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Lesson 10 & 11, When BP is low, prorenin is cleaved to renin released…
Lesson 10 & 11
HYPERTENSION
Systolic BP: highest pressure in arteries drg ventricular contraction
Diastolic BP: min pressure when ventricles relax
(mai)
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Signs & Symptoms:
- throbbing headache
- nausea/vomiting
- giddiness/ blurred vision
(mai)
Risks: (jonathan)
- heart disease
- kidney disease
- vascular dementia
- peripheral arterial disease
- underlying conditions: obesity, diabetes, COPD
Types of hypertension: (jonathan)
- Essential hypertension: idiopathic or primary hypertension
- Masked: elevated BP at home but normal office BP
- Resistant: elevated BP despite concurrent use of 3 antihypertensive drugs of different classes
- Secondary: due to an identifiablle, potentially curable cause
Pharmacologic Treatments
Effect on RAAS - Achala
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(2) Angiotensin converting enzyme inhibitors (ACE-I) : Enalapril, Lisinopril
Reversible competitive inhibition of ACE (enzyme) - prevents conversion of angiotensin I to angiotensin II
Adverse effects: angioedema, persistent dry cough, hyperkalaemia
(3) Angiotensin II Receptors blockers (ARB) : Valsartan, Losartan
Prevents binding of angiotensin II to AT1 receptors (antagonist) in arteriolar smooth muscle & adrenal gland - arteriolar dilation & decreased Na reabsorption - water follow Na - preventing water retention - decreased blood vol. - decreased PVR (* therapeutic effects only exerted on ACE-pathway: not as effective)
Adverse effects: angioedema, hyperkalaemia, low incidence of dry cough
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(9) Other Vasodilators
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Adverse effects: Postural hypotension, Tachycardia,
fluid retention, lupus-like syndrome
e.g. Hydralazine
Rapidly and extensively absorbed with half life
of 3 to 7 hours. Excreted mainly as metabolites in the urine
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BP REGULATION (mai)
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Renin-angiotensin-aldosterone system (RAAS)
- regulates BV and systemic vascular resistance
- Angiotensin II --> systemic vasoconstriction of the arterioles, Na reabsorption in proximal convoluted tubules of kidney, release aldosterone from adrenal cortex
- Hypothalamus gets stimulated for thirst and water intake
- reduces sensitivity of baroreceptors to increase BP so it will not counteract the RAAS effect
Thus, increase BV and BP
Baroreceptors reflex
- negative feedback
- aorta and carotid artery sense changes in BP
in the vascular system and input to vasomotor center (VC)
High BP,
- stretches the wall of aorta and carotid arteries
- baroreceptors fire action potentials > normal rate
- Nucleus of tractus solitarius (NTS) in brainstem activate
parasymp system
- inhibit SNS
- since activation of PSNS and inhibition of SNS works oppsosite
- decrease in CO and vasodilation to reduce BP
LIPOPROTEIN (monica)
Lipoprotein and cholesterol --> transported in bloodstream. --> consist of central core of hydrophobic lipid encased in hydrophilic coat or polar phospholipid, free cholesterol & apoprotein.
4 Main Classes:
( classified based on size and density)
- High-density lipoprotein (carry cholesterol)
--> contains apoA1, apoA2
--> 7-20 nm
--> <1 mmol/L
- Low-density lipoprotein (carry cholesterol)
--> apoB-100
--> 20-30 nm
--> <3.4 mmol/L
- Triglycerides (VDL and Chylomicrons)
--> apoB-100, apoC2
--> VDL: 30-80 nm
--> Chylomicrons: 100-1000nm
--> < 2.3 mmol/L
- Total cholestrol
--> no apoprotein
--> no diameter
--> < 5.2 mmol/L
Lipoprotein Transport
- Chylomicrons --> transport triglycerides and cholestrol from GI tract to the tissues --> triglyceride split and releases --> free fatty acids & glycerol --> taken up in muscle and adipose tissues. :
- Chylomicron remnants --> taken up in liver --> cholesterol is stored and secreted in blie , oxidised to bile acids/ converted into very low-density lipoprotein
- Very low-density lipoprotein --> transport cholesterol & newly synthesised triglycerides to the tissues --> TGs are removed --> leaves intermediate density and low density lipoprotein particles with large component of cholesterol --> some LDL cholesterol taken up by the tissues and by liver --> via endocytosis by specific LDL receptors.
- High-density lipoprotein particles absorb cholesterol derived from cell breakdown in tissues --> transfer to liver
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Dyslipidaemia
Drugs used (monica)
Bile acid sequestrants
Binds to bile acids in gut -> prevents reabsorption
-> increased cholesterol catabolism; up-regulates LDL receptors
Toxicity: constipation, bloating,
interferes with absorption of some
drugs and vitamins
Fibrates
peroxisome proliferator-activated receptors agonist. increase gene transcriptions
Causes VLDL clearance. Lower LDL, higher HDL
(zian)
- Omega 3 Fatty Acid: reduce hepatic VLDL production and increases VLDL clearance --> reduce plasma triglyceride concentrations
- Statins (ORAL)
Inhibit HMG-CoA recutase --> decrease in cholestrol synthesis and up regulate LDL receptors on hepatocytes, decrease VLDL secretion
Toxicity : high, myopathy jaundice
Types of Dyslipidaemia
- Hypercholesterolemia --> TC, LDL
- Mixed Dyslipidaemia --> TC, LDL, TG
- Hypertriglyceridemia (>4.5 mmol/L or 400 mg/dL) (TG)
- Severe hypertriglyceridemia (>10 mmol/L or 900 mg/dL) (TG)
(Mai)
- When BP is low, prorenin is cleaved to renin released into blood
- conversion of angiotensinogen (liver) into angiotensin I by renin
- Angiotensin I converted to angiotensin II by angiotensin converting enzyme (ACE, lungs and kidney)
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