Term
| 3 components of the JG apparatus |
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Definition
1)Macula Densa 2)Juxtaglomerular cells 3)Mesangial cells |
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Term
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Definition
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Term
| where are JG cells located? |
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Definition
| Mostly in the afferent arteriole but some in efferent |
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Term
| The macula densa responds to changes in _______ concentration in the distal convoluted tubule. |
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Definition
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Term
| Low Na in the DCT causes the release of what 3 mediators? |
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Definition
1)adenosine 2)Prostaglandin 3)NO |
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Term
| When macula densa cells swell NO is produced leading to the upregulation of ________ which synthesizes prostaglandins from arachidonic acid. |
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Definition
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Term
| What are the three pathways that contribute to renin release from the JG cells during hypotension? |
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Definition
1)intrarenal artery baroreceptors 2)carotid sinus baroreceptors through B1 3)Macula densa release of mediators |
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Term
| Angiotensinogen is converted to Angiotensin I by ______________ |
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Definition
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Term
| Angiotensin I is converted to Angiotensin II by ____________ |
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Definition
| ACE (angiotensin converting enzyme) |
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Term
| 5 effects of angiotensin II |
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Definition
1)increase in sympathetic activity leading to vasoconstriction 2)Tubular Na & Cl reabsorption and K excretion 3)release of aldosterone from the adrenal gland (also, increases absorption of Na & Cl and release of K) 4)arteriolar vasoconstriction causing increased blood pressure 5)ADH secretion by pituitary gland (acts on collecting duct for H2O absorption) |
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Term
| What are some negative long term effects of angiotensin II? |
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Definition
| vascular and cardiac hypertrophy and remodeling |
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Term
| If you block ACE you will increase __________ |
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Definition
Bradykinin which is a potent vasodilator (bradykinin is usually broken down by ACE) |
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Term
| 3 areas that may be targeted by drugs to counteract effects of angiotensin? |
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Definition
| 1)renin site 2)ACE itself 3)receptors for Angiotensin II (which would circumvent the secondary effect of increasing bradykinin when targeting ACE itself) |
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Term
| only renin inhibitor we discussed? |
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Definition
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Term
| Aliskiren is used to treat _________ |
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Definition
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Term
| 3 side effects of aliskiren |
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Definition
1)hyperkalemia 2)renal impairment 3)teratogen |
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Term
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Definition
1)Captopril 2)Enalopril 3)Fosinopril 4)Lisinopril |
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Term
| ____________ is the only ACE inhibitor which may be given parenterally. |
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Definition
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Term
| Indications for ACE inhibitor use (7) |
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Definition
1)Hypertension 2)congestive heart failure 3)acute MI (diabetic and hypertensive pts) 4)pts with cardiovascular risk(thrombotic disorders) b/c ACE helps maintain higher level of plasminogen 5)chronic renal failure (diabetes/diabetic nephropathy) 6)prevent glomerulosclerosis in diabetes even in absence of hyoertension 7)Scleroderma renal crisis |
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Term
| In the case of secondary HTN associated with fibromuscular dysplasia or atherosclerosis of the renal arteries do not use __________ to treat hypertension |
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Definition
| ACE inhibitors; b/c the sclerotic renal arteries caused drop in GFR that caused renin-angiotensin syst activation. Angiotensin II caused constriction in the efferent vessels to increase GFR and overcome lack of hydrostatic pressure in afferent due to the sclerotic artery. Use of ACE will cause GFR to drop and kidneys to fail. |
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Term
| Most common side effect of ACE inhibitors is _________ |
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Definition
| dry cough likely from increased bradykinin (this would be circumvented if receptors of ACE were targeted rather than ACE itself |
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Term
| Angioedema and cough distinguish ACE inhibitors from __________ |
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Definition
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Term
| Toxicity of ACE inhibitors (9, simple list) |
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Definition
1)Hypotension 2)cough 3)Hyperkalemia 4)Acute renal failure 5)teratogenic 6)skin rash 7)proteinuria 8)angioedema 9)dysgeusia (change in sense of taste) |
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Term
| 5 main Angiotensin II receptor blockers |
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Definition
1)Irbesartan 2)Losartan 3)Olmesartan 4)Telmisartan 5)Valsartan |
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Term
| Toxicity of angiotensin II receptor blockers (3) |
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Definition
1)Hyperkalemia 2)acute renal failure 3)teratogenic |
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