Hypertension

Question 1

what is hypertension?

Answer 1

Persistently elevated BP measured on 3 separate occasions, minimum of 2 days apart, systolic ≥140 and / or diastolic ≥90 mmHg.When severely elevated, minimum of 3 readings on same visit.
NB with correct blood taking techniques :
- Rested patient, seated 5-10 mins, arm at heart level supported.
- correct Size of the cuff. (Upper arm cuff is the most reliable). Wrist cuff or finger pulse not recommended
- correct cuff placement ->over brachial artery,2-3 cm above antecubital fossa
- placed on the bare arm or over a thin sleeve. The patient’s sleeve should not be rolled up, as this may act as a tourniquet, nor should the measurement be taken over a thick sleeve, as this may lead to an overestimate of the patient’s BP.

Question 2

Even though left side is prefered when taking blood pressure ,Conditions such as aortic dissection do necessitate BP reading rom both arms anda difference in these readings is difference but what is the threshold of this difference ?

Answer 2

The threshold difference is >20mmHg.

Question 3

describe the pathophysiology of hypertension .

Answer 3

different organs play a part .
Brain ->inappropriaely high sympathetic outflow -> catecholamines ->NE and E ( this then can because the root oof evrything )
Blood vessels -> increased large arterial stiffness (arteriolar sclerosis in old age )->increased systemic resistance
– Abnormal venoconstriction and high venous return .
KIDNEYS :
- inappropriate high renin release
- abnormal renal salt/water handling

Question 4

explain the mechanism of hypertension

Answer 4

• Blood Pressure = CO Cardiac Output (volume of blood that the body pumps in 1 minute [Stroke volume – volume of blood pumped out of the left ventricle during each systolic cardiac contraction ]
• Heart Rate [number of beats per minute] x PVR [ Peripheral Vascular Resistance] Resistance in the circulatory system that is used to create blood pressure, flow of blood and is also a component of cardiac function
  = When blood vessels constrict, this leads to an increase in PVR/SVR this is also called the afterload.
  =Preload – volume of blood in the ventricles, determined by venous return.
  =Afterload – pressure against which the heart has to pump.
• Sympathetic outflow > noradrenaline and adrenaline (alpha 1, B1, Alpha 2, B2).

Question 5

what is the general approach to management of HTN?

Question 6

What are the therapeutic objectives in the management of HTN?

Question 7

Explain the non-pharmacological measures /management .

Question 8

what are the determinants of BP?

Answer 8

Volume overload/salt overload
⇧ systemic vascular resistance
⇧ central drive to increase BP
⇧ sympathetic nerve stimulation.

BP = CO x PVR

[CO= SV x HR]

BP = SV x HR x PVR

Question 9

list the hypertension stages

Answer 9

systolic/diastolic

Optimal BP=<120/<80
Normal <130/<85
Prehypertension 130 to 139 /85-89
Grade 1 hypertension (mild)=140 to 159/90 to 99
Grade 2 hypertension (moderate )=160 to 179/100 to 109
Grade 3 hypertension (severe)= >180 />110
Isolated systolic hypertension (grade 1)= 140 to 159 /< 90
Isolated systolic hypertension (Grade 2)=>160/<90

Question 10

explain the suggested algorithm in HTN management (SA hypertension management algorithm 2015)

Answer 10

STEP1 :
Risk Factor Assessment / Target Organ Damage / Complications.
Levels of the BP:
-
STEP 2:
STEP 3:
STEP4:

Question 11

Explain the initial choice of antihypertensive treatment or combination

Question 12

Explain the causes of primary hypertension

Question 13

Explain the causes of secondary hypertension

Question 14

Which drugs causes secondary hypertension?explain how .

Question 15

List the group of drugs used in hypertension

Answer 15

1. Diuretics (low ceiling and High ceiling )
2. Angiotensin converting enzyme inhibitor (ACEi) and Angiotensin receptor blockers (ARBs)
3. Calcium chanel blockers
4. Mineralocorticoids antagonists
5. Sympatholytic agents
   - Beta Blockers
   - ALPHA2 recepter agonist
6. Alpha receptor blocker
   7.Vaspdilators

Question 16

Explain the concept of glomerular filtration,sexcretion,secretion and reabsorption.

Answer 16

Concept of excretion, secretion and reabsorption.
Afferent arteriole -> Glomerular capillaries fenestrated (Filtration) glucose, ions like Na, amino acids, into the Bowmans capsule -> not filtered, out through the Efferent arteriole
2. Filtered reabsorbed into the peritubular capillaries.
3.Some of what was (molecules from the blood not filtered can be secreted (occurs in PCT) from the capillaries into the nephron [antibiotics, toxins, molecules that are in excess].
4. Whatever is not absorbed will be excreted in urine.

Question 17

what are the 4 sites of Sodium reabsorption

Answer 17

4 sites of Sodium reabsorption:
1. Proximal convoluted tubule – Na+HCO3- cotransporter (65%)
2. Thick ascending limb – Na+K+CL- symporter (25%)
3. Distal convoluted tubule – Na+Cl- symporter (5%)
4. Collecting duct – Na reabsorption/K+-H+ excretion (2-4%)

Question 18

generally which drugs acts on the different sites of Na+ reabsorption?

Answer 18

4 sites of Sodium reabsorption:
1. Proximal convoluted tubule – Na+HCO3- cotransporter (65%)->Carbonic anhydrase inhibitors and osmotic diuretics
2. Thick ascending limb – Na+K+CL- symporter (25%)-> Loop diuretics
3. Distal convoluted tubule – Na+Cl- symporter (5%)->Thiazides
4. Collecting duct – Na reabsorption/K+-H+ excretion (2-4%)-> Aldosterone antagonist and ADH antagonists.

