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The development of cardiorespiratory disease > PBL 49 > Flashcards

PBL 49 Flashcards

1
Q

Explain the MoA of ACE inhibitors

A

Block ACE in the lungs, this prevents Ang I to Ang II conversion.
Fall in BP from EFFERENT arteriole CONSTRICTION due to increased GFR, this leads to >filtration fraction and therefore increased urine OUTPUT

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2
Q

Side effects of ACE inhibitors

A
  • Dry cough
  • Rash
  • Angio-oedema
  • Hyperkalaemia
  • Dizziness (from hypotension)
  • Fatigue
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3
Q

MoA of warfarin

A

Vitamin K reductase inhibitor which is used to make clotting factors, so it is an anti-coagulant

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4
Q

Which clotting factors are affected by vitamin K reductase inhibition?

A
  1. Prothrombin
  2. VIIa (7a)
  3. IX (9)
  4. Protein C
  5. Protein S
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5
Q

Side effects of warfarin

A
  • Severe bleeding incl. heavier than usual menstrual bleeding
  • Red or brown urine
  • Black or bloody stool
  • Severe headache or stomach pain
  • Haemoptysis
  • Joint pain
  • Vomiting blood
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6
Q

MoA of heparin

A

ANTICOAGULANT
Binds to enzyme inhibitor antithrombin III (AT)
AT will then inactivate thrombin, factor Xa and other proteases to inhibit thrombosis

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7
Q

Side effects of heparin

A
  • Bruising more easily
  • Bleeding that takes longer to stop
  • Irritation/pain/redness/sores at injection site
  • Allergic reactions such as hives/chills/fever
  • Increased liver enzymes on liver function test
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8
Q

Give examples of selective, non-selective and additional alpha-blocking beta blockers

A

Selective: Atenolol, bisoprolol, metoprolol

Non-selective: Propanolol, timolol

Alpha-blocking: Carvedilol, labetolol

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9
Q

MoA of beta blockers

A
  • Inhibit sympathetic stimulation by blocking the effects of adrenaline on B1 and B2 receptors (depending on selectivity)
  • Reduces HR, contractility and blood pressure to improve myocardial O2 supply/demand ratio
  • Reduces excitability of cardiac tissue and prevalence of arrhythmias (adrenaline increases inward Na+ and Ca2+ current)
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10
Q

Side effects of beta blockers

A
  • Worsen heart failure
  • Fall in BP –> can affect kidneys so you start with a low dose bb
  • Fall in HR
  • General sluggishness
  • Cold peripheries
  • Wheeze (contraindicated in brittle asthmatics)
  • Dizziness/lightheadedness
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11
Q

MoA of alpha blockers

A

Block peripheral alpha-1 receptors which mediate sympathetic vasoconstriction, so you get vasodilation and a reduction in BP

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12
Q

Examples of alpha blockers

A

Doxasozin
Prazosin
Tamsulosin
Phenoxybenzamine

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13
Q

Side effects of alpha blockers

A

Postural hypotension
Headaches
Nausea
Dizziness
Lethargy
Swollen legs/ankles
Sleep disturbances
Tremor

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14
Q

Mechanism of diuretics: thiazides

A

Act on the DCT where they inhibit the sodium-chloride symporter leading to increased Na & Cl EXCRETION and therefore >H2O excretion, lowering the BP

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15
Q

Side effects of thiazides

A

Feeling thirsty w/dry mouth
HYPERURICAEMIA
Nausea/vomiting
Stomach pain
Diarrhoea
Loss of appetite
Constipation
Severe joint pain
Feeling dizzy and faint

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16
Q

Mechanism of diuretics: Mineralocorticoid receptor (aldosterone) antagonist
- What is the function of the receptor in general?

