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What type of blood pressure would be considered normal?
Systolic <120 & Diastolic <80
What is Hypertension?
-An increase in blood pressure
* Remember it can involve pulmonary circulation or systemic circulation. Systolic >140 and/or diastolic BP >90
What is Primary Hypertension?
- Aka: Essential hypertension that is idiopathic and tends to be familial.
What are the risk factors involved in Primary HTN?
-Race ( increased in African Americans and Decreased in Asians)
-Lack of Physical Activity
- High Salt Diet
Does Secondary HTN have an identifiable etiology?
(Renal Diseases, Endocrine Diseases and Vascular Diseases)
* Remember those diseases can cause HTN
What are the main 4 Etiologic Factors in the Pathogenesis of HTN?
-Increased Sympathetic Tone
- Genetic abnormality in Na metabolism
-Excess Salt intake
-Increased Stiffness of the aorta
How can an increase in sympathetic tone increases blood pressure in a patient?
- Increased sympathetic tone will cause vascular spasms and sclerosis/stenosis of the Renal artery
- Juxtaglomerular Cells will get signaled to secrete Renin--> converts Angiotensinogen to angiotensis I
- ACE in the lungs converts Ang I to Ang II
-ANG II--> contracts arteriolar smooth muscle increasing TPR--> increasing blood pressure
- ANG II--> also promote aldosterone release to reabsorb sodium and water in the renal tubules-->increasing blood volume --> increasing blood pressure.
* Remember it also causes an increase in CO by B1 receptors and Alpha 1 receptors and B2
Which cells signal the juxtaglomerular cells to secrete renin?
- Macula Densa cells
* Remember they are chemoreceptors that monitor the delivery of the sodium to the distal tubule. The JG cells are surrounding the afferent arteriole.
How else can you classify HTN?
What is Benign HTN?
-Mild to moderate elevation of BP that is clinically silent and causes vessels and organ damage slowly over time.
What type of Pathology do you see in Benign HTN?
- Visceral Pathology
Mild Hypertensive Retinopathy would be classified under what type of Pathology due to Benign HTN?
How will a patient present to the clinic if they have mild hypertensive retinopathy?
- Eye will "hurt"
- loss of visual acuity
*Along with HTN signs and symptoms but remember this is how the patient will present and what you should look for in a vignette .
What three organs are affected in visceral pathology of Benign HTN?
* Remember these are small vessels that are affected.
What is Arteriolosclerosis?
- Narrowing of Small arterioles--> divided into Hyaline and hyperplastic
If you have proteins leaking into the vessel wall which produces a vascular thickening and upon microscopy you see pink hyaline (protein) what is this a consequence of?
* remember diabetes can also cause Hyaline arteriolosclerosis and can slowly progress to chronic renal failure
Explain the mechanism of arteriolosclerosis in benign HTN?
- increased BP --> Vessel wall damage-->increased the permeability of the walls and protein leaks in -->causing sclerosis.
In LV hypertrophy what do you see on histology?
Increased cell size (diameter)
Large, hyperchromatic, and rectangle
How do you describe the nuclei of the cardiomyocyte in LV hypertrophy?
-Hyperchromatic (increased in staining)
A Black patient with a 22 year Hx of Diabetes and hypertension presents with chest pain. In the past she has suffered from a stroke and she currently is suffering from proteinuria with evidence of periods of accelerated or poorly controlled BP. Based on the presentation what is the mechanism of the disorder she most likely has?
- Patient most likely has Hypertensive Nephrosclerosis
--> poorly controlled bp and long standing arteriolosclerosis leads to a reduced vessel caliber with end organ ischemia--> glomerular scarring that slowly progresses to chronic renal failure
A young african american male comes to the ED with a Hx of severe cocaine and amphetamine use presents with symptoms of nausea,vomiting, blurry vision and headache. Upon fundoscopy there is a bilateral optic disk swelling and the patients blood pressure is 190/126 . What is the most likely Diagnosis and what is the most effective treatment at this current moment?
-Hypertensive Emergency ( Malignant HTN)
-Treatment--> Rapid lowering of BP (Usually with IV nitroprusside but now a days the first line DOC for Hypertensive ER is a L type calcium channel blocker)
What are the causes of Malignant HTN?
-Preexisting HTN or Withdrawal of short acting antihypertensive drugs
How is the brain affected in a Hypertensive Emergency?
- Stroke due to thickening of the vessel wall by hyperplasia of smooth muscle
Reduced vessel caliber in the brain disrupts the autoregulation leading to the development of cerebral edema, increase intracranial pressure and hypertensive encephalopathy.
How will the surface of the kidneys look in a patient with fibrinoid necrosis?
- Microinfarctions and microhemorrhages ( Petechia)
* remember Fibrinoid Necrosis is fibrin-containing conglomerate of necrotic tissues and plasma proteins.
Explain the mechanism of hypertensive encephalopathy:
-High BP → dilation of cerebral arterioles →
increased permeability → cerebral edema
→ raised intracranial pressure
What is HYpertensive Urgency?
-Severe BP elevation (>180/120 mm Hg)
without an acute target-organ damage
- NO PAPILLADEMA
If you are given a a gross specimen of a kidney and you see petechia what is your first thought?
- Malignant (Acute Hypertensive) Nephrosclerosis
How will the Histology slide look of a patient with hypertensive encephalopathy?
- Aggregates of necrotic tissue with plasma proteins
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