The Kidney and Hypertension Flashcards

1
Q

Renal causes of HTN

A

Abnormalities in primary
Parenchymal dz
Vascular dz

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2
Q

Renal damage from HTN

A

Progression of chronic
Benign HTN nephrosclersis
Malignant nephroscleoriss

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3
Q

Salt sensitivie kidney

A

No matter how high the CO or TPR is, renal excretion has the capacity to return BP to normal

Therefore maintenance of crhonic HTN requires renal participation

Maybe result of decreased ability to excrete Na load…a higher AP required to maintan Na balance

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4
Q

Salt wasting disorders

A

Associated with low BP disorders

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5
Q

Salt sensitivity

A

High salt intake correlate with increase prevalene of ess HT

INceease sensitivity due to genetics…more in AA

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6
Q

OTher causes of salt-sensitive HTN

A

Low brith weight (nephron underdosing)

Primary glomerular dz

Aging, diabetes, obesity

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7
Q

Secondary HTN causes

A

Monogenetic tubular defects (Liddle syndrome)

Renal parenchymal
renal vascular dz

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8
Q

Renal parenchymal dz

A

Leading cause of HTN

RPomotes HTN and HTN promotes progression of kidney dz

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9
Q

Circle of HTN and kidney

A

Primary dz…dec neprhon number…hypertrophy and vasodilation of sruving neprhon and increased pressure…increase GFR and pressure…increase glomerular scelorisis…decrease neprhon number

COnstriction of the efferent arteriole and dilatio nof afferent to increase the pressure

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10
Q

Vascular causes of renal HTN

A

Ateromatous renal artery stenosis and fibromuscular renal artery hyperplasia

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11
Q

Renovascular HTN

A

Most commonly atherscelorsis

Less common fibromuscular dysplasia

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12
Q

Renovascular HTN clinical

A

Onset under 30 or over 55

SUdden onset uncontrolled in previously well controlled

Accelerated/malignant HTN

Intermittnet pulm edema

Epigastric bruit, particularly systolic/diastolic

Azotemia induced by ACEI

Unilateral small kdiney

Unexplained hypokalemia

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13
Q

Stensosi effects

A

INcreased renin…goes to AT2…Vasoconstriction, renal sodium retention, aldosterone secretion

Constricts efferent arteriole to help increase the GFR

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14
Q

Unilateral renal artery stenosis

A

Reduced perfusion…increased in RAAS system in that side…leads to increased renal perfusion in the ther kidney (increased Na excretion and suppressed RAS)

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15
Q

Effect of RAS blockade

Dx tests

Unilateral renal artery stenosis

A

Reduced AP, enhanced lateralization of diagnostic tests, GFR in stenotic kidney may fall

Plasma renin activity elevated
Lateralized features

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16
Q

ACEI effect in affected unilaterla renal steoniss dz

A

Will drop the GFR by dilating the effernt artieole

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17
Q

Bilateral renal stenosis path

A

Bilateral…reduced perfusion…activated RAS and impaired Na and water excretion…volume expansion so RAS is then turned off…then increased arterial pressure

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18
Q

Effect of blockade and dx tests of bilateral

A

Reduced arteril pressure only after volume depletion..may lower the GFR

Dx - plasma renin activity normal or low and no lateralized features

19
Q

Renovascular HTN dx

A

Duplex doller US, CTA, MRA

20
Q

Fibromuscular dysplasia

A

Young female 15-40

Medial in 90% and often in distal RA

Tx (PTRA) - successful in most…restenosis in 5-11, cured in 60

Total occlusion rare

21
Q

Atheroscleotic RAS

A

Usually men over 55

ESRD in 11%

Progressesi n more than half

Tx is emphasis on medical managmenet…stent success is very high but cure is low

22
Q

Medical rx of renovascular HTN

A

Aggressive risk fx mods

ACEI/ARB safe in unilateral if careful…but contraindiciated in bilateral RAS or solitary kidnye RAS

23
Q

HTN nephrosclerosis

A

Due to HTN damage ot renal vasculature

Abnormalities in walls of small pre-glomeraular arterioles

Patchy ischemic atrophy gloemruli and less extent in the tubules

Slowly progressive renal failure

24
Q

HTN neprhosclerosis demographics

A

Not everyone

Tx early on may help and less common than other HTN complications

25
Factors of developemnt of NTH neph
Degree of HTN Transmission of pressure to glom Tissue susceptibiltiy to barotrauama..pro-inflam or diabetes Decreased neprhon mass
26
Pathh of HTN neprho
INcreased systemic pressure Affarent constriction to dec intragolmerular pressure...efferent arteriole dilates
27
Hyaline arterioloscelrosis
Medial and intimal thickening Mostly of the affarnet Haline deposition caused by extravasation of proteins throgu hendothelium and partly by increase BM deposition
28
HYlainization of glmeruli
Narrowing of lumen of AA leads to dec blood flow and results in ischemia and glomerular damge Hyalinization of glomerulus and loss of glomerular function
29
Tubular hyalizniation
Dec blood flow to the tubules and interstitium leads to cell death and loss of nephron function Progressive loss of neprhons
30
Bad synergy with DM
Diabetic nephropathy increase in the RAA via AT2 leads to efferent arterial constriction further increased the glomerular HTN and accelerating the damage
31
Hx of patients with HTN nephro
HTN for a long time with evidence of uncontrolled BP More comps than you think they should have
32
Features usggesting HTN neprho
Proteinuria is a big one Black HTN dx prior to proteinuria LEft ventricular hypertrophy
33
HTN neprho tx
ACE inhibitors but diuretic needs ot be co-admin
34
HTN emergency
Severe HTN (diastolic above 120) with rapid decomp of organ system OR life-therating conditions aggravated by presence of elevated BP Lower over minutes ot horus
35
HTN emergency clinical cues
Moderate to severe HTN retinopathy (malignant HTN)
36
Severe asx HTN
Relatively asx or completely asx patient iwth a BP in the severe range...maybe a mild headache Does NOT require rapid reduciton of BP Rapid reduciton of BP may be harmful BP reduced over a period of days
37
HTN emergencies clinical
Reflects consequens of BP on tagret organs Depends on level and rate of BP Affected by pre-existing HTN
38
CLinical pres of malignant HTN
``` HA - worse in morning Visual Ischemic CP Renal N//V Neurologic ``` Depends on involved organ system
39
Etiology of malignant
Essential HTN most common with renal parenchymal as seocndary
40
Pathophys of malignant
Crticial evaluiatioj of BP Loss of autoregulation Vascular endothelai damage - loss of permeability with deposition of fibrinogen and plasma proteins in walls...activation of mediators of coagulatio nand cell proliferation Localized intravasc activation of clotting cascade - microangiopathic hemolytic anemia Act of RAAS Natriuresis from pressure POsitive ffedback to increase more
41
Patho of Malig HTN
Proliferative endarteritis (onion skin) Fibrinoid necrosis Kidney - fibrinoid neprho of glomeruli, heorrhage and fibrosis of intersittium, tublar artophy or ATN
42
Microangiopathic hemolytic anemia
RBCs traverse an injured vascular endothelilum with associated fibrin depositon and platelet aggrgeation Fragmentation hemolysis Mech disruption of RBC membrane IV hemolysis and appearance of schistocytes
43
Malignant HTN therpay
ICU Arterial line Rapid reduciton of MAP by 20% 160-170/100-110 SHort acting IV agents
44
Malig HTN prognosis
75% survive 5 years and 50% survive with restoration of pre-crisis renal function