GP ILAs Flashcards
What is needed to confirm a diagnosis of Hypertension
24hr ABPM or a week of at home readings
At what BP reading should treatment be offered
all with BP ≥160/100mmHg or ABPM ≥150/95mmHg.
Health conditions which can cause hypertension
- Kidney disease/long term infections
- Diabetes
- Glomerulonephritis
- Hormone issues- underactive thyroid, Cushing’s, Acromegaly, hyperaldosteronism, phaechromocytoma
Medications which can cause hypertension
- contraceptives
- steroids
- NSAIDs
- Cocaine/amphetamines
- Some SSNRIs e.g. venlafaxine
How can hypertension affect the kidney?
○ People with hypertension and normal kidney function have a significantly reduced number of nephrons in each kidney
○ Individual nephrons are enlarged as a result of glomerular hyperfiltration
what tests are used to quantify overall risk of a hypertension diagnosis?
fasting glucose and cholesterol
what tests are used to look for end-organ damage from hypertension
- ECG/Echo (LVH or history of MI?)
- Urine analysis (protein, blood)
What test can exclude secondary causes of hypertension
Bloods- U&E: decreased K+ in Conn’s, increased Ca2+ in hyperparathyroidism
Explain pathophysiology of essential hypertension
Primary (essential hypertension): arteriosclerosis of major renal arteries, and changes in intrarenal vasculature (nephrosclerosis)
- blood vessel wall becomes hyalinised in small vessels and arterioles as the intima thickens with reduplication of the internal elastic lamina
- Concentric reduplication of internal elastic lamina and endothelial proliferation lead to ‘onion skin’ appearance
- both kidneys reduce in size- can be asymmetrical if one major vessel is affected
- proportion of sclerotic (scarred) glomeruli increases
What is the range for stage 1 Hypertension
a systolic BP of 130-139 or a diastolic BP of 80-89
What is the range for stage 2 hypertension
systolic>140, diastolic>90
is the cause of essential (primary) hypertension known or unknown?
unknown
what percentage of hypertension cases are secondary hypertension and what is secondary hypertension?
5% . Secondary Hypertension= Hypertension with an identifiable cause i.e. secondary to another condition.
what are some causes of secondary hypertension?
- renal disease (intrinsic issues such as glomerulonephritis, systemic sclerosis and PCKD & renovascular diseases which are usually atheromatous)
- Endocrine disease e.g. Cushing’s, Conn’s, Phaechromocytoma, Acromegaly, Hyperparathyroidism
- coarctation, pregnancy, drugs (steroids, oral contraceptive, cocaine, amphetamines)
Treatment pathway for a patient with type 2 diabetes diagnosed with hypertension? (4 steps)
(1) ACEi/ARB
(2) (ACEi/ARB) + CCB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
Treatment pathway for patient <55, not of black/afro-Caribbean descent and with no diabetes who is diagnosed with hypertension? (4 steps)
(1) ACEi/ARB
(2) (ACEi/ARB) + CCB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
Treatment pathway for patient age 55 or over with no diabetes?
(1) CCB
(2) (CCB) + ACEi/ARB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
Hypertension treatment algorithm for patient with black african or afro-caribbean family origin (any age)?
(1) CCB
(2) (CCB) + ACEi/ARB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
How often should patients with hypertension be monitored:
1- adjusting their hypertension medication
2-once stabilised
3- serum potassium and creatinine
1- when adjusting medication BP should be monitored every 2-4 weeks
2- Once stabilised, BP should be checked and medications reviewed every 6-12 months
3- Serum Potassium and Creatinine should be checked yearly
What are the 3 most likely complications of hypertension?
Coronary artery disease, cerebrovascular accidents (e.g. stroke) and Left Ventricular Hypertrophy
hypertension medications which can result in erectile dysfunction
thiazide-like diuretics and beta blockers
hypertension medication which results in ankle swelling
calcium channel blockers
hypertension medications which result in dry cough
ACE inhibitors e.g. ramipril
Most common cause of HF in the developed world
Ischaemic heart disease
Pathophysiology of HF (3 basic steps)
1- initial stressful event (e.g. infarction/inflammation/pressure or volume overload) leads to myocardial damage which causes increased myocardial wall stress. This results in initial HF
2- compensatory mechanisms are activated which attempt to maintain cardiac output snd peripheral perfusion. As HF progresses, these are overwhelmed. These include the RAAS, sympathetic nervous system, ventricular dilatation/remodelling and release of cytokines e.g. TNF
3-The compensatory physiological changes become pathological and damaging; All of this leads to further wall stress- vicious cycle
Explain the RAAS role in hypertension
(1) Renin (enzyme) released from granular cells of the renal juxtaglomerular apparatus in response to (i) reduced sodium delivery to distal convoluted tubule detected by macula densa cells, (ii) reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole and (iii) sympathetic stimulation of the JGA via B1 adrenoreceptors. Renin release is inhibited by ANP which is released by stretched atria in response to increases in BP
(2) Angiotensinogen (produced in the liver) is cleaved by renin to form Angiotensin I
(3) Angiotensin I is converted to Angiotensin II by ACE (angiotensin converting enzyme)
(4) Angiotensin II stimulates the release of Aldosterone from the adrenal cortex. Aldosterone acts on the principal cells of the collecting ducts in the nephron, increasing expression of ENaC to reabsorb urinary sodium, and increase the activity of basolateral Na/K/ATPase is increased. This increases sodium reabsorption of urinary sodium. In exchange, potassium is moved from the blood into the principal cell of the nephron and exits the cell into the renal tubule to be excreted into the urine.
Actions of Angiotensin II (4)
(1) stimulates release of Aldosterone
(2) cardiovascular- acts on AT1 receptors in endothelium of arterioles throughout the circulation to achieve vasoconstriction, resulting in an increase in TPR and consequently BP
(3) Neural effects: acts at hypothalamus to stimulate the sensation of thirst, resulting in an increase in fluid consumption, which helps raise the circulating volume and in turn the BP. Also increases secretion of ADH from the posterior pituitary gland, which results in the production of more concentrated urine to reduce the loss of fluid from urination. This allows circulating volume to be better maintained until more fluids can be consumed. Also stimulates the sympathetic nervous system to increase release of noradrenaline which is typically associated with fight or flight and increases CO, vasoconstricts arterioles and releases renin
(4) Renal effects: acts on kidney to produce a variety of effects including afferent and efferent arteriole constriction and increased Na+ reabsorption in the proximal convoluted tubule
most likely pathological heart sound for heart failure
S3 sound
risk factors for HF
hypertension, ischaemic heart disease, smoking, alcohol, obesity, (possibly diabetes?), sedentary lifestyle
main causes of RVF
LVF
Tricuspid valve disease
cor pulmonalae
Left ventricular systolic dysfunction (LVSD) is also known as
heart failure with reduced ejection fraction. Commonly caused by ischaemic heart disease but can also occur with valvular heart disease and hypertension
causes of right ventricular systolic dysfunction
left ventricular systolic dysfunction, primary and secondary pulmonary hypertension, right ventricular infarction, adult congenital heart disease
diastolic heart failure is also known as
heart failure with normal ejection fraction. Where the patient has symptoms and signs of heart failure with a normal or near-normal left ventricular ejection fraction (45-50%) and evidence of diastolic dysfunction on echo (e.g. abnormal left ventricular relaxation and filling, usually with left ventricular hypertrophy). This leads to impairment of diastolic ventricular filling and hence decreased cardiac output. Diastolic failure is more common in elderly hypertensive patients but may occur with cardiomyopathy.
