Hypertension Flashcards

1
Q

what signs and symptoms of hypertension

A

end organ damage

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2
Q

What are the three stages of hypertension

A

Stage 1
- 140/90 and ABPM 135/85

Stage 2
- 160/100 and ABPM 150/95

Stage 3
- Systolic> 180 or diastolic >110

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3
Q

ABPM what does it stand for

A

ambulatory blood pressure mean - get a day time mean and and a night time mean - the figure is for the day time mean

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4
Q

How do you measure postural hypotension

A
  • Measure BP seated or supine
  • Stand the patient for 1 minute
  • Systolic drops by more than 20mm
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5
Q

What is the definition of postural hypotension

A
  • this is when systolic drops by more than 20mm
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6
Q

What is the definition of malignant hypertension

A
  • BP > 180/110 AND signs of papilloedema or retinal haemorrages
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7
Q

Describe how a ABPM work

A
  • 24 hr monitoring

Machine size of half a BNF

  • Take BP 3 times an hour during the day and hourly at night
  • BP should dip at night; if not worse prognosis
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8
Q

in ABPM what should drop at night

A

BP should dip at night; if not worse prognosis

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9
Q

guidelines suggests that all patients should have a

A

ABPM before treatment

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10
Q

What is the alternative to ABPM

A
  • Week of home blood pressure monitoring and then ask them to average it out
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11
Q

How should you take a history

A

CO

HPC

  • Ask about pregnancy and the pill
  • Ever had a BP check at work or for work eg HGV

PMH

  • Diabetes
  • CVA
  • MI
  • Renal disease

FH

  • Cause and age of death
  • Specifically ask about MI and CVA
  • Parents and siblings

SH

  • Smoking
  • Alcohol
  • Salt
  • Dairy
  • 5 a day
  • Exercise
  • Caffeine
  • snoring
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12
Q

What should you look for in systems review for hypertension

A
  • Cardiovascular
  • Angina
  • Claudication
  • Exercise tolerance
  • Erectile function

Females
- Pregnancy plans /contraception

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13
Q

How do you examine a patient with blood pressure

A
  • Measure BP in both arms
  • APBM before starting treatment

Look for end organ damage

  • eyes
  • urine - proteinuria

Look for secondary causes

  • cushings
  • coarctation
  • renal artery stenosis
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14
Q

What does coarctation look like

A

Between the two arms

radial delay

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15
Q

What investigations can you use

A
  • ABPM
  • Urinalysis - for protein, albumin:creatine ratio and haematuira

U&E

  • Conns
  • hyperparathyroidism

Blood tests

  • glucose
  • electrolytes
  • creatine
  • eGFR
  • total and HDL cholesterol
  • Fundoscopy - check for retinopathy
  • ECG - check for left ventricular hypertrophy

Secondary care

  • ECHO
  • Urinary Metanephrines
  • Renin/aldo ratio (Conns)
  • Renal/liver ultrasound
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16
Q

What are the two things can can effect measurement of blood pressure not due to hypertension

A
  • Wrong cuff size - lead to wrong measurement
  • White coat - doctors make patients anxious - picked up on ABPM
  • masked hypertension - relaxed when they see the doctor but BP is high the other time - picked up on ABPM
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17
Q

What can cause essential hypertension

A

Genetic

Environmental

  • City living
  • Alcohol
  • Obesity
  • Salt
  • Lack of exercise
  • OSA - obstructive sleep apnea
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18
Q

What causes secondary hypertension

A
  • Phaeochromocytoma
  • Cushings
  • OSA
  • Obesity
  • Conns
  • Renal disease
  • Renal artery stenosis

Drugs

  • OC
  • Steroids
  • Recreational drugs e.g. cocaine
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19
Q

What type of end organ damage presents in hypertension

A

Heart

  • MI
  • CCF

Brain
- CVA

Kidney

  • Nephrosclerosis
  • Accelerates other forms of kidney disease

Depends on ethnicity

Legs

Erectile function

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20
Q

How do you manage stage 1 hypertension

A

Assess cardiovascular risk

  • If target organ damage or 10% over 10 yrs risk give drugs
  • Younger adults; consider drug treatment at a lower risk
  • Life style intervention
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21
Q

