Case 2/ multisystem 1

Hypertensive Headache Is due to overstretched cranial blood vessels. Hypertensive headache characterize by: A dull or tight pressure moderate aches, with sensation of band round the head. Radiates forward from the occipital region. No associated vomiting or photophobia excluding ICP. More prominent in early morning & improves through mid-day. Worsened by movement. Hypertension Primary hypertension is commoner than secondary hypertension. Primary essential hypertension is due to abnormalities in the physiological mechanisms involved in the regulation of blood pressure. Pathophysiology: All of the mechanisms factors below that are involved in the normal regulation of BP are likely to participate in the pathophysiology. The initial changes in essential HTN are due to overlap of abnormal changes in the following factors, NOT due to one single factor, and it isnt necessary to have all the factors. Is due to many contributed factors Renin-angiotensin- aldosterone system The circulating Renin-angiotensin- aldosterone is not thought to be directly responsible for the rise in BP.
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Case 2/ multisystem 2

Not all persons with essential HTN have an elevated renin in plasma; some of patients have low renin plasma concentrations.

Sympathetic nervous system: overactivity Peripheral resistance Most patients with HTN have normal cardiac output at beginning but a raised total peripheral resistance. This elevation is due to persistent contraction of smooth muscles in arterioles resulting in the release of growth factors (mainly mediated by angiotensin II as it cause vasoconstriction) , growth factor cell proliferation arteriolar wall thickening. The thickening results in irreversible rise in peripheral vascular resistance. Smooth muscles contraction is also maintained by sympathetic NS SNS overactivity. Increase intracellular Ca may also have a role as it increase the contraction of smooth muscles.

Obesity BMI > 27 considered as obese. The mechanism that link obesity with essential HTN include insulin resistance, activation of SNS & RAAS, where they have produce their effect on kidney blood volume BP. Adipose tissue is also a major site of production of angiotensinogen, hence obese persons are likely to have increased concentrations of angiotensinogen angiotensin producing their effect BP.

Salt intake People on high salt intake with genetic defect in the ability to extrude Na from cells are at higher risk of HTN. Because this leads to increase in intracellular Na intracellular Ca arteriolar smooth muscle tone (vasoconstriction).
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Case 2/ multisystem 3

Insulin resistance Endothelial dysfunction discussed in vasoactive substance. Genetics Genetic factors account for up to 30%, the factors encodes most of the proteins involved in regulation of BP. Vasoactive substance Substance produced by vascular endothelium cells, they are either vasodilator or vasoconstrictor. Nitric oxide is a vasodilator in nature.

In HTN, production is impaired due to endothelial dysfunction no dilation constriction BP In addition normal vasodilatory response to endothelial agonists (acetylcholine) is diminished. Endothelin is a potent vasoconstrictor in nature

It cause constriction of blood vessels through its activation of local RAAS (Reninangiotensin- aldosterone system) It plays a role in abnormal pressure-natriuresis relationship. Atrial natriuretic peptide (ANP) hormone secreted from the atria of the heart.

Defect in ANP may cause fluid & Na retention essential hypertension. Bradykinin (BK) a vasodilator in nature. (physiological information only) Hypertensive retinopathy Changes in optic fundi can estimate the severity of HTN, which provide an indication of the arteriolar damage occurring anywhere in body.
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Case 2/ multisystem 4

Grade 1 Grade 2 Grade 3 Grade 4

Sliver wiring: Arteriolar thickening, tortousity & reflectiveness. arteriovenous nipping: G1 + constriction of veins at arterial crossing. Flame or blot haemorrhages, cotton wool exudates: G2 +evidence of retinal ischaemia. G3 +Papilledema

Diabetic retinopathy Changes occur in varying combinations & are used to classify the retinopathy *1 Microaneurysms The earliest clinical abnormality detected. Near & separated from retinal vessels. Blot Hemorrhage Occur in the deeper layers of retina. Also, Flame-shape haemorrhages occurs particularly if the patient is hypertensive. *2 Exudates (patches) Are characteristic of diabetic retinopathy. Found at the perimacular area. Results from leakage of plasma from abnormal retinal capillaries. Cotton wool spot Similar to those seen in HTN. A feature of pre-proliferative diabetic retinopathy. Intra-retinal microvascular abnormalities
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Case 2/ multisystem 5

Are *3 dilated, tortuous *capillaries indicating sever pre-proliferative retinopathy. *4 Neovascularisation Occurs in response to ischaemic retina. If they rupture causes pre-retinal (sub-hyoloid) or vitreous hemorrhage. Serous products leaking causing adhesion and contraction retinal detachment. Venous changes *5 venous tortuous dilatation early feature Beading sausage-like change. Increased tortuosity including oxbow lakes or loops advanced preproliferative retinopathy. Rubeosis iridis Development of new vessels on the anterior surface of the iris may obstruct the drainage angle secondary glaucoma. Classification of diabetic retinopathy b ased on prognosis for vision 840 The effect of hypertension on Heart High BP introduce a pressure load on the heart causing cardiac workload leading to hypertrophy & thickening of the left ventricle (left ventricular hypertrophy). Presence of forceful apex beat & 4th heart sound. Left ventricular hypertrophy leads to congestive heart failure as complication (presence of dilated Left ventricle) As HTN accelerates atherosclerosis it will initiate coronary arterial atherosclerosis Ischemic heart disease (common).
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Case 2/ multisystem 6

