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Year 3 TCDs > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Why is staging of hypertension important?

A

Risk stratification of patients that helps guide towards next management steps

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2
Q

What is hypertension a major risk factor for?

A
  1. Stroke
  2. Ischemic heart disease
  3. Heart failure
  4. Chronic kidney disease
  5. Cognitive decline
  6. Premature death
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3
Q

When trying to diagnose someone with hypertension how do you measure BP?

A

Measure BP in both arms

  • Difference > 15mmHg, repeat
  • If BP > 140/90mmHg, repeat
  • Record lower of 2 measurements

If the recording is 140/90mmHg - 180/120mmHg offer ambulatory blood pressure measurement

  • 2 recordings at least 1min apart
  • Morning + evening
  • Continue for 4-7d
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4
Q

What is the clinical definition of hypertension?

A

HTN ≥ 140/90mmHg in clinic + ABPM average of ≥ 135/85mmHg

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5
Q

Name the grades of HTN

A 
Grade 1 (Mild): 140-159/90-99mmHg
Grade 2 (Mod): 160-179-100-109mmHg
Grade 3 (Severe): >180/>110mmHg
Isolated systolic HTN: >140/<90mmHg
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6
Q

What is a hypertensive crisis? Hypertensive urgency?

A

Hypertensive urgency:

  • No sudden organ damage (i.e. to kidney, heart, brain)
  • Approx 180/110mmHg
  • Symptoms: headache, SOB, nosebleeds, severe anxiety
  • Management: Oral hypertension meds

Hypertensive crisis/malignant hypertension:

  • Target organ damage (~180/120mmHg)
  • Symptoms: chest pain, SOB, back pain, numbness/weakness, vision changes, encephalopathy (cerebral oedema + increased ICP)
  • Management: IV vasodilator, b-blocker, Ca2+ channel blocker (to decrease BP by vasodilating arteries)
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7
Q

What is the pathophysiology of hypertension?

A

BP = CO x PR

Cardiac Output = how much blood each ventricle pumps/min
Peripheral Resistance = resistance to blood flow increases resistance = increased difficulty of blood to get through vessels

  1. HTN = decreased blood flow to kidney -> kidney releases RENIN -> angiotensin -> AT1 -(ACE)–> AT2 -> vasoconstriction -> increased peripheral resistance
  2. Renin also causes the release of Aldosterone -> increased Na+ and H2O absorption -> increased blood volume -> increased CO

Increased PR + CO = Increased blood flow = increased BP

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8
Q

What is the short-term control of BP?

A
  1. Baroreceptors
  2. Chemoreceptors
  3. ANS
    - SNS vasomotor nerve fibres leave cord thru thoracic + lumbar spinal nerves
    - SNS chain: SNS nerves (viscera), Spinal nerves (vasculature)
  • PSNS = vagus nerve
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9
Q

Describe the vasomotor centre

A
  1. Vasoconstrictor area = origin of excitatory preganglionic vasoconstrictor neurons
  2. Vasodilator area = internal inhibition of vasoconstriction
  3. Sensory area = input from vagus and glossopharyngeal nerves modulate vasoconstrictor/vasodilator area activity
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10
Q

What are the vasomotor centre influences?

A
  1. Reticular substance (pons/mesencephalon)
  2. Hypothalamus
  3. Cerebral cortex
  4. Other: cingulate, hippocampus
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11
Q

What are the 4 things to raise arterial pressure?

A
  1. SNS release NA from nerve terminals
  2. NA acts on a-adrenergic receptors of the VSMC (vascular smooth muscle cells)
  3. All arterioles constricted
  4. Heart directly stimulated
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12
Q

What 3 vessel areas are not innervated?

A
  1. Capillaries
  2. Pre-capillary sphincters
  3. Metarterioles
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13
Q

Where are the baroreceptors?