How do you manage stage 2 hypertension

A
  • Check with ABPM

- Drugs and lifestyle

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22
Q

How do you manage stage 3 hypertension

A
  • Treat now with drugs
  • then do an ABPM
  • then recommend lifestyle
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23
Q

Describe what medications to give to what patients

A
Younger than 55 
Step 1
- ACE 1st 
Step 2
- ACE + CCB or ACE + Thiazide type diruetics 
Step 3
- ACE + CCB + Thiazide like diuretics 
step 4 
- add a further direutics 
or
- alpha blocker 
or 
- beta blocker 
and consult specialist advice 
Older than 55 or afro-carrabean or black patients of any age 
Step 1 
- CCB or Thiazide 
Step 2 
- ACE + CCB or ACE + thiazide 
Step 3 
- ACE + CCB + Thiazide 
Step 4 
- add a further direutics 
or
- alpha blocker 
or 
- beta blocker 
and consult specialist advice
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24
Q

Why do black and Afro-Caribbean patients not respond to ACE inhibitors

A
  • They have lower plasmin renin therefore something that acts on the RAAS it is less effective
  • but if you stimulate the RAAS you raise the renin aldosterone levels and they become sensitive to the ACE
25
Q

Describe what you should check before you prescribe an ACE

A
  • Check pregnancy plans (can be tetrogenic)
  • Under 55
  • Not as monotherapy in Africans or Caribbean
26
Q

Who should you give CCBs to

A
  • over 55

- African or Caribbeans

27
Q

What can be contradicted in calcium channel blockers

A
  • Can cause ankle swelling - therefore caution if worried about heart failure or oedema
28
Q

Name the types of calcium channel blockers

A
  • Verapamil
  • Dilitiazem

Dihydropyridines

  • Amlodipine (common)
  • nifedepine (in pregnancy and breast feeding)
  • lacidipine (less ankle oedema)
29
Q

Name a side effect of calcium channel blockers

A
  • All cause gum hyperplasia - good dental hygiene is needed

- can cause ankle oedema

30
Q

Name some examples of a loop diuretics

A
  • Bumetanide

- Furosemide

31
Q

Name some examples of a potassium sparing diuretics

A

Amilioride

32
Q

Name some examples aldosterone antagonist

A
  • Spironolactone

- eplenerone

33
Q

What are the side effects of ACE inhibitors

A
  • Angioedema
  • dry cough
  • causes high potassium
34
Q

Name some examples of ACE inhibitors

A
  • Ramipril
  • perindopril
  • lisinopril
35
Q

What is the mechanism of action of ARBs

A

Block the A2 angiotensin receptor

36
Q

What are the side effects of ARBs

A
  • Increase potassium
37
Q

Name some examples of ARBs

A
  • Irbesarten
  • losarten
  • valsarten
  • candarsarten
38
Q

How does spironlactone work

A
  • Aldosterone antagonist

- Affects renin angiotensin system

39
Q

What are the side effects of aldosterone antagonists

A
  • Spironolactone = Gynacomastia due to oestrogen effects

- Eplenerone less oestrogen effects so no gynacomastia

40
Q

What blood pressure drugs can be used in pregnancy

A
  • Labetolol
  • Methyl Dopa
  • Nifedipine
41
Q

What are the targets for hypertension

A
  • Reduce clinic BP to below 140/90

- ABPM or home monitoring 135/85

42
Q

what would a U and E show if conns was the cause of hypertension

A
  • decrease in potassium
43
Q

What would a U and E show if hyperparathyroidism was a cause of hypertension

A
  • increase in calcium
44
Q

What are examples of end organ damage

A
  • LVH
  • Previous medical history of MI or angina
  • previous medical history of stroke/TIA
  • peripheral vascular disease
  • renal failure
45
Q

How does conns disease present in the clinical history and physical examination

A
  • Muscle weakness
  • family history of early onset hypertension
  • cerebrovascular events aged before 40

