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41 Cards in this Set
- Front
- Back
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is arterial pressure lower or higher in infants?
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LOWER
70mmHG |
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How is renin released and activated?
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It is released as pro-renin and is proteolytically processed
Renin antagonists like aliskiren can bind to the active site of renin |
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Where is renin released from?
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The afferent arteriole of the kidney
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What are the types of AT receptors?
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Type 1 and 2 and only type 1's effect is known and this is the only receptor that angiotensin blockers affect
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What are the primary roles of the RAA system?
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To prevent hypotension and maintain renal perfusion
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What do prostaglandins do to renin production? What does ANP do?
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They increase it
ANP causes a decrease in renin production |
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What does 11 beta hydroxysteroid dehydrogenase do?
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It is co-expressed with mineralcorticoid receptors
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What does the angiotensin 2 receptor type 1 do exactly?
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It is responsible for promoting aldosterone release and vasoconstriction
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What percent of salt is reab. in the tubule?
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99%
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What are the aldosterone sensitive nephron segments?
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The CCTand ICT
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What does aldosterone stimulate within the cel?
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1. Na/K ATPase on the BL side
2. ENaC activity on the apical side |
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How does hyperaldosteronism look clinically?
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Hypokalemia and Hypertensive
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The ENaC channel is the product of three different components--mutation in any of these leads to what?
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Liddle's Syndrome
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Infants presenting with Hypotension and hypokalemia probably have what disorder?
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Liddle Syndrome
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A mutation in the ACE allele causing overproduction would cause what?
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High BP
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What is glucocorticoid remediable HTN?
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Gene defect that allows a crossover of ACTH responsive promotor to aldosterone synthase = ALDOSTERONE OVERPRODUCTION
ADMIN. of GLUCOCORTICOIDS CAUSES A DECREASE IN ALDOSTERONE EXPRESSION |
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What is syndrome of apparent mineralcorticoid excess?
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Gene defect in 11 beta-HSD that causes HTN because the enzyme doesn't readily cleave cortisol to cortisone
The built up cortisol can bind to mineralcorticoid receptors and cause HTN |
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Renal artery stenosis causes what?
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Promotion of renin overproduction and RAAS facilitation
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A patient presents with HTN and hypokalemia as well as a mass on one kidney..what is the diagnosis?
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Aldosteronoma or Conn's Syndrome
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What can overeating licorice cause?
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Glycyrrhetic acid over-ingestion can lead to hypokalemia and hypertnesion due to 11-beta HSD inhibition
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What does 11-Beta HSD do?
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Converts cortisol to cortisone--there is far more cortisol in the body than aldosterone but both can bind mineralcorticoid receptors
If you convert cortisol to cortisone then it can't bind the mineralcorticoid receptors |
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Why do we put people with HTN on a low salt diet?
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Because the RAAS system is relatively inactive at high salt levels...this means that it is not a critical determinant of BP
If you lower salt levels then RAAS is important and controlling it with an ACEi will lower BP |
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Lack of ETB receptors causes what?
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Hypertension on a high salt diet
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Lack of ETA receptors can cause what?
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Hypotension
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Where is ETA located and what are its affinities?
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Located in vascular smooth muscle and has far more affinity for ET-1 than the other types
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Where is ETB located and what are its affinities?
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Located in the Collecting duct endothelium and has equal affinities for all ET's
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How is ANP released?
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Atrial stretch causes cleavage of Pro-ANP to active ANP with Corin which then binds to guanylyl cyclase receptors to convert GTP to cGMP which causes vasodilation and alters salt transport in the CD
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How does ANP work?
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It causes decrease in BP mediated by cGMP through...
1. Zona glomerulosa: DECREASE in release of aldosterone in response to angiotensin II and KCl Vascular myocyte: Vasorelaxation Endothelium:Increased vascular permeability Glomerulus: INCREASE IN Glomerular filtration rate Collecting tubule: DECREASE in Sodium reabsorption |
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Underproduction of ANP leads to what? Overproduction?
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HTN due to gene knockout
If heterozygous then: will have circulating ANP but sensitive to high Na+ Overproduction = low BP |
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Increase in urinary sodium causes what?
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Increase in urine cGMP
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How is NO normally produced? How can that be screwed up?
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Oxidation of L-arginine to NO
ADMA or Symmetric dimethyl ARG will bind NO synthase and inhibit NO production competitively |
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True/False: The end product of ANP and NO is the same.
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TRUE--it is cGMP
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What is the mechanism for NO production and action?
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Arginine is brought into the endothelial cell and it binds the calmodulin and is converted to NO and citruline
NO then diffuses into the adjacent smooth muscle cell and increases cGMP production |
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Oral administration of NO syntthase inhibitors causes...
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Increased BP
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What can happen with regards to NO during sepsis?
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Overproduction of NO synthase and fall in BP
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Salt sensitive individuals do well with what?
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thiazide diuretics!
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True/False: There is no way to reverse increase in vascular stiffness that accompanies age.
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FALSE--low salt diet can have an immediate effect and lower stiffness
High salt diets cause TGF-B levels to increase and this promotes vascular stiffness through matrix produection and smooth muscle hardening |
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How does TGF-B cause vascular hardening?
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It downregulates Matrix Metalloproteinases
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True/False: BP MUST be lowered to below normal in order to maintain health.
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FALSE--just get it below 140/90
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What is essential HTN?
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Idiopathic HTN that is established between 30 and 50 years
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What labs should be evaluated in order to assess an adult HTN patient?
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Med history
Family history of kidney disease Two BP readings prior to starting treatment Thigh cuff pressure once on a young patient Serum K+ |
