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CR > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Pathophysiology of atherosclerosis

A

1) Dysfunctional epithelial cells + high circulating LDLs
2) LDLs move into tunica intima
3) Endothelial cells release ROS and oxidise the LDLs, trapping them
4) Triggers endothelial cells to express adhesion molecules for WBCs
5) Monocytes move into intima and become macrophages
6) Macrophages take up LDLs and become foam cells
7) Foam cells release chemokines and IGF-1 and also die
8) Attraction of more macrophages, smooth muscle cell migration and proliferation, production of more collagen, and release of lipid contents/ROS/cytokines
9) Increased inflammation in area (plaque)
10) Plaque grows and can rupture

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2
Q

Mechanisms of hypertension

A

Atherosclerosis - increases SVR

Low renal blood flow - kidneys secrete renin which helps kidneys retain water, leading to higher pressure

Pathology in RAAS system seems to be main mechanism, rather than baroreceptor pathology

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3
Q

Symptoms and signs

A

Usually asymptomatic

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4
Q

Secondary causes of hypertension

A

1) Renal disorders - chronic pyelonephritis, diabetic nephropathy, glomerulonephritis, PKD, obstructive uropathy, renal cell carcinoma
2) Vascular disorders - coarctation of aorta, renal artery stenosis
3) Endocrine disorders - primary aldosteronism, phaeochromocytoma, Cushing’s, acromegaly, hypo or hyperthyroidism
4) Drugs - alcohol, ciclosporin, cocaine, COCP, steroids, EPO, leflunomide, liquorice, NSAIDs, sympathomimetics, venlafaxine
5) Others = CTDs, retroperitoneal fibrosis, OSA

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5
Q

Normal blood pressure

A

<120/80

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6
Q

Categorisation of hypertension (clinic BPs)

A

Stage 1 = 140/90 - 159/99 AND ABPM >=135/85

Stage 2 = 160/100 - 180/120
AND ABPM >=150/95

Stage 3 = 180 or higher/120 or higher (either diastolic or systolic)

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7
Q

Risk factors for primary hypertension

A

Old age, obesity, salt-heavy diet, sedentary lifestyle, black people, genetics, social deprivation, smoking, alcohol, anxiety and stress

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8
Q

Hypertensive crisis symptoms

A

Confusion, drowsiness, chest pain, breathlessness

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9
Q

How to confirm hypertension

A

BP in clinic - 3 readings

Confirmed by ambulatory BP monitoring or home BP monitoring (if clinic BP 140/90-180/120)

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10
Q

Accelerated (or malignant) hypertension definition

A

Severe increase in blood pressure to 180/120 mmHg or higher (and often over 220/120 mmHg) with signs of retinal haemorrhage and/or papilloedema. It is usually associated with new or progressive target organ damage.

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11
Q

If BP is 180/20 or higher?

A

Refer for same day specialist assessment if signs of retinal haemorrhage and/or papilloedema, life-threatning symptoms e.g. confusion, chest pain, heart failure, AKI
If no symptoms/signs –> carry out investigations for target organ damage ASAP

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12
Q

Investigations for target organ damage/cardiovascular risk

A

Urine dip - haematuria
Urine ACR (protein in the urine)
HbA1C
Electrolytes, creatinine, and EGFR (for CKD)
Fundoscopy (for hypertensive retinopathy)
ECG (for cardiac function/LVH)
Serum total cholesterol and HDL cholesterol
QRISK assessment

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13
Q

Symptoms/signs of renal causes of secondary hypertension

A

Chronic pyelonephritis - usually detected unexpectedly on USS

Diabetic nephropathy — microalbuminuria or proteinuria

Glomerulonephritis — microscopic haematuria.

Polycystic kidney disease — abdominal or flank mass, microscopic haematuria, or family history.

Obstructive uropathy — abdominal or flank mass.

Renal cell carcinoma — haematuria, loin pain and a loin mass

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14
Q

Symptoms/signs of coarctation of aorta

A

Upper-limb hypertension. Significant difference in BP between arms.
Absent or weak femoral pulses, radio-femoral delay, palpable collateral blood vessels in the back muscles, and a suprasternal murmur radiating through to the back.

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15
Q

Symptoms/signs of renal artery stenosis

A

Peripheral vascular disease Abdominal bruit

BP resistant to treatment Raised plasma renin

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16
Q

Primary hyperaldosteronism signs/symptoms

A

Hypokalaemia, alkalosis, and plasma sodium level greater than 140 mmol/L,
Tetany, muscle weakness, nocturia, or polyuria.

