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Scenario Three

Scenario Three

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Scenario 3
Contents
\u2022Hypertension
o
Physiology \u2013 RAA system
o
Drugs
\u2022Complications and risk factors for hypertension - hersh
\u2022Anatomy and histology of pancreas -
laura

\u2022Control of glucose: insulin and glucagon
\u2022Diabetes pathophysiology
\u2022Risk factors of diabetes
\u2022Genetics of diabetes
\u2022Diabetes sx and signs
\u2022Diabetes diagnosis and investigations
\u2022Management of diabetes

o
Annual review
o
Drugs

\u2022Microvascular complications of diabetes
\u2022Macrovascular complications of diabetes
\u2022Atherosclerosis
\u2022Peripheral vascular disease and foot ulcers
\u2022Diabetic emergencies
\u2022Psychosocial aspects of diabetes
\u2022Economics and diabetes
\u2022Economics of chronic disease

o
Expert patient programmes

\ue000Economics and epidemiology of obesity
\ue000Metabolic Syndrome
\ue000Malnutrition and nutrition

1. Water
2. Food
3. Fat Soluble Vitamins
4. Water Soluble Vitamins

5. Carbohydrates
6. Protein Synthesis
7. Fat lysis

\ue000HONK and Ketoacidosis
\ue000Nephrotoxic Drugs
\ue000Glome Nephritis
\ue000eGFR
\ue000Ischaemic Foot Paul

\ue000MDT diabetes
\ue000Infections immune compromised
\ue000Tests diabetes
\ue000BMI
\ue000Obesity
\ue000Anatomy of Glom
\ue000CKD

Blood Pressure
Control of blood pressure
The mean arterial pressure is determined by two factors: cardiac output and total peripheral resistance
\u2022Cardiac output depends on heart rate and stroke volume
\ue000Heart rate increases due to sympathetic nervous system and decreases by the action of parasympathetic
nervous system
\ue000Stroke volume increases in response to sympathetic activity and it increases as venous return increases.
Venous return is increased by sympathetically induced venous vasoconstriction, the skeletal muscle
pump, the respiratory pump, cardiac suction and blood volume.
\ue001Blood volume depends on magnitude of passive bulk-flow fluid shifts between plasma and
interstitial fluid across capillary walls and on the activity of the rennin-angiotensin-aldosterone
system.
\u2022Total peripheral resistance depends on arteriolar radius and blood viscosity.
\ue000Blood viscosity depends mainly on number of red blood cells
\ue000Arteriolar radius is influenced by sympathetic activity that causes vasoconstriction and so increases
total peripheral resistance and blood pressure. It is also influenced by local metabolic controls and
hormones (vasopressin, angiotensin II)
Barorecptor reflex is a very important short-term regulator of blood pressure that stimulates or inhibits
sympathetic or parasympathetic activity accordingly.
\u2022Carotid sinus and aortic arch barorecptors are mechanoreceptors sensitive to changes in mean arterial and
pulse pressure that trigger the baroreceptor reflex
\u2022Generated action potential are integrated in the cardiovascular control centre in medulla which alters
accordingly the balance between sympathetic and parasympathetic activity to effector organs
\ue000Sympathetic stimulation increases heart rate and contractile strength of heart = cardiac output increases =

blood pressure increases. It also causes arteriolar vasoconstriction and increases total peripheral
resistance. It also causes venous vasoconstriction which increases venous return, stroke volume, cardiac
output and blood pressure

\ue000Parasympathetic stimulation has the opposite effects.
Rennin- angiotensin-aldosterone system is long-term regulator of blood pressure

Rennin is an enzyme that is secreted by the juxtaglomerular apparatus in the following cases:
1. Low blood pressure leading to low renal perfusion pressure
2. A fall in Na concentration in distal tubule

3.Renal sympathetic nerve activity, \u03b2-adrenoreceptor agonist and PGI2
Angiotensin II and atrial natriuretic peptide inhibit rennin release.
Rennin acts on angiotensinogen (made in liver) to produce angiotensin I which is converted to angiotensin II by
angiotensin converting enzyme when it passes from lung.

Angiotensin II has the following actions:
1. Vasoconstriction (direct and via increased noradrenaline release from sympathetic nerves)
2. Salt retention due to secretion of aldosterone and due to increased Na tubular reabsorption.
3. Vascular growth (hyperplasia and hypertrophy in heart and arteries)

Hypertension
\u202295% of cases have essential hypertension with poorly understood mechanism
\u20225% of cases have secondary hypertension due to chronic renal parenchymal or vascular disease or a
catecholamine or aldosterone-secreting adrenal tumour or due todrugs (NSAIDs, steroids, oral
contraceptive pill).
Pathophysiology
\u2022Increased peripheral vascular resistance due to widespread constriction of arterioles and small arteries.
Cardiac output and viscosity of blood are normal.
\u2022In chronic hypertension structural changes take place that cause further hypertension or complications
\ue000High peripheral resistance = increased work of heart = left ventricular hypertrophy = hypertrophy outstrips
coronary blood supply =fibrous tissue deposition= heart failure
\ue000Hypertension causes thickening of tunica media = arteries lose compliance = more pronounced pressure
wave = mechanical stress and endothelial dysfunction = atherosclerosis
\ue000Changes in renal vasculature = reduced renal perfusion = reduced glomerular filtration rate = activation of
rennin-angiotensin system = increase in blood pressure
Risk factors

\u2022Genetic factors:polygenic definite influence of heredity and family history
\u2022Fetal factors: low birthweight possibly due to changes in blood vessel structure or hormonal changes
\u2022Environment: obesity, sleep disordered breathing, alcohol intake, sodium intake, stress
\u2022Diabetes is associated with hypertension. The described metabolic syndrome includes hyperinsulinemia,

glucose intolerance, low HDL, hypertriglyceridaemia and central obesity, all of which are associated with
insulin resistance.
Investigations of hypertension

\u2022ECG (check for LV hypertrophy, ischemic heart disease)
\u2022Urinalysis for proteinuria if renal disease, vanillyl mandelic acid for malignant hypertension)
\u2022U&Es (high urea suggests renal impairment, low potassium without diuretic might suggest Conn\u2019s

(mineralocorticoid) or Cushing\u2019s syndrome(corticosteroid)

\u2022Lipids (high cholesterol is cardiovascular risk factor)
\u202224-hour ambulatory blood pressure monitoring
\u2022Echocardiography (check for left ventricular hypertrophy)

Management of hypertension
\u2022Smoking cessation, weight reduction, alcohol intake reduction, salt intake reduction, healthy diet (no
saturated fats, more fruits and vegetables), regular physical exercise
A= ace and alpha- B= bendroflumethiazide C= calcium channel- D= diuretic
Young < 55 & non Black
Older > 55 or Black
Step 1
ACE inhibitor or B-blockers
Calcium channel blockers or Diuretics
Step 2
A (or B) + C or D
C (or D) + A or B
Step 3
A+C+D
A+C+D
Step 4
+ alpha blocker or spironolactone
+ alpha blocker or spironolactone

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