A

The action of the mineralocorticoid receptor (DCT) is to promote renal sodium retention, potassium excretion and inducing hypertension upon excessive activation
- This is blocked by antagonists which will lead to Na+ EXCRETION and K+ RETENTION (K+ sparing)

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17
Q

Examples of mineralocorticoid receptor/aldosterone antagonists

A

Spironolactone
Amiloride
Eplerenone

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18
Q

Side effects of mineralocorticoid receptor/aldosterone antagonists

A

HYPERKALAEMIA
Gynaecomastia (but NOT with eplerenone)
Drowsiness
Dizziness
Light-headedness
Upset stomach –> diarrhoea/nausea/vomiting
Headache

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19
Q

Mechanism of diuretics: loop diuretics

A

Inhibit the Na/K/2Cl co-transporter in the thick ascending loop of Henle in the renal tubule
- This prevents the transport of sodium ions from the lumenal side into the basolateral side for reabsorption. This inhibition results in increased excretion of H2O along with Na, Cl, Mg, Ca, H+, and K+ ions

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20
Q

Example of a loop diuretic

A

Furosemide

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21
Q

Side effects of loop diuretics

A

Hypokalaemia
Hyponatraemia
Hyperuricaemia –> gout
Nausea/vomiting
Diarrhoea
Constipation
Stomach cramping
Vertigo
Dizziness
Headache
Blurred visions

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22
Q

Mechanism of diuretics: osmotic diuretics

A
  • Elevate blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and CSF, into interstitial fluid and plasma
  • Promotes diuresis in kidneys by increasing the concentration of filtrates in the kidney and blocking reabsorption of water by kidney tubules
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23
Q

Example of an osmotic diuretic

A

Mannitol

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24
Q

Side effects of osmotic diuretics

A

Dehydration
Headache
Nausea
Vomiting
Diarrhoea
Dry mouth
Thirst
Blurred vision

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25
Q

Mechanism of diuretics: Carbonic anhydrase inhibitors

A
  • Inhibits CA and therefore causing an accumulation of carbonic acid
  • The mechanism of diuresis involves the proximal tubule of the kidney. CA is found here allowing the resorption of bicarbonate, sodium, and chloride. By inhibiting this enzyme, these ions are excreted, along with excess water, lowering BP, ICP and intraocular pressure.
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26
Q

Example of a carbonic anhydrase inhibitor

A

Acetazolamide

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27
Q

Side effects of carbonic anhydrase inhibitors

A

Blurred vision
Dry mouth
Drowsiness
Loss of appetite
Nausea/vomiting
Diarrhoea
Changes in taste

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28
Q

MoA of digoxin

A
  • Inhibits the Na/K+ ATPase, allowing more Na+ to remain within the cell. This will work upon the NCX, allowing more Ca2+ to be released by SERCA and more available for troponin C, >inotropy
  • Has parasympathomimetic effects on the AV node, so it activates vagal efferent nerves to the heart, slowing electrical conduction in the AV node, therefore, decreasing heart rate,
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29
Q

Side effects of digoxin

A

Confusion
Dizziness
Malaise
Loss of appetite
Nausea/vomiting
Diarrhoea
Blurred vision
Skin rashes

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30
Q

MoA of oral anticoagulants

A

Inhibit the formation of fibrin clots in the final common pathway of the coagulation cascade, decreased fibrin formation and reduced thrombin-stimulated platelet aggregation will prevent the formation of thrombin

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31
Q

What are oral anticoagulants used for?

A

Prevent blood clots
Prevent stroke and embolism in those with AF

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32
Q

Examples of oral anticoagulants

A

Rivaroxaban (FXa)
Dabigatran (FIIa)
Apixaban (FXa)
Edoxaban (FXa)
Betrixaban (FXa)

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33
Q

Mechanism of angiotensin receptor blockers

A
  • AKA angiotensin II receptor antagonists
  • Block angiotensin II action at the AT1R and AT2R
  • Ang II has a powerful vasoconstricting effect, increasing blood pressure. - - It also has aldosterone-secreting effects which are selectively blocked by ARBs as they block the binding of angiotensin II to the AT1 receptor.
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34
Q

Examples of ARBs

A

Losartan
Candesartan
Valsartan
Irbesartan

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35
Q

Side effects of ARBs

A

Headache
Fainting
Dizziness
Fatigue
Respiratory symptoms
Vomiting
Diarrhoea
Back pain
Leg swelling

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36
Q

MoA of calcium channel blockers
- What is the difference between dihydropyridines and non-dihydropyridines?

