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Q1) Higher blood glucose level --> more water in blood to regulate the blood glucose --> blood pressure increase

Q2) Glibenclamide --> Oral Sulphonylureas à Hypoglycaemia, weight gain

Gliclazide --> Oral Sulphonylureas à Hypoglycaemia, weight gain

Glipizide --> Oral Sulphonylurease à Hypoglycaemia, weight gain

Side effects of Sulphonylurease is weight gain. The patient is already obese and hence should not be given a drug that would further increase her BMI.

Q3) Ace Inhibitors à Angiotensin-converting enzyme (ACE) inhibitors prevent or delay microvascular and macrovascular complications of diabetes and are recommended as first-line antihypertensive agents in patients with diabetes. ACE inhibitors delay progression of diabetic kidney disease and more effective than other medications in delaying onset kidney failure (glomerular filtration rate) ACEIs may be used alone for BP lowering but are much more effective when combined with a thiazide-type diuretic or other antihypertensive drug.

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Clinical uses & side effects

antidysrhythmic (mainly verapamil)

angina (e.g. diltiazem)

hypertension

Adverse Effects :

Non-dihydropyridines (diltiazem and verapamil)

-Bradycardia (↓ HR) due to decreases cardiac contractility

-Constipation

Dihydropyridines (amlodipine and nifedipine)

-    Peripheral oedema

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Ca2+ antagonists block Ca2+ entry to cells by preventing the opening of voltage gated L-type calcium channels

site of action: heart and smooth muscles (inhibits the Ca2+ entry caused by the depolarization in these tissues

↓contractility, ↓conductivity of the heart; ↓O2 demand

Verapamil which is relatively cardioselective (antidysrhythmic action) whereas most of the dihydropyridines (example : nifedipine) and exerts a greater effect on the smooth muscle (mainly on resistance vessels) and reduces PVR , diltiazem is intermediate.

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- act of increasing the amount of urine produced by the kidneys
-  it increases the secretion of Na+ (natriuresis) and H2O by decreasing the reabsorption of Na+ and Cl- from filtrate
- most diuretics have direct action the nephron act from the tubular lumen and reaches their sites of action by being secreted into proximal tubule

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Therapeutically useful diuretics :

- Loop diuretics :

act on thick ascending loop of Henle

most powerful diuretics in comparison with thiazides

capable of causing excretion 25% of filtered Na+

can cause torrential urine flow and Hypokalemia (muscle cramp and weakness)  and postural hypertension

-   Thiazide diuretics :

act on early distal tubule

reduces Ca2+ excretion ( advantages in older patients  at risk of osteoporosis)

adverse effects of Hypokalemia

- Potassium-sparing diuretics/ aldosterone antagonists –

act on collecting tubules and ducts

limited diuretic action alone because distal Na+/K+ exchange the site on which they act accounts for reabsorption of only 2% of filtered Na+

can help to prevent hypokalemia when combined with loop diuretics or thiazides , compete with aldosterone for its intracellular receptor  , which thereby inhibits distal Na+ retention and K+ secretion

side effects are Hyperkalemia and postural hypertension

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Background: renin aids in the series of enzymatic step to cleave off amino acid from angiotensinogen to angiotensin I and then to angiotensin II which is a potent vasoconstrictor

This prevent angiotensin II to be formed and prevent stimulation of Aldosterone that is also part of raising blood pressure

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1.blocks all effect of angiotensin II by blocking AT1 receptor in the arteriole smooth muscle and in adrenal gland. thus what it does is preventing binding of Angiotensin II which is a vasoactive hormone that induces vasoconstriction and stimulates the secretion of aldosterone by the adrenal cortex, which results in sodium and water retention.

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competitively inhibits ACE so to prevent the conversion of angiotensin I to Angiotensin II via ACE pathway which will lead to sympathetic activation, vasoconstriction and etc.

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Angiotensin II subtype 1 receptor blocker (ARB)

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Angiotensin II subtype 1 receptor blocker (ARB)

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What is hypertension and how it is form?

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What is hypertension and how it is form?

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1. chronic elevation of either systolic or the diastolic BP

2. Should be consistently measured on average of 2 or more reading taken at each of 2 or more visit after initial screening

3. normally asymptomatic until organ damage is imminent

4. signs and symptoms: throbbing headache, nausea, or vommiting and etc

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1. Why do diabetic patients have higher risk of hypertension?

2. One of the drugs in this case study should ideally not be recommended. Which drug is it? And why?

3. Which antihypertensive agents are recommended for patients with diabetes?

https://diabetesjournals.org/clinical/article/22/3/137/1660/Case-Study-Treating-Hypertension-in-Patients-With

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1.  Antidiuretic hormone(ADH)
produced by hypothalamus a strong vasoconstrictor that can increase BP by raising blood volume--> increase cardiac output

2. Nitric oxide and endothelium-derived relaxing factor
produced locally by the vascular endothelium, a monolayer of endothelial cells

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MOA:
α1 selective antagonist --> vasodilatation through blocking alpha1 receptors on arterioles and veins --> arterial pressure decrease due to decrease in resistance and capacitance vessels.

Adverse Effects:
1. Postural hypotension --> reduced blood pressure by reduced venous retun
2. Reflex tachycardia --> baroreceptor
3. Nasal congestion --> vasodilation in the nasal mucosa

E.g., Prazosin

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1. regulates smooth muscles constriction and relaxation of tunica media

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Main Function: Reduce sympathetic outflow from vasomotor centers

Drug --> false neurotransmitter α-methylnoradrenaline (MeNA) --> alpha2/ alpha1 potency ratio is much greater than that of noradrenaline --> tips scale from excitation to autoinhibitory feedback mechanism --> reduced activity of sympathetic nerves --> reduction in arterial pressure

Adverse Effects: Drowsiness, Rebound hypertension and Dry mouth

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1. Regulates cardiac output and heart rate

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1. release epinerphrine, norepniephrine, renin (RAAS)

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1. collection of integrating neurons/ group of neurons
2. Found medulla oblongata
3. Regulated on min to min basis
4. Connected to the main 4 control site of BP
5. controls the cardiac output as well as peripheral vascular resistance

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1. Specialized neurons
2. located at aortic arch and carotid sinus in the carotid artery
3. sense change in BP e.g. increase in BP --> causes the wall of aorta and carotid artery to stretch--> more action potential from the baroreceptors