B4.042 - Renal Failure due to Hypertension Flashcards

1
Q

what is high blood pressure

A

resting blood pressure persistently above 130-140/90

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2
Q

epidemiology of hypertension

A

Age Male gender African American Obesity High Na intake Low K intake Genetic predisposition Excess alcohol

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3
Q

what is prehypertension

A

120/80 - 139/89

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4
Q

what is stage 1 HTN

A

140/90 - 159/99

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5
Q

what is stage 2 HTN

A

= or > 160/100

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6
Q

what is early stage HTN due to

A

young patients high cardiac output - normal TPR

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7
Q

what is adult stage HTN

A

>40 yo High TPR normal or below normal CO

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8
Q

what is late stage HTN

A

high peripheral resistance, LVH, maybe low CO

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9
Q

what is primary HTN

A

no underlying cause and is a diagnosis of exclusion

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10
Q

what does primary HTN result from

A

a complex interaction of genetic and environmental factors (high Na intake; lack of exercise, obesity, depression)

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11
Q

secondary HTN causes

A

Renal parenchymal disease Reno-vascular disease Endocrinology disease Cardiac Disease Drugs

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12
Q

what are some renal parenchymal diseases that can cause secondary HTN

A

Glomerulonephritis Chronic renal failure Polycystic kidney disease Liddles syndrome Familial Hyperaldosteronism

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13
Q

what are reno-vascular diseases than can cause secondary HTN

A

Renal arterial stenosis (athoerosclerosis) Fibromuscular dysplasia

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14
Q

what are endocrinology diseases that can cause secondary HTN

A

pheocromocytoma and neuroblastoma corticosteroid excess congenital adrenal hyperplasia thyroid disorders

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15
Q

what are cardiac diseases than can cause secondary HTN

A

coarctation of aorta

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16
Q

what are drugs that can cause secondary HTN

A

cocaine amphetamines epinephrine phenylephrine

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17
Q

what are large artery pathologies than can cause HTN

A

accelerated atherosclerosis elastic hyperplasia aneurisms all lead to decreased compliance and palpable rigidity of artery

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18
Q

what are pathologies of the small arteries caused by HTN

A

Hypertrophy of smooth muscle

elastic laminal enlargement

hyaline sclerosis growth of the intima

all lead to obstruction of flow, weakness/absence of pulses

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19
Q

what are pathologies of the heart from HTN

A

LVH

left ventricular failure

Diastolic dysfunction

lead to 4th heart sound, ECG with increased QRS, signs of hypertrophy/insufficiency

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20
Q

what are pathologies of the brain due to HTN

A

atherosclerosis

little aneurisms predisposition to stroke can lead to transient ischemic attacks. stroke

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21
Q

what are pathologies of the retina due to HTN

A

atherosclerosis

aterial wall thickening

hemorrhage

arteriolar spasm

edema of retina and optic nerve lead to blurry vision

22
Q

what is hypertensive kidney disease

A

damage of the kidney due to chronic HTN

23
Q

how is CKD noted initially

A

initially CKD goes without symptoms and only detected by increased serum creatinine or proteinuria. Eventually leads to renal insufficiency.

24
Q

GFR characteristics of CKD, who gets it?

A

GFR < 60 mL/min/m2 1:8 adult americans have CKD 24.5% of 60 year olds or older have CKD