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17
Q

Symptoms/signs phaeochromocytoma

A

Intermittently high or labile blood pressure, or postural hypotension, headaches, sweating attacks, palpitations, or unexplained fever and abdominal pains.

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18
Q

Hyperthyroidism signs/symptoms

A

tremor, anxiety, sweating, weight loss, diarrhoea, and heat intolerance.

19
Q

Hypothyroidism signs/symptoms

A

fatigue, weight gain, dry skin and hair loss, constipation, and muscle weakness.

20
Q

Cushing’s signs/symptoms

A

Truncal obesity and striae

21
Q

Acromegaly signs/symptoms

A

Enlargement of hands and feet, facial changes, sweating

22
Q

BP target for non-diabetics etc.

A

Adults aged under 80 years — clinic blood pressure below 140/90 mmHg.
Adults aged 80 years and over — clinic blood pressure below 150/90 mmHg.

23
Q

BP targets for diabetics

A

If end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg
otherwise < 140/80 mmHg

24
Q

Investigations for secondary causes

A
  • U&E + estimated GFR (renal disease)
  • Renal ultrasound/arteriography (renal artery stenosis)
  • 24h urinary meta-adrenaline (raised in pheochromocytoma)
  • Urinary free cortisol (raised in Cushing’s)
  • Renin aldosterone ratio (aldosterone high in Conn’s)
  • MR aorta (coarctation)
25
Q

Non-pharm managament of cardiovascular risk factors

A 
Healthy diet + regular exercise
Weight loss 
Reduce caffeine
Low dietary sodium
Smoking cessation 
Reduce alcohol
26
Q

Step 1 in pharm treatment

A

If <55 or T2DM = ACE inhibitor (or ARB)

If >=55 or black = calcium channel blocker

27
Q

Step 2 in pharm treatment

A

A + C

28
Q

Step 3 in pharm treatment

A

A + C + D (thiazide-like diuretic)

29
Q

Step 4 in pharm treatment

A

A + C + D
+ spironolactone if potassium =<4.5
+ alpha or beta blocker if potassium >4.5

30
Q

Step 5 in pharm treatment

A

Refer for specialist review if on 4 drugs and not controlled

31
Q

ACE inhibitors

- mechanism, SEs

A

Inhibit the conversion angiotensin I to angiotensin II

S/Es - cough, angioedema, hyperkalaemia, can worsen renal function

32
Q

ARB

- mechanism, SEs

A

Block effects of angiotensin II at the AT1 receptor

S/E - hyperkalaemia

33
Q

Calcium channel blockers

- mechanism, SEs

A

Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction
S/Es - flushing, ankle swelling, headache

34
Q

Thiazide like diuretics

- mechanism, SEs

A

Inhibit sodium absorption at the beginning of the distal convoluted tubule
S/Es - hyponatraemia, hypokalaemia, dehydration

35
Q

Spironolactone

- mechanism, SEs

A

Aldosterone antagonist which acts in the cortical collecting duct
S/E - hyperkalaemia, gynaecomastia

36
Q

Alpha blockers SEs

A

postural hypotension
drowsiness
dyspnoea
cough

37
Q

Beta blockers

A

Reduce cardiac output, alter baroceptor reflex sensitivity, and block peripheral adrenoceptors. Some beta-blockers depress plasma renin secretion. May have central effect.
S/Es - abdo discomfort, bradycardia, peripheral coldness, dizziness, can cause AV block and bronchospasm (uncommon)

38
Q

Management of hypertensive emergency

A

IV antihypertensive therapy - reduce BP by 20-25% within 2 hours
e.g. with labetalol, GTN, nitroprusside, hydralazine…

39
Q

Management of hypertensive urgency

A

Gradually reduce BP over 24-48 hours with oral antihypertensive therapy e.g. labetalol or amlodipine or felodipine

40
Q

In hypertensive crisis, why should BP be reduced gradually?

A

If reduced too quickly, there is a risk of reduced organ perfusion leading to cerebral infarction, blindness, deterioration in renal function, and myocardial ischaemia.

41
Q

What is BP determined by? (2)

A

Cardiac output x systemic vascular resistance

42
Q

Stages of hypertensive retinopathy

A 
1 = arteriolar narrowing and tortuosity, silver wiring
2 = AV nipping
3 = cotton wool exudates, flame and blot haemorrhages
4 = papilloedema
43
Q

Pathology of target organ damage caused by accelerated hypertension

A

A rise in systemic vascular resistance starts the cycle

  • -> increase in BP
  • -> mechanical stress and endothelial injury
  • -> increased permeability
  • -> activation of the coagulation cascade and platelets, and deposition of fibrin
  • -> ischaemia and release of vasoactive mediators, generating ongoing injury

CR (19 decks)

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