A
  1. Carotid body (sinus)
  2. Arch of aorta
  • Activated on stretch

Carotid: Hering’s nerve -> Glossopharyngeal nerve to tractus solitarius in brainstem

Aortic: Vagus nerve -> tractus solitarius

Increased BP = secondary signals from tractus solitarius = inhibition of vasoconstrictor centre + excitation of vagal PSNS centre

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14
Q

Where are the chemoreceptors?

A

Sensitive to low O2, high CO2, and acidosis

Organs:

  1. 2 carotid bodies
  2. 1-3 aortic bodies
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15
Q

How does the atrial volume reflex work?

A

Atrial stretch due to Pressure -> reflex dilation of renal afferent arteriole -> increased glomerular cap pressure -> increased filtration of fluid into renal tubule -> decreased secretion of ADH via hypothalamus -> decrease in H2O resorption from renal tubule - >fluid loss by kidneys

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16
Q

What are the 2 long-term blood pressure control mechanisms?

A
  1. Renin-Angiotensin Aldosterone System

2. Vascular remodelling + contractility

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17
Q

Explain the RAAS system

A

Decrease in arterial P -> decrease in glomerular hydrostatic P -> decreased GFR -> decreased flow in loop of Henle -> Increased NaCl reabsorption -> decreased macula densa NaCl -> increased renin -> increased AT2 -> increased efferent arteriole resistance -> increased GFR

Decreased macula densa NaCl -> decreased afferent arteriole resistance -> increased GFR

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18
Q

What are the effects of Angiotensin II?

A
  1. Increased sympathetic activity
  2. Increased tubular Na+, Cl-, reabsorption + K+ excretion, H2O retention
  3. Increased aldosterone secretion
  4. Increased arteriolar vasoconstriction, increase in BP
  5. Increase in ADH secretion (posterior pituitary) -> increase in H2O absorption in collecting duct
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19
Q

How does aldosterone increase the absorption of Na+ and secretion of K+ and H+?

A
  1. Principal cells of collecting tubules
  2. Distal tubules
  3. Collecting ducts
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20
Q

What is primary hyperaldosteronism?

A

Increased aldosterone = decrease K+ and decrease H+

- hypokalemic alkalosis

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21
Q

What are the causes of primary hyperaldosteronism?

A
  1. Unilateral aldosterone-producing adenoma
  2. Conn’s Syndrome (50-60%)
  3. Bilateral adrenal hyperplasia (40-50%)
22
Q

What are the symptoms of hypokalemia?

A
  • Muscle weakness
  • Cramps
  • Palpiatations
  • Polyuria + Polydipsia (in nephrogenic disease)

** Complication of long-standing HTN**

23
Q

What is Addison’s Disease?

A

The opposite of Conn’s disease. The failure of glucocorticoid/mineralocorticoid release

Treatment = IV hydrocortisone; synacthen (synthetic ACTH)

24
Q

What is the pathophysiology of essential hypertension in terms of the blood vessels? Type 2 diabetes?

A

Essential HTN:

  1. Increased wall thickness
  2. Decrease in lumen diameter
  3. Increase in wall-lumen ratio
  4. Preservation or mild impairment of endothelial function

Type 2 Diabetes:

  1. Increased wall thickness
  2. No change in lumen diameter
  3. Impairment of endothelial function
25
Q

Which protein from fat tissue can increase BP in obesity?

A

Adiponectin

26
Q

Outline the treatment regimen for hypertension

A

<55y: ACE inhibitor -> A + C OR A + D -> further diuretic therapy, a-blocker, b-blocker

≥55y + Black: Ca2+ blocker + diuretic -> A + C OR A + D -> further diuretic therapy, a-blocker, b-blocker

Where A = ACE inhibitor or low-cost angiotensin II receptor blocker (ARB)
C = Calcium-channel blocker
D = thiazide-like diuretic

27
Q

What are the possible end-organs that are damaged by HTN?

A
  1. Eyes: Hypertensive retinopathy
    - Flame hemorrhage
    - Hard exudates (lipids)
    - Cotton wool spots
    - Papilloedema
  2. Brain: Hypertensive cerebrovascular disease
  3. Heart: LV hypertrophy, ischemic heart disease with our without heart failure
  4. Kidney: Hypertensive retinopathy
28
Q

What is secondary hypertension and 17 causes?