A
  • Class IV anti-arrhythmia drugs
  • Dihydropyridines have MORE effect on vasodilation and LESS on heart function, whereas non-dihydropyridines have less effect on vasodilation and more on heart function
  • Blocking Ca2+ entry to the heart will cause a reduced HR, LV contraction, BP and reduced myocardial O2 demand
37
Q

What are calcium channel blockers used for?

A

Hypertension
Angina
Arrhythmia

38
Q

Examples of dihydropyridine vs non-dihydropyridine calcium channel blockers

A

DHPR: amlodipine, nifedipine

NDHPR: verapamil, diltiazem

39
Q

Side effects of calcium channel blockers

A

Leg swelling
Constipation
Dizziness
Palpitations
Fatigue
Flushing
Headache
Nausea
Rash

40
Q

What is heart failure?

A

The inability of the heart to pump blood around the body, mainly due to LV failure/impairment

41
Q

What is the meaning of left ventricular end diastolic volume?

A

The volume of blood in the left ventricle just prior to the heart beat

42
Q

What is the meaning of left ventricular end systolic volume?

A

The volume of blood in the left ventricle at the end of the heart beat

43
Q

The difference between acute heart failure and chronic heart failure

A

Acute heart failure occurs suddenly and is a medical emergency, whereas chronic heart failure develops over time, they have different pathophysiologies

44
Q

What are the typical presentations of AHF?

A

Pulmonary oedema and anasarca (peripheral oedema)

45
Q

Explain the pathophysiology of AHF

A
  1. LV impairment
  2. Increased LVEDV –> Increased LVEDP since there is less blood being pumped around the body per cardiac cycle
  3. Increasing LVEDP will cause an increase in LA pressure and when LA pressure > capillary colloid osmotic pressure of pulmonary veins (the force that pushes fluid into the blood capillaries), the fluid from the intravascular space will be forced into the alveoli –> PULMONARY OEDEMA
  4. Fluid in the alveoli will lead to hypoxia, as the alveoli are filled with fluid and cannot transport sufficient O2
46
Q

Explain how AHF can lead to anasarca/peripheral oedema

A
  • Same mechanism as cor pulmonale
  1. Pulmonary oedema causes hypoxia
  2. Hypoxia causes pulmonary hypertension
  3. Pulmonary hypertension causes RV strain which can lead to RV hypertrophy and RV impairment
  4. RV impairment causes increased in pressure build up in the RV
  5. Increased RV pressure leads to increased RA pressure
  6. Increased RA pressure will cause a back-log onto the vena cava, specifically the SVC, as it can no longer pump blood to the lungs efficiently through the pulmonary arteries
  7. Fluid travels backwards through the SVC to the legs, ankles and abdomen where it accumulates and presents as peripheral oedema
47
Q

Signs and symptoms of AHF

A

Breathlessness
Difficulty talking
Orthopnoea and PND
Accessory muscle use ++
Pink, frothy sputum
Sweating
Cold/clammy
Cyanosed
Extreme hypotension due to cardiogenic shock

48
Q

Risk factors for AHF

A
  • Coronary artery disease
  • Hypertension
  • Diabetes
  • MI
  • Arrhythmia
  • Pulmonary embolism
  • Cardiomyopathy
  • Medications
  • Sleep apnoea
  • Heart defects
  • Alcohol misuse or other toxic drugs
  • Viral infections affecting the heart
  • Kidney problems
49
Q

Diagnosis of AHF

A
  • CV examination
  • CXR
  • ECG
  • ECHO
  • Angiogram
  • NT-proBNP - elevated in those with heart failure
  • CT
  • MRI
50
Q