25
symptoms of CKD
loss of appetite, nausea, vomiting, weight loss, fatigue sleepiness, changes in urine output, itching, weight loss
26
what are signs of CKD
HTN, peripheral edema, shortness of breath, chest pain, GFR increase, increased creatinine and BUN
27
what is this indicative of
narrowing of arteriolar lumen thickening and hyalinazation of the walls seen in nephrosclerosis
28
what is shown here
medial hypertrophy reduplication of elastic lamina growth of intima
29
what is shown here
glomeruli areas of thrombosis and necrosis hemorrhages of parenchyma
30
what is shown here
tubules patchy ischemic atrophy interstitial fibrosis
31
describe the pathophysiology of hypertension and kidney disease
HTN --\> vessel damage, slerosis/reduced lumen --\> increased intraglomerular pressure --\> glomerular damage (podocyte injury) --\> microalbuminuria proteinuria --\> decreased perfusion --\> GFR initially maintained --\> glomerular damage, edothelial cell proliferation, messangial cells proliferation --\> renin angiotensin-aldosterone system --\> increased sympathetic n. activity --\> decreased renal blood flow --\> increased tubular Na reapsorption --\> decreased GFR Renal insufficiency
32
what is Kuf
ultrfiltration constant reflects teh net filtration pressures, surface area and permeability of the glomerular membrane
33
describe pressures in renal circulation that are altered in HTN
oncotic pressure stays constant Hydrostatic pressure starts out high in the renal arteries and afferent arterioles, then drops in glomerular capillary, drops more drastically in efferent arterioles and then slowly drops more through peritubular capillaries, intrarenal vein and the renal vein
34
what is ultrafiltrate
plasma without proteins only ions and small molecules filter
35
describe glomerular membrane selective permeability
only things smaller than albumin can pass through filtration favors cationic molecules compared to anionic ones In HTN damage of glomerular membrane allows passage of proteins
36
describe the function of glomerular mesangial cells
provide structural support for the glomerular capillaries regulate glomerular filtration via their contractile capacity function as phagocytes secrete paracrine substances
37
what stimulates the renin angiotensin aldosterone system
increased sympathetic n activity decreased renal blood perfusion decreased Na delivery to macula densa
38
what does renin do
stimunates angiotensinogen to be converted to angiotensin 1
39
what does angiotensin II do
inhibits renin vasoconstricts Na retention Na reabsorption in proximal tubules
40
what happens in CKD when GFR is reduced
clearance of creatinine and urea is reduced Urea leads to azotemia uremia causing lethargy, pericarditis and ecephalopathy potassium accumulates in blood producing heart problems
41
what are the stages of chronic renal disease based on GFR estimates
42
what are important indicators of glomerular nd tubular function
BUN/Creatinine ration (BUN/Cr)
43
what information does creatinine tell you
its mainly filtered and little is secreted so gives you info on glomerular function
44
what information does urea (resonsible for BUN) tell you
its filtereed and reabsorbed in the tubules, so it gives an estimate of GFR but also tubular function
45
what is a normal BUN/Cr and what does a high BUN/Cr or low BUN/Cr indicate
normal is 15 if BUN/Cr \> 15 glomeruli more affected if BUN/Cr \<15 tubules more affected
46
what causes volume overload due to CDK
decreased glomerular function, GFR High Cr, uremia olguria Electrolyte imbalance (less K secretion, hyperphosphatemia **Na retention** **L**eads to peripheral edema, pulmonary edema, HTN
47
what causes HTN in CKD
Increased intravascular volume Na retention Alteration of kidney reg mechanisms controlling ECF volume and osmolarity Renin agniotensin Aldosterone
48
what causes acidosis in CKD
lack of acid secretion
49
what caues anemia in CKD
kidneys cant make EPO altered oxygen sensing mechanism in kidney leads to: decreased delivery of oxygen to tissues increased CO ventricular hypertrophy CHF Impaired host defense against infection growth retardatio in kids
50
how does bone disease become a consequence of CKD
GFR declines as a result of underlying renal disease This leads to less inorganic phosphage excretion Decreased serum calcium and calcitrol stimulate PTH production Phosphate retention also stimulates PTH secreation Metabolic acidosis affects bone
51
treatment of CKD
1. treat HTN early on 2. Na restriction 3. diuretics 4. ACE Inhibitors 5. Ca blockers 6. potassium binders to preven hyperkalemia 7. dyalissi with vitamin D eventually and EPO replacement