A

Occurs in 10% of people with hypertension, usually under the age of 40. There’s an underlying cause to their hypertension.

Renal diseases: no regulation of H2O + sodium -> increased fluid retention -> increased P

  1. Polycystic kidney disease (inherited; fluid-filled cysts damage kidney)
  2. Glomerular disease (primary renal disease)
  3. Renovascular hypertension (narrowing of arteries)
  4. Cushing’s Syndrome (increased glucocorticoids = Na/H2O retention)
  5. Primary aldosteronism (Too much aldosterone = increased water retention)
  6. Pheochromocytoma (Tumour of the adrenal glands = increased norepinephrine + epinephrine release = increased BP)
  7. Sleep apnea (breathing stops, hypoxia, increased P at night)
  8. Obesity (increased body weight = increased BP)
  9. Brain tumours + encephalitis (inflammation = decreased blood flow = increased P)
  10. Oral contraceptives
  11. NSAIDs
  12. Stimulants (i.e. Cocaine, methylphenidate)
  13. Calcineurin inhibitors
  14. Antidepressants
  15. Coarctation of the aorta
  16. Hypothyroidism
  17. Primary hyperparathyroidism
29
Q

What are the suggestive clinical features of secondary HTN in general?

A
  1. Acute rise in BP over a previous stable value
  2. Proven age of onset before puberty
  3. Age < 30y with no family history of HTN and no obesity
30
Q

What are the suggestive clinical features of secondary HTN due to renovascular disease?

A
  1. Acute elevation in serum creatinine of at least 30% after administration of ACE inhibitor or ARB
  2. Mod-severe HTN in a patient with diffuse atherosclerosis, unilateral small kidney, asymmetry in renal size of more than 1.5cm that cannot be explained by another reason
  3. Mod-severe HTN in patients with recurrent episodes of flash pulmonary oedema
  4. Onset of stage II HTN after 55y
  5. Systolic/diastolic abdominal bruit (not very sensitive)
31
Q

What are the suggestive clinical features of secondary HTN due to primary renal disease?

A
  1. Elevated serum creatinine concentration

2. Abnormal urinalysis

32
Q

What are the suggestive clinical features of secondary HTN due to oral contraceptives, NSAIDs, stimulants, and antidepressants?

A

New elevation in BP temporally related to use

33
Q

What are the clinical signs of 2º HTN due to pheochromocytoma?

A
  1. Paroxysmal elevations in BP

2. Triad of headache (pounding), palpitations, sweating

34
Q

What are the clinical signs of 2º HTN due to primary aldosteronism?

A
  1. Unexplained hypokalemia with urinary potassium wasting; however more than 1/2 of patients are normokalemic
35
Q

What are the clinical signs of 2º HTN due to Cushing’s syndrome?

A
  1. Cushingoind facies
  2. Central obesity
  3. Proximal muscle weakness
  4. Ecchymoses
36
Q

What are the clinical signs of 2º HTN due to sleep apnea syndrome?

A
  1. Primarily seen in obese men who snore loudly while asleep
  2. Daytime somnolence, fatigue, morning confusion
37
Q

What are the clinical signs of 2º HTN due to coarctation of the aorta?

A
  1. HTN in arms with diminished/delayed femoral pulses + low/unobtainable BP in the legs
  2. L brachial pulse is diminished and equal to the femoral pulse if origin of the L subclavian artery is distal to the coarct
38
Q

What are the clinical signs of 2º HTN due to hypothyroidism?

A
  1. Symptoms of hypothyroidism

2. Elevated serum thyroid stimulating hormone (TSH)

39
Q

What are the clinical signs of 2º HTN due to primary hyperparathyroidism?

A

Elevated serum calcium

40
Q

What are lifestyle changes people can make to reduce their blood pressure?

