L12- Secondary HTN Flashcards
Name the 6 causes of secondary HTN that we discuss in this lecture
Chronic Kidney Disease (5%)
Renovascular Disease (4%)
Adrenal Disease (.5%)
Pheochromocytoma (.2%)
Genetic causes
Obstructive Sleep Apnea
Discuss pathology of CKD and HTN
Kidney damage results in fewer functioning nephrons to filter blood (extra sodium and water) so the remaining ones have to work harder – get intraglomerular HTN and retention so increased CO – more damage to kidney exacerbating cycle
Damage leads to inappropriate volume retention and activation of RAS, SNS and NO dysregulation
What are other problems in CKD treatments that can also contribute to HTN?
Treatment of CKD can lead to secondary Hyperparathyroidism with higher intracellular Ca concentrations leading to stiffer vessels
Erythropoietin treatment leads to higher Hb and therefore more CO
What happens in renal artery stenosis?
Reduced flow to those selfish, selfish kidneys causes the Glomerulus to compensate by increasing Renin release to preferentially act on efferent arteriole to constrict it and maintain GFR
HOWEVER increased AG2 causing increased BP
When would you suspect Renal Artery stenosis?
**start treatment on patient for HTN with Ace-Inhibitor and BP plummets!!! **
So, that’s good that you cured the HTN but also discovered the underlying problem is renal artery stenosis. STOP ACE-Inhibitor so you can maintain GFR and prevent kidney damage - dont want to cause CKD!
What is Captopril?
How can does the Captopril nuclear scan work?
What would be diagnostic results?
Captopril = ACE-Inhibitor
In scan, inject radio-nucleotide tracer to measure uptake into kidneys and then into bladder/urine over time. Then add Captopril
DDX = Renal Artery Stenosis if add captopril and see SLOWER renal uptake of drug bc less renal perfusion pressure AND *Longer time to get drug to appear in urine *
Serum diagnosis for renovascular disease?
HIGH renin levels in plasma
Profound drop in BP with ACE-Inhib
Where is Aldosterone released from? What does it do? What can cause Hyper-release?
Aldosterone released from Adrenal Cortex (Glomerulosa) and acts on the Kidney to cause increase Na Retention and K Secretion
Hyper-Aldosteronism results from Adrenoma, Carcinoma or Hyperplasia of adrenal cortex
How do you Diagnose Primary HyperAldosteronism?
High Aldosterone
LOW RENIN (suppressed from aldosterone)
LOW SERUM POTASSIUM!!! (high urinary potassium)
What drugs can block Aldosterone’s effects on the kidney?
Spironolactone or Eplerenone
aldo antagonists acting at distal tubule
How does Licorice ingestion (or Kushing’s Disease or Obesity or 11-beta-OH deficiency) cause HTN?
Excess Cortisol!!!
outcompetes Aldosterone at mineralcorticoid receptor and acts similarly
What are the Monogeneic determinants of HTN?
1) Congenital Adrenal Hyperplasia
- 21 OH deficiency (90%) = salt wasting
- 11 OH deficiency = HTN, Hypokalemia, elevated 11-deoxycorticosterone
- 17 OH deficiency = rae but has sexual problems!!
**2) Liddle’s Syndrome!! **
(constituitive activation of Amiloride sensitive NA channels and so No ALDOSTERONE at all!)
What is Liddle’s syndrome and classica diagnosis for that?
Constant activation of Amiloride sensitive NA channels resulting in HTN and Hypokalemia (reabsorbing too much like excess aldosterone condition)
**DX with High BP, Low K+, and NO ALDOSTERONE! **
What is Glucocorticoid remedial HTN?
_Autisomal Dominan_t form of low renin HTN with hyperaldosteronism bc Aldosterone secretin is controlled by ACTH rather than by AG2
Therefore, complete suppression of Aldosterone by exogenous glucocorticoid use (like dexamethasone)
Treatment - inhibit mineralcorticoid receptor
What are the possible causes of HTN when you see High Aldosterone and High Renin?
Renovascular (renal artery stenosis)
Hypovolemia
LV failure
OR
Renin secreting tumor
