericardium?
Restrains the filling volume of the heart
122
Describe the properties of the pericardium
Similar properties to rubber - initially stretchy but becomes stiff at high tension
Sac has a small reserve volume
123
Define tamponade physiology
Small amount of volume added to space has a dramatic effect on filling
But so does removal of a small amount
124
Describe chronic pericardial effusion and its effect of filling
Chronic accumulation allows adaptation of the parietal pericardium
This reduces effect of diastolic filling of the chambers
∴ V Slow accumulating effusions rarely cause tamponade
125
What are the main clinical indications for ACE inhibitors?
Hypertension
Heart failure
Diabetic nephropathy
126
What are the main adverse effects for ACE inhibitors?
**1. Related to reduced angiotensin II formation**
results in ->
Hypotension, Acute renal failure, Hyperkalaemia, Teratogenic effects in pregnancy
**2. Related to increased kinin production**
results in ->
Cough, Rash, Anaphylactoid reactions
127
What are the main clinical indications of ARB?
Hypertension
Diabetic nephropathy
Heart failure (when ACE - I contracindiated)
128
What are the main adverse effects of ARB?
Symptomatic hypotension (esp. vol deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema
Contraindicated in pregnancy
Usually very well tolerated though
129
What are the main clinical indications of CCB?
Hypertension
Ischaemic Heart Disease - angina
Arrhythmia (tachycardia)
130
What are the three types of CCB?
1. Dihydropyridines
2. Phenylalkylamines
3. Benzothiazepines
131
Give examples of dihydropyridines
Nifedipine, amlodopine, felodipine, lacidipine
132
Give an example of phenylalkylamines
Verapamil
133
Give an example of Benzothiazepines
Diltiazem
134
Give the adverse effects of CCB and what is it due to?
1. Due to **peripheral vasodilation** (mainly dihydropyridines)
Flushing
Headache
Oedema
Palpitations
2. Due to negatively **chronotropic effects** (mainly verapamil/diltiazem)
Bradychardia
Atrioventricular block
3. Due to **negatively inotropic effects** (mainly verapamil)
Worsening of cardiac failure
4. Verapamil causes constipation
135
What are the main clinical indications?
IHD
Heart failure
Arrhythmia
Hypertension
136
What are the main clinical indications of Diuretics?
Hypertension
Heart failure
137
What effect does aspirin have when taken for angina?
Antiplatelet effect ∴ avoids thrombosis
138
Name a side effect of aspirin
Gastric ulceration
139
How does aspirin reduce platelet aggregation?
COX inhibitor
∴ ↓prostaglandin synthesis (incl. TxA2)
∴ ↓platelet aggregation
140
What do betablockers do when prescribed for angina?
Reduces force of contraction of heart
141
What are the side effects of BB?
Fatigue
Trouble sleeping/nightmares
Bradycardia
Erectile dysfunction
Cold hands/feet
**Worsens asthma, heart failure, hypotension and bradyarrhythmias !!!**
142
Describe how betablockers reduce the force of contractions
Act on B1 receptors in heart (adrenergic sympathetic pathway)
∴
↓ Heart rate
↓ LV contractility
↓ Cardiac output
143
How does GTN spray reduce angina symptoms?
Dilates systemic veins
∴ ↓ Reduces venous return to right heart
∴ Reduces preload
∴ ↓ Workload of heart and O2 demand
ALSO dilates coronary arteries
144
State the side effects of GTN spray
Headache immediately after use
145
GTN spray is a nitrate that is a ______dilator
**Veno**dilator
146
CCB is a primary _____dilators
**Artero**dilators
147
How do CCBs work to treat angina?