Treatment of AHF

A

N.B it is a medical emergency so treatment is in hospital

  1. IV opiates to relieve anxiety and vasodilation = MORPHINE/DIAMORPHINE
  2. O2 as the patient will be hypoxic
  3. IV furosemide for the pulmonary and peripheral oedema
  4. IV nitrate as a vasodilator to reduce preload and afterload
  5. CPAP or IPPV
  6. Dobutamine as inotropic support as patients will often be in cardiogenic shock
51
Q

What makes furosemide ideal for treatment of pulmonary oedema?

A

Furosemide exerts direct vasodilatory effects, which results in its therapeutic effectiveness in the treatment of acute pulmonary oedema

Vasodilation leads to reduced responsiveness to vasoconstrictors, such as angiotensin II and noradrenaline, and decreased production of endogenous natriuretic hormones with vasoconstricting properties.

It also leads to increased production of prostaglandins with vasodilating properties

52
Q

Characteristics of anasarca/peripheral oedema

A

Pitting oedema
Ascites
Pleural effusions

53
Q

Treatment of anasarca/peripheral oedema

A

Bed rest to get help from gravity - LMWH as prophylaxis for DVT

  • IV furosemide until the patient is euvolemic then bumetanide which has a better absorption and fewer side effects than furosemide. Commonly use diuretics with different mechanisms to increase effectiveness such as a thiazide
54
Q

Explain the pathophysiology of CHF

A
  • Occurs gradually, over time
  1. LV pump failure causes reduced BP, causing steps 2 and 3
  2. Firstly, activation of the sympathetic nervous system causes vasoconstriction, this causes increased AFTERLOAD to restore BP and perfuse organs
  3. Secondly, RAAS is activated to increase the BP. You get increased Na and H2O retention, leading to increased BP and increased PRELOAD, advantageous in this moment but not in the long term
  4. Increased preload and afterload causes the heart to become over-worked and leads to further negative remodelling and exacerbation of LV pump failure & function.
55
Q

What is preload?

A

Volume of blood in the ventricles at the end of diastole (EDP)

56
Q

What is afterload?

A

The resistance that the left ventricle must overcome to circulate blood

57
Q

Consequences of CHF

A
  1. Reduced kidney perfusion causes more aldosterone release from the adrenal gland which has an important role in heart failure, it will lead to myocardial fibrosis
  2. > ANP and >BNP release
  3. Cachexia as there is a reduction in muscle strength and endurance
  4. Impaired ergoreflex: much greater spike in ventilation required for the same amount of exercise. Also, increased resting energy expenditure & resting O2 consumption
58
Q

Signs and symptoms of CHF

A

Breathlessness
Fatigue
Ankle swelling
Chest pain
Persistent cough which may be worse at night

  • Less common:
    Loss of appetite
    Wheezing
    Weight gain or loss
    Bloated stomach
    Confusion
    Dizziness/fainting
    Tachycardia
    Pounding, fluttering or irregular heart beat
59
Q

Risk factors for CHF

A
  1. CAD
  2. Hypertension
  3. Diabetes
  4. Cardiomyopathy
  5. Damaged or inflamed heart
  6. Arrhythmia
  7. Congenital heart conditions
  8. Disease of the heart valve
  9. Myocarditis
  10. Chemo drugs and cocaine
  11. Xs alcohol consumption
  12. Thyroid gland disease
  13. Anaemia
60
Q

Diagnosis for CHF

A

CV examination
CXR
ECG
ECHO
Angiogram
NT-proBNP
CT
MRI

61
Q

Treatment for CHF

A
  • If it is heart failure with preserved ejection fraction, where the problem is NOT the LV failing to pump, but more so relaxation of the LV, treat the cause which is most commonly OBESITY, DIABETES and HYPERTENSION
  • If it is due to left ventricular dysfunction, first line is ACEi and beta blocker
    If intolerant to ACEi, give an ARB

