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Renal and Urinary 3 > The Kidney and Hypertension > Flashcards

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
Q

Factors of developemnt of NTH neph

A

Degree of HTN

Transmission of pressure to glom

Tissue susceptibiltiy to barotrauama..pro-inflam or diabetes

Decreased neprhon mass

26
Q

Pathh of HTN neprho

A

INcreased systemic pressure

Affarent constriction to dec intragolmerular pressure…efferent arteriole dilates

27
Q

Hyaline arterioloscelrosis

A

Medial and intimal thickening

Mostly of the affarnet

Haline deposition caused by extravasation of proteins throgu hendothelium and partly by increase BM deposition

28
Q

HYlainization of glmeruli

A

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
Q

Tubular hyalizniation

A

Dec blood flow to the tubules and interstitium leads to cell death and loss of nephron function

Progressive loss of neprhons

30
Q

Bad synergy with DM

A

Diabetic nephropathy increase in the RAA via AT2 leads to efferent arterial constriction further increased the glomerular HTN and accelerating the damage

31
Q

Hx of patients with HTN nephro

A

HTN for a long time with evidence of uncontrolled BP

More comps than you think they should have

32
Q

Features usggesting HTN neprho

A

Proteinuria is a big one

Black

HTN dx prior to proteinuria

LEft ventricular hypertrophy

33
Q

HTN neprho tx

A

ACE inhibitors but diuretic needs ot be co-admin

34
Q

HTN emergency

A

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
Q

HTN emergency clinical cues

A

Moderate to severe HTN retinopathy (malignant HTN)

36
Q

Severe asx HTN

A

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
Q

HTN emergencies clinical

A

Reflects consequens of BP on tagret organs

Depends on level and rate of BP

Affected by pre-existing HTN

38
Q

CLinical pres of malignant HTN

A 
HA - worse in morning
Visual
Ischemic CP
Renal 
N//V
Neurologic

Depends on involved organ system

39
Q

Etiology of malignant

A

Essential HTN most common with renal parenchymal as seocndary

40
Q

Pathophys of malignant

A

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
Q

Patho of Malig HTN

A

Proliferative endarteritis (onion skin)

Fibrinoid necrosis

Kidney - fibrinoid neprho of glomeruli, heorrhage and fibrosis of intersittium, tublar artophy or ATN

42
Q

Microangiopathic hemolytic anemia

A

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
Q

Malignant HTN therpay

A

ICU

Arterial line

Rapid reduciton of MAP by 20%

160-170/100-110

SHort acting IV agents

44
Q

Malig HTN prognosis

A

75% survive 5 years and 50% survive with restoration of pre-crisis renal function

Renal and Urinary 3 (22 decks)

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