Atrial fibrillation Common Caused by diastolic dysfunction caused by lt. ventricular hypertrophy. Or by the effect of coronary artery (ischemic heart) disease. Antihypertensive agents The major drugs are: thiazides, B-blockers, Ca antagonist, ACE inhibitors, & alpha blockers. Thiazides: Have diuretic action 1st choice in treatment of HTN Other diuretics As loop diuretic which are more potent. E.g.furosemide or bumetanide Are not used in renal impairment or in conjunction with ACEI B blockers: 1. Cardioselective type blocks B1 receptors only, e.g. atenolol, metorprolol, bisoprolol. Adrenergic blockers: Are combined B & alpha adrenoceptor antagonist E.g. carvedilol, labetalol, the latter is used in malignant hypertension. ACE inhibitors: Inhibit the conversion of angiotensin I to angiotensin II. E.g. enalapril ,ramipril, lisinopril. Not favorable in pt. with impairment renal function or renal artery stenosis.
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Case 2/ multisystem 7

S.E. include: hypotension, rash, cough, hyperkalemia, & renal dysfunction. Angiotensin receptor blocker: e.g. losartan, valsartan, tolerated better than ACEI. Ca antagonist: E.g. nifedipine, amlodipine. Well tolerated in elderly, their S.E. are flushing, palpitation, fluid retention (How, while it treat HT Other drugs: Centrally acting drugs: (methyl dopa, clonidine) Bind to alpha2 receptor decrease sympathetic outflow. Methyl dopa preferred in pregnancy. Vasodilators: Minoxidil, & hydralazine, acts directly on smooth B.V. Minoxidil not preferred in female as it increases facial hair. Selective alpha1 blockers: as prazosin, indoramin, doxazosin. Main pathophysiology of stroke types & underlying causes: A PDF file Ischemic stroke risk factors 26.60, (1202 ( Hemorrhagic stroke risk factors 26.61, (1203 ( Cortical stroke clinical features any feature caused by lesion on the cortex: Examples: Any impairment of, memory, speech, or level of consciousness. Defects as aphasia, neglect syndrome.
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Case 2/ multisystem 8

Subcortical stroke clinical features any feature caused by lesion at any place away from the cortex such as brainstem, cerebellum: Examples: ataxia, diplopia, vertigo, bilateral weakness. Clinical features of facial N palsy: Preserved function in upper face. Loss of nasolabial fold Mouth deviated to normal side. Drooping of mouth with dropeling of salavia at affected side. Loss of frontal wrinkling. Bells phenomenon: no closure of eye with up rolling of eye. Loss of nasolabial fold. Mouth deviated to normal side. Drooping of mouth with dropeling of saliva at affected side.
UMN

LMN

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Case 2/ multisystem 9

Speech defects resulting from stroke Expressive (Braocas) aphasia A motor lesion , location is at the inferior frontal gyrus, 44, 45 areas.

Language is understood but not easily produced. So they are unable to produce easily speech, they have difficulties, (nonfluent) They can write the words.

Receptive (Wernickes) aphasia A sensory lesion, location is at the sensory speech centers (e.g. angular gyrus at posterior parietal lobe). Language is not understood, means loss of the ability to understand the spoken & written word. But the speech is unaffected, they can produce fluent speech but unaware of the meaning of the words, they might use incorrect of nonexistent words. Wernickes aphasia Sensory lesion Lesion at the sensory speech center Cant understand the spoken written words Fluent meaningless speech Braocas aphasia Motor lesion 44, 45 frontal gyrus Understand the spoken written language, Not fluent, but understood speech

Global aphasia Destructive lesions in both sensory & motor area.

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Case 2/ multisystem 10

Speech is nonfluent (loss of production of words), and the language in not understood.

Conductive aphasia The defect is inability to repeat the words, although the 1st spontaneous speech production is not affected. The lesion is in arcuate fasciculus. Hemiplegias see the UMNL clinical features as hemiplegia is a UMNL UMNL Power Weak upper limbs>> extensors weaker lower limbs>> flexors weaker Tone Reflex Babiniski sign Babiniski sign Scratching the skin along the lateral aspect of the sole will lead to dorsal flexion of the great toe & the other toes fan outward. The normal response (it means ve Babiniski sign), is plantar flexion of all the toes. Hemiplegic gait Leg is extended & the toes forced downward. When walking, abduction of circumduction at the hip preventing the toes from catching the ground. Posture
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LMNL Weak

Spasticity Increases exaggerated Positive in UMNL

Flaccidity Reduced/absent Negative in LMNL

Case 2/ multisystem 11

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