Term
| Why might you see HTN in liddle's syndrome? |
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Definition
| LIddle's syndrome involves GOF mutation in ENaC channel, leading to increased sodium reabsorption in the collecting duct and increased intravascular volume. |
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Term
| What happens to CO following volume expansion in the context of reduced kidney function? |
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Definition
1) Giving salt and water will initially increase CO, by increasing preload (this increases MAP)
2) After a few days, CO drops, but MAP remains high, because of increased blood delivery to vascular beds, which causes Autoregulation and increased TPR.
**In young hypertensive patients, CO remains high with low TPR, but after years of chronic high salt intake, CO decreases, but TPR is now elevated because of vascular remodeling** |
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Term
| What are the 4 major hypothesis of abnormal sodium excretion in HTN? |
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Definition
1) Altered Pressure Natriuresis
- Patient may regulate around a "higher baseline pressure" or have decreased sensitivity to volume expansion (IT TAKES MORE PRESSURE TO CAUSE EXCRETION)
2) Deficient natriuretic hormone
- ANP usually inhibits N-K-ATPase, thereby decreasing the force for sodium reabsorption. Therefore a deficit would enhance reabsorption.
3) Renin and Nephron heterogeneity (Laragh-Sealy Hypothesis)
- Sub-population of ischemic nephrons releasing too much renin, or abnormality in RAAS system
4) Reduced nephron number
- Fewer nephrons to excrete Na+
4) Reduced nephron number |
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Term
| Why might deficient ANP cause hypertension? |
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Definition
1) ANP cannot sufficiently inhibit Na/K ATPase, so there will be increased sodium reabsorption
2) Increased sodium reabsorption leads to more intravascular water retention. |
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Term
| How can the sympathetic nervous system contribute to renal-mediated hypertension? |
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Definition
SNS activity decreases renal blood flow, leading to RAAS activation and increased sodium reabsorption, with decreases in RPF and eventually GFR
Remember, stress can cause epinephrine release, which increases BP and acts on pre-synaptic beta 2 receptors to cause NE release. |
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Term
| What role does TPR play in the pathogenesis of HTN? |
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Definition
1) TPR is regulated by vascular endothelial and smooth muscle cells and maintains high blood pressures.
2) TPR is increased due to structural remodeling that increases arterial stiffness and causes various cell membrane alterations. |
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Term
| What is the role of mineral metabolism in HTN? What mineral changes cause HTN? |
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Definition
1) Hypocalcemia
2) Decreased dietary K+ and Mg2+ intake
3) Tobacco, Caffeine and Alcohol |
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Term
| What are the most common (3) causes of HTN in young patients with no family history who have an abrupt onset of disease and fail empiric therapy? |
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Definition
Secondary HTN
1) Renal parenchymal disease
- sodium excretion goes down and CO goes up. Autoregulation will decrease CO and increase TPR.
2) Renovascular HTN (stenosis)
- Decreased perfusion and RAAS causing increased BP and atheroslerosis, aneurysm, emboli and arteritis.
3) Adrenal gland causes
- Pheochromocytoma (chromaffin tumor)
- Primary aldosteronism (aldosterone)
- Cushing's syndrome (cortisol excess because of ACTH) |
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Term
What are the common consequences of HTN in each of the following systems?
1) Cardiac
2) Cerebrovascular
3) Peripheral vasculature
4) Renal
5) Retina |
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Definition
1) CAD and LVH, leading to MI and CHF.
2) TIA/CVA and stroke.
3) Atherosclerosis of distal arteries with diminished circulation to extremities.
4) Serum creatinine >1.5 (clinical proteinuria), microalbuminuria
5) Retinopathy (grade 1-4)
**Grade 3-4 have correlation with renal failure** |
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Term
| What are the 5 phases and associated age ranges of essential hypertensive renal disease? |
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Definition
Phase 1 (20-30)
- increased renal vascular resistance
Phase 2 (30-40)
- Functional and structural disturbances of vasculature with decreased perfusion (GFR PRESERVED)
Phase 3 (40-50)
- Sustained rise in FF with proteinuria and arteriolar nephrosclerosis
Phase 4 (50-)
- Renal mass decrease with progressive decrease in GFR (with increased glomerular capillary hydraulic pressure)
Phase 5 (50-)
- Chronic renal insufficiency progressing to ESRD |
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