Physical examination
- arrhythmias if severe hypokalaemia

46
Q

What are the laboratory investigations for primary aldosteronism confirmation

A
  • Hypokalaemia in U and E
  • aldosterone:renin ratio under standardised conditions
  • fludrocortisone suppression test
  • adrenal CT scan
  • adrenal vein sampling
47
Q

what are the clinical presentation and physical examination on pheochromocytoma

A
  • Paroxysmal hypertension
  • headache
  • sweating
  • palpitations
  • pallor
  • family history

Physical examination
- skin stigmata of neurofibromatosis - cafe-au-lait spots

48
Q

What investigations do you use to diagnose pheochromocytoma

A
  • incidental discovery of adrenal mass
  • measurement of urinary fractionated metanephrines or plasma free metaneprhines
  • CT or MRI of abdomen and pelvis
  • genetic screening
49
Q

What are the clinical history of cushings syndrome

A
  • weight gain
  • polyuria
  • polydipsia
  • psychological disturbances

Physical examination

  • central obesity
  • moon face
  • buffalo hump
  • red striae
  • hirsutism
50
Q

What tests can you do to confirm Cushings syndrome

A
  • hyperglycaemia
  • 24 hour urinary cortisol excretion
  • dexamethasone suppression tests
51
Q

What is the clinical history of renal artery stenosis and what would you find on a physical examination

A

Fibromuscular dysplasia
- early onset hypertension

Atherosclerotic stenosis

  • abrupt onset hypertension
  • worsening or difficult to treat
  • flash pulmonary oedema

physical examination
- abdominal bruit

52
Q

What is the clinical history of renal parenchymal disease and what would you find on a physical examination

A

Clinical history

  • history of urinary tract infection or obstruction
  • haematuria
  • family history of polycystic kidney disease

physical examination
- abdominal mass

53
Q

Define accelerated hypertension

A

Accelerated hypertension is defined as a recent significant increase over baseline BP that leads to target organ damage

54
Q

when is same day referral given with accelerated hypertension

A
  • with palpilloedema and retinal haemorrhages
  • with new onset confusion, chest pain, signs of heart failure or acute renal failure
  • with suspected phaeochromocytoma
55
Q

Describe the mechanism of action of atherosclerosis

A
  1. Endothelial wall damage
    - shear stress - hypertension
    - toxic damage - e.g. cigarette smoke
    - exposure to high levels of LDL
  2. Uptake and modification of LDL
    - Following endothelial damage, LDL and monocytes infiltrate subendotheilal space

Once taken up LDL is modified

  • oxidation - in the presence of reactive oxygen specific
  • glycation in the presence of increased glucose
  1. Infiltration of macrophages into subendothelial space
    - Oxidised LDL stimulates endothelial cells to produce inflammatory mediators required for uptake of monocytes
    - Monocytes taken up and transform into macrophages
  2. Formation of fatty streaks
    - Macrophages take up excess LDL van scavenger receptors and transform into foam cells
  3. Smooth muscle proliferation and fibrous cap formation
    - Endothelial cells and macrophages release growth factors, inducing smooth muscle proliferation and collagen deposition (can form fibrous cap)
    - Ca2+ deposits onto plaque, hardening it
    - Smooth muscle cells can also take up LDL and become foam cells
    - Fibrous cap is very fragile and can break off: collagen exposed to blood 🡪 thrombus formation (can break off and embolise)
56
Q

What are the signs of accelerated phase HTN

A
  • Severe hypertension (SBP>200, DBP >130)
  • bilateral retinal haemorrhages
  • exudates +/- papilloedema
57
Q

What are the symptoms of accelerated phase hypertension

A

Headache +/- visual disturbance

58
Q

What is the treatment for accelerated phase hypertension

A
  • oral therapy unless there is encephalopathy or CCF
  • aim is controlled reduction in blood pressure over days not hours
  • avoid sudden drops in blood pressure as cerebral auto regulation is poor
  • bed rest and hypotensive drug - atenolol or long acting CCBs
59
Q

What are the grades of hypertensive retinopathy

A
  1. Tortuous arteries with thick shiny walls (silver or copper wiring)
  2. AV nipping
  3. Flame haemorrhages and cotton wool spots
  4. Papilloedmea