Question 19

what is meant by High ceilingg diuretics ?

Answer 19

• Effect of diuresis increases with increasing dose
• Cause substantial diuresis
• Loop diuretics (e.g Furosemide)

Question 20

what is meant by Low ceiling diuretics ?

Answer 20

• Effect of diuresis flattens with dose increase
  -Increased risk of adverse effects ( when you keep increasing the dose you are only increasing the side effects at this point not the effect )
• Thiazide diuretics (e.g Hydrochlorothiazide)

Question 21

explain the MOA of Thiazide diuretics

Answer 21

-act mainly on the early segments of the distal convoluted tubule,
- where they inhibit NaCl reabsorption by binding to the symporter responsible for the electroneutral cotransport of Na and Cl.
- Excretion of Cl, Na and accompanying H2O is increased.
- The increased Na load in the distal tubule stimulates Na exchange with K and H, increasing their excretion and causing hypokalaemia and a metabolic alkalosis
- Initially, the BP falls because of a decrease in body Na, blood volume, venous return and cardiac output. With chronic administration, thiazides can cause vasodilatation due to the loss of sodiu
- Diuretics have no direct effect on vascular smooth muscle and the vasodilatation they cause seems to be associated with a small but persistent reduction in body Na (fall in smooth muscle Na causes a secondary reduction in intracellular Ca, so that the muscle becomes less responsive)
- Long-term effect maintained through reduced vascular resistance (Opening of Ca2+ activated K+ channels)
EXAMPLE
Prototypical thiazide: Hydrochlorothiazide (HCTZ)

Question 22

explain the adverse effecst of Thiazide diuretics

Answer 22

1.Hypokalaemia
- The blockade of the Na/Cl cotransporter causes an increase in Na delivery to the distal segment of the DCT & collecting duct
-This increased delivery causes the aldosterone sensitive Na/K pump to increase sodium reabsorption in the principal cells.
-This exchange increases Na transfer into the interstitium and ↑K transfer into the the collecting tubules and lumen.
2. Hyponatraemia
3.Gout
- Diuretics inhibit uric acid excretion,
- TZD directly cause an ↑ urate reabsorption in the PCT via OAT 1 – Organic anion transporters.
- results in hyperuricaemia

4.Metabolic changes
- TZD cause hypokaelemia, beta pancreatic cell hyperpolarization deceased insulin secretion.
- Impaired carbohydrates tolerance-> glucose intolerance and metabolic Alkalosis

Question 23

explain the MOA of loop diuretics

Question 24

Explain the side effects of loop diuretics

Answer 24

1.Hyponatremia
2. Hypokalemia
3.Hypocaleamia
4. Postural hypotension
5.Metabolic ->Dyslipidemia and metabolic alkalosis
6.Hearing impairement -> can be irreversible

Question 25

Give example of Thiazide diuretics

Question 26

Explain the MOA of Mineralocorticoid antagonist(potassium sparing diuretics)->Spironolactone

Question 27

Explain the Adverse effects of nMineralocorticoid antagonist(potassium sparing diuretics)

Answer 27

1. Hyperkalemia
   2.Osteogen related effects :Gynaecomastia
   3.Erectle dysfunction

Question 28

Give example of Mineralocorticoid antagonist (potassium sparing diuretics)

Question 29

what other potassium sparing diuretics can be used in pts complaining of oestrogen related effects such as gynaecomastia?

Question 30

Explain MOA of ACE -inhibitors and angiotensin receptor blockers

Question 31

Give examples of ACE -inhibitors and angiotensin receptor blockers

Answer 31

Analapril , captopril and peridopril

Question 32

explain the adverse efects of ACE inhibitors

Answer 32

Dry cough that is caused by the accumulation of bradykinin
Angioedema is also due to the accumulation of bradykanin
Hyperkalaenia - because the angiotensin 2 is inhibited therefore it does not stimulate release of aldosterone - no sodium retuention and K is also not being excreted
First dose hypotension/ postural hypotension

Question 33

which other patient subgroups benefits from ACE inhibitors ? and How?

Answer 33

Diabetic patients - reduce progression to diabetic glomerulopathy
Renal desease - reduduce the risk of disease progression - glomerulisclerosis
IHD/post MI
Prevent the effect of angiotensin 2 which is hypertrophy of the heart muscle and fibrosis- remodelling of the heart muscle

Question 34

Gives the 2 types of Calcium channel blockers, the difference between the 2 groups and drugs that fall under each

Question 35

Explain the MOA of CCB

Question 36

what are the Adverse effects of CCB?

Question 37

What cautions need to be taken with CCB and what are the contraindications?

Question 38

Explain the classification of Beta blockers and which drugs fall under this group

Question 39

which cardiac conditions are Beta blockers indicated in ?

Question 40

Explain the MOA of Beta blockers

Question 41

Explain the adverse effect of beta blockers

Question 42

what are the contraindications for beta blockers .

Question 43

What is the MOA of Methyldopa and wht are he adverse effects?

Question 44

What is the MOA of Doxazosin ?

Question 45

What is the MOA of Hydralazine?

Question 46

What is the MOA of Minoxidil ?

Question 47

What is the MOA of Nitroprusside?

Question 48

Explain the HPN associated cardiovascular risk

Question 49

What are the benefits and risks of intensive BP control ?

Question 50

what is a hypertensive emergency ?

Question 51

what are changes caused by uncontrolled HTN in other organs ?