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
Q

symptoms of CKD

A

loss of appetite, nausea, vomiting, weight loss, fatigue sleepiness, changes in urine output, itching, weight loss

26
Q

what are signs of CKD

A

HTN, peripheral edema, shortness of breath, chest pain, GFR increase, increased creatinine and BUN

27
Q

what is this indicative of

A

narrowing of arteriolar lumen

thickening and hyalinazation of the walls

seen in nephrosclerosis

28
Q

what is shown here

A

medial hypertrophy

reduplication of elastic lamina

growth of intima

29
Q

what is shown here

A

glomeruli

areas of thrombosis and necrosis

hemorrhages of parenchyma

30
Q

what is shown here

A

tubules

patchy ischemic atrophy

interstitial fibrosis

31
Q

describe the pathophysiology of hypertension and kidney disease

A

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
Q

what is Kuf

A

ultrfiltration constant

reflects teh net filtration pressures, surface area and permeability of the glomerular membrane

33
Q

describe pressures in renal circulation that are altered in HTN

A

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
Q

what is ultrafiltrate

A

plasma without proteins

only ions and small molecules filter

35
Q

describe glomerular membrane selective permeability

A

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
Q

describe the function of glomerular mesangial cells

A

provide structural support for the glomerular capillaries

regulate glomerular filtration via their contractile capacity

function as phagocytes

secrete paracrine substances

37
Q

what stimulates the renin angiotensin aldosterone system

A

increased sympathetic n activity

decreased renal blood perfusion

decreased Na delivery to macula densa

38
Q

what does renin do

A

stimunates angiotensinogen to be converted to angiotensin 1

39
Q

what does angiotensin II do

A

inhibits renin

vasoconstricts

Na retention

Na reabsorption in proximal tubules

40
Q

what happens in CKD when GFR is reduced

A

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
Q

what are the stages of chronic renal disease based on GFR estimates

A
42
Q

what are important indicators of glomerular nd tubular function

A

BUN/Creatinine ration (BUN/Cr)

43
Q

what information does creatinine tell you

A

its mainly filtered and little is secreted so gives you info on glomerular function

44
Q

what information does urea (resonsible for BUN) tell you

A

its filtereed and reabsorbed in the tubules, so it gives an estimate of GFR but also tubular function

45
Q

what is a normal BUN/Cr and what does a high BUN/Cr or low BUN/Cr indicate

A

normal is 15

if BUN/Cr > 15 glomeruli more affected

if BUN/Cr <15 tubules more affected

46
Q

what causes volume overload due to CDK

A

decreased glomerular function, GFR

High Cr, uremia

olguria

Electrolyte imbalance (less K secretion, hyperphosphatemia

Na retention

Leads to peripheral edema, pulmonary edema, HTN

47
Q

what causes HTN in CKD

A

Increased intravascular volume

Na retention

Alteration of kidney reg mechanisms controlling ECF volume and osmolarity

Renin agniotensin Aldosterone

48
Q

what causes acidosis in CKD

A

lack of acid secretion

49
Q

what caues anemia in CKD

A

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
Q

how does bone disease become a consequence of CKD

A

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
Q

treatment of CKD

A
  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