Dilates systemic arteries ∴ ↓ BP drop
∴ ↓ afterload on heart
∴ ↓ Energy req. to produce same cardiac output
∴ ↓ work on heart and O2 demand
148
Describe the physiology of Tetralogy of Fallot
Stenosis of RV outflow -> RV is at a higher pressure than LV
∴ Deoxygenated blood passes from RV to LV
∴ Patients are 'blue'
149
Describe Ventricular septal defect (VSD)
Abnormal connection between the 2 ventricles
150
Describe the physiology of Ventricular septal defects
↑ Pressure LV
↓ Pressure RV
∴ Blood flows from high pressure -> low pressure (not blue)
∴ Increased blood flow through lungs
151
State some symptoms of VSD
↑↑ High pulmonary blood flow in infancy
Breathless
Poor feeding
Failure to thrive
152
State some clinical signs of VSD
Small, breathless, skinny baby
↑Resp rate
Tachycardia
Big heart on CXR
Murmur varies in intensity
153
eisenmengers syndrome
154
What is Atrial Septal Defect? (ASD)
An abnormal connection between two atria
155
Describe the physiology of ASD
Slightly higher pressure in LA than RA
∴ Shunt is left to right (∴ not blue)
↑ Flow into R.Heart and lungs
156
State some symptoms of ASD
↑↑ Flow through R Heart and lungs in youth
R heart dilation
Shortness of breath on exertion
↑ Chest infections
157
State some clinical signs of ASD
Pulmonary flow murmur
Fixed split second heart sound (bc delayed closer of PV bc more blood to get out)
Big heart and pulmonary arteries on CXR
158
Describe a Atrio-ventricular septal defect
A hole in the centre of heart
Can be complete of partial
Involved ventricular septum, atrial septum & mitral and tricuspid valves
Instead of 2 AV valves, there is one big malformed valve
159
What occurs with ASD (complete defect)?
Poor feeding / poor weight gain
Torrential pulmonary blood flow
Breathless as neonate
Needs repair or PA band in infancy
160
What occurs with ASD (partial defect)?
Presents like a small VSD/ASD
Can present in late adulthood
May be left alone if no R heart dilation
161
What occurs with patent ductus arteriousus?
Ductus arteriosus fails to close after birth
∴ Vessel formed connecting aorta and pulmonary artery
162
What are some clinical signs of PDA?
Continuous murmur
If large - BIG heart, breathless
Eisenmenger's syndrome - cyanosis
163
What symptoms does PDA present?
Breathless
Poor feeding
Failure to thrive
Torrential flow from aorta to pulmonary arteries in infancy
164
What is usually done to treat PDA?
Surgical closure under local anaesthetic.
(Has low risk of complications)
165
Define Conn's syndrome
The overproduction of aldosterone due to unilateral adrenal adenoma.
166
What does Conn's syndrome result in?
Sodium and water retention
167
Name the causes of Hypertension and what % of cases they result in
85% are primary and aetiology is unknown
10% are due to overproduction of aldosterone (Conn's syndrome)
5% are due to cases such as renal failure, drugs and rare hormone secreting tumours
168
What are some drugs that cause hypertension?
NSAIDs
Combined oral contraceptive
Corticosteroids
Ciclosporin
Cold cures
Antidepressants
Illicit drugs e.g. cocaine, amphetamines
169
Name some lifestyle causes of hypertension
Excessive salt and alcohol intake
Obesity
170
What is the Framingham scale?
Framingham Coronary Heart Disease Risk Score estimates risk of heart attack in 10 years
171
Name the methods of treatment for hypertension
CCBs
ACE inhibitors
ARBs
Thiazide diuretics
172
How do CCBs work?
Inhibit the opening of voltage-gated calcium channels in vascular smooth muscle
∴ ↓ Calcium entering muscle
∴ ↓ Calcium available for muscle contraction
173
Give an example of a CCB
Dihydropidines
174
Describe how ACE inhibitors work
Prevent the generation of Angiotensin II from Angiotensin I
175
Give examples of ACE inhibitors
Ramipril
Captopril
176
Describe how ARBs work
Block the action of angiotensin II at peripheral angiotensin II receptors
177
Which drug inhibits renin?
Aliskiren
178
How do Thiazide diuretics work?
They inhibit sodium reabsorption by DCT
∴ ↓ ECF vol (which is elevated in hypertension)
179
Give an example of a thiazide diuretic
Bendroflumethiazide