A
  1. Healthy diet
  2. Reduce sodium intake
  3. Reduce excess caffeine intake
  4. Stop smoking
  5. Reduce alcohol intake
  6. Regular exercise
  7. Relaxation therapies (not available on NHS)
41
Q

What are 10 causes of high blood pressure?

A
  1. Obesity
  2. Stress
  3. Excess salt intake
  4. Excess alcohol intake
  5. Excess caffeine intake
  6. Smoking cigarettes
  7. Not enough fruit/veg
  8. Not enough exercise
  9. Family history
  10. Caribbean/African descent
42
Q

What is the QRISK-3 score and what factors does it use?

A

Calculates a person’s risk of developing a heart attack or stroke over the next 10 years.

It includes factors such as:

  • Smoking
  • Diabetes
  • Heart attack/angina in relative < 60
  • AF
  • BMI
  • BP treatment
  • Rheumatoid arthritis
  • Cholesterol
  • Chronic Kidney disease
  • Migraine
  • Corticosteroids
  • Systemic lupus erythematous (SLE)
  • Atypical antipsychotics
  • Severe mental illness (schizophrenia, bipolar disorder, moderate/severe depression)
  • Erectile dysfunction
  • A measure of systolic BP variability
43
Q

What drug and dose is used for primary prevention of CVD?

A

Atorvastatin 20mg

44
Q

A 60y old lady has been confirmed to have BP of 156/95mmHg for the last 3-4mo with no evidence of end organ damage. Her BMI was 31. Her GP gave her some advice to reduce weight and salt in her diet. 3mo later her BP is 150/91 and BMI hasn’t changed.

What should the next step be?

A

Continue lifestyle measures AND start Ca2+ channel blocker

45
Q

How would you manage the following 3 scenarios:

Inability to control BP even after 4 agents

180/110 but no evidence of end organ damage

170/120 with hematoproteinuria

A

Inability to control BP even after 4 agents: Consider specialist referral to rule out 2º causes

180/110 but no evidence of end organ damage: Manage in primary care

170/120 with hematoproteinuria: Urgent referral to 2º care for IV antihypertensives

46
Q

A 57y old English gentleman known to be on treatment for HTN has come to his GP for annual checkup. He is taking ramipril 10mg OD. His repeated BP readings this time are 155/95mmHg. He has a BMI of 24. He has a good lifestyle of regular exercise and low salt diets.

What will the next management step be?

A

Continue lifestyle measures and add calcium channel blocker

47
Q

Which of the following statements about 2º HTN are false:

  1. Secondary HTN is more common than essential hypertension
  2. Cocaine causes it
  3. Primary hyperaldosteronism is a cause of it
  4. Licorice causes it
  5. Oral contraceptive pills cause it
A

2º HTN is NOT more common than essential HTN

48
Q

What is BP dependent on?

A

Cardiac output + peripheral resistance

49
Q

What are the main side effects of the following drugs:

  1. ACE inhibitors
  2. B-blockers
  3. Ca2+ channel blockers
  4. Thiazide diuretics
  5. Loop diuretics
  6. Aldosterone antagonists
A
  1. ACE inhibitors -> dry cough
  2. B-blockers -> bradycardia
  3. Ca2+ channel blockers -> ankle swelling
  4. Thiazide diuretics -> hyponatremia
  5. Loop diuretics -> gout attack
  6. Aldosterone antagonists -> hyperkalemia
50
Q

Name 3 antihypertensives that can be used safely during pregnancy?

A
  1. Labetalol
  2. Methyldopa (antihypertensive, centrally acting)
  3. Nifedipine (Ca2+ channel blocker)
51
Q

What is medial fibromuscular dysplasia?

A

It is a “string of beads” appearance involving the renal vessels. The appearance is caused by areas of stenosis alternating with small aneurysms, the diameters of which exceed the normal diameter of the artery. This is a secondary cause of HTN.

52
Q

Prescribe a calcium channel blocker for a patient who is 70y with NKDA.

A

Lercanidipine, 10mg PO

Year 3 TCDs (24 decks)

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