If symptoms persist then consider (in order of symptoms still persisting):
1. Aldosterone antagonist
2. ARB
3. Hydralazine in combination with nitrate
4. CRT or digoxin
- Can offer triple therapy of ACEi + BB + aldosterone antagonist

  • Ivabradine and entresto can be offered
62
Q

MoA of ivabradine

A

Inhibits the If channel in SAN, reducing HR and can reduce hospitalisation for those with heart failure

63
Q

MoA of entresto

A

New medication prescribed ONLY by cardiologists
- Combination of sacubitril (NEP) and valsartan (ARB)

64
Q

People with CHF should not be given which medications?

A
  1. Calcium antagonists –> Amlodipine
  2. Aspirin
  3. Statins
65
Q

Lifestyle and dietary changes for CHF

A
  1. Stop smoking
  2. Limit alcohol intake
  3. Lose weight –> less stress on heart
  4. Regular exercise
  5. Mediterranean diet
  6. Keep on top of existing health conditions
  7. Limit salt intake –> reduces fluid retention
  8. Weigh yourselves daily –> if weight increases by >2kg over 1-3 day period, contact a doctor
66
Q

Which blood pressure values show hypertension?

A

140/90mm/Hg or 150/90 if >80y/o

67
Q

What is primary vs secondary hypertension?

A

Primary hypertension represents 90-95% of hypertensive patients, where there is NO KNOWN CAUSE and develops over many years

Secondary hypertension is when there is an identifiable underlying cause, approx 5-10% of cases

68
Q

What are the changes seen in primary hypertension?

A

Early:
1. Increased blood volume and CO
2. Increased Na+ retention

Longer term:
1. Blood volume and CO become normal
2. Increased vascular tone due to >sympathetic activity and >AngII levels
3. Thickening of resistance vessels walls and reduction in lumen diameters
4. Abnormal endothelial function, esp those with diabetes, less NO production by the endothelium and smooth muscle cells are less responsive to NO

69
Q

For the blood pressure to increase, there has to be 1 of:

A
  1. Increased CO
  2. Increased systemic vascular resistance
  3. Increased neurohumoral activation
  4. Increased blood volume
70
Q

Give some causes of secondary hypertension

A
  1. Renal artery stenosis
  2. Chronic renal disease
  3. Primary hyperaldosteronism
  4. Phaeochromocytoma
  5. Coarctation of the aorta
  6. Other causes:
    - Cushing syndrome
    - Pregnancy
    - Thyroid disease
    - Sleep apnoea
    - Alcohol
    - SAME
    - Certain medications: birth control, cold remedies, decongestants, over-the-counter pain relief
71
Q

Explain how renal artery stenosis leads to hypertension

A
  • Commonly seen in young women
  • Severe narrowing at the origin of the renal artery, leading to renin release and therefore >AngII and >Aldosterone
  • Ang II causes cardiac and vascular hypertrophy via sympathetic activation which leads to >blood volume, CO and vascular resistance
72
Q

Explain how chronic renal disease leads to hypertension

A
  • IT IS A COMMON CAUSE OF HYPERTENSION
  • Lots of underlying causes such as diabetic neuropathy and glomerulonephritis
  • Whichever process is causing it, there will be Na and H2O retention, whilst also an increase in renin, so the increase in BP is an attempt by the body to restore GFR which makes the problem worse
73
Q

Explain how primary hyperaldosteronism can lead to hypertension

A
  • CONN’S SYNDROME
  • Adenal tumours or, more commonly, adrenal hyperplasia will lead to Xs aldosterone production
  • > aldosterone leads to >Na and H2O retention
74
Q

What is phaeochromocytoma and how can this lead to hypertension
A - Other adverse effects of this?
B - How is this diagnosed?

A
  • It is when the adrenal glands release too many catecholamines (A/NA)
  • You get alpha mediated vasoconstriction and beta mediated cardiac stimulation which leads to >BP and tachycardia

A - May cause cardiomyopathy so they can present with heart failure
B - Diagnosed with 24hr urinary catecholamine presence

75
Q

What is coarctation of the aorta and how can this lead to hypertension?

A
  • Stenosis of the aorta just below the level of the left subclavian artery
  • Causes hypoperfusion of the kidneys leading to activation of RAAS
76
Q

What is accelerated hypertension?

A

A recent significant elevation over baseline blood pressure that is associated with target organ damage

77
Q

How does accelerated hypertension normally present?

A

• You see fibrinoid necrosis of the small arteries and arterioles
• Damage to RBCs as they negotiate vessels obstructed by fibrin with resulting microangiopathic haemolytic anaemia
• You lose auto-regulation of cerebral blood flow, so you get dilatation of cerebral arteries
• As auto-regulation fails, the arterioles dilate, causing hypoperfusion which can cause cerebral oedema and lead to hypertensive encephalopathy. So you get papilloedema due to high levels of pressure within the brain, this is a life-threatening emergency and can lead to seizure and death

78
Q

Who is at risk of accelerated hypertension?

A

Men
Smokers
Those with 2y hypertension

79
Q

Signs and symptoms of hypertension

A
  • Most people have no signs or symptoms
  • Visual disturbances
  • Headaches
  • Irregular heart rhythm
  • SOB
  • Nose bleeds

Severe hypertension can cause:
- Fatigue
- Nausea
- Vomiting
- Confusion
- Anxiety
- Chest pain
- Muscle tremors

80
Q

Complications of hypertension

A
  • MI
  • Stroke
  • Aneurysm
  • Heart failure
  • Weakened or narrowed kidney blood vessels
  • Thickened, narrowed or torn blood vessels in the eye
  • Metabolic syndrome
  • Trouble with memory or understanding
  • Dementia
81
Q

Risk factors for hypertension

A
  • Age
  • FHx
  • African or Caribbean origin
  • High salt diet
  • Obesity
  • Lack of exercise
  • Xs alcohol consumption
  • Smoking
  • Long-term sleep deprivation
82
Q

Diagnosis of hypertension

A

Sphygmomanometer
Ambulatory 24hr BP monitoring
Home testing

83
Q

Treatment of hypertension

A

ABCD
1. ACEi
2. BB
3. Calcium channel blocker
4. Diuretic

  • <55y/o start with ACEi
  • > 55 or black of African or Caribbean family origin, start with a calcium channel blocker
  • If more is needed give: A + C, then A + C + D, then A + C + D + further diuretic, or alpha blocker
84
Q

Long term consequences of hypertension on end organs: heart

A
  • Coronary atheroma –> Increased MI risk
  • Pulmonary atheroma
  • LV hypertrophy
85
Q

Long term consequences of hypertension on end organs: aorta

A
  • Atheroma
  • Aneurysm - may rupture/dissect
  • Aortic dissection (intima is torn off the rest of the aorta by pressure)
86
Q

Long term consequences of hypertension on end organs: brain

A
  • Stroke both ischaemic and haemorrhagic
  • Ischaemic = more common in hypertension, increased carotid atheroma, small penetrating arteries
  • Haemorrhagic = small arteries (charcot-bouchard aneurysms) which are tiny aneurysms developing in small arteries and may rupture causing intra-cerebral haemorrhage
87
Q

Long term consequences of hypertension on end organs: kidneys

A
  • Small vessel (hypertensive) disease causes glomerular damage
  • Gradual parenchymal loss accelerates decline in function
  • Large vessel atheromatous disease - atheroma in renal arteries causing renal artery atenosis
  • Kidney damage causes hypertension and hypertension causes kidney damage - often difficult to find out which came first
88
Q

Long term consequences of hypertension on end organs: eyes

A
  • Hypertensive retinopathy
  • Papilloedema if severe
  • AV nipping developed early – as the arteriole crosses the vein, the vein is nipped

The development of cardiorespiratory disease (23 decks)

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