Renal. FMD+ renal athero + hypoalb (07-30) (1) Flashcards
FMD. patients to screen.
Women age < 50 with 1 of the symtoms? 5
1.severe/resistant HTN
2. onset HTN < 35 yo
3. sudden incr. from baseline
4. incr. Cr after startint ACEI/ARB and without significant effect on BP
5. Systolic-diastolic epigastric bruit
FMD. clinical presentation (2 esminiai)?
Resistant HTN (due to renal a. involvement)
CAROTID or VERTEBRAL artery involvement –> non specific s. such headache, tinnitus, dizziness
FMD. clinical presentation 2 more apart ,,main”?
Cerebrovascular FMD with symtpoms of brain ischemia (eg amaurosis fugax, Horner’s, TIA, stroke”
Can involve iliac, subclavian and visceral arteries
FMD. diagnosis? noninvasive - preferred. what?
Non-invasive testing preferred (CT with angiography, duplex US)
FMD. diagnosis? invasive - for patients with inconclusive noninvasive testing.
what?
catheter-based digital subtraction arteriography for patients with inconclusive noninvasive testing.
FMD. follow-up when?
what test/methods?
Medically treated patients need follow-up BP and Cr ever 3-4months.
AND
renal UG every 6-13 months.
FMD. in what patients?
90 proc women (young)
FMD. if internal carotid a. stenosis –> symptoms? 4
recurrent headaches, pulsatile tinnitus,
TIA, stroke
FMD. renal a. stenosis –> symptoms? 2
HTN, flank pain
FMD. examination physical? 2
Subauricular SYSTOLIC bruit
Abdominal bruit
FMD. again, what 2 diagnostics?
Imaging preferred: duplex UG, CTA, MRA
Catheter-based arteriography
FMD. treatment?
antihypertensives (ACEI/ARB)
PTA (percutaneous transluminal angioplasty)
Surgery (if PTA unsuccessful)
FMD. what is first line revascularization procedure?
PTA (percutaneous transluminal angioplasty) - without stent placement.
Stent spacement is reserved for arterial dissection or renal a. perforation.
Renal a. s.
HTN-related symptoms? 5
Resistant HTN (uncontrolled despite 3 drugs)
Malignant HTN (with end organ damage)
Onset of severe HTN (180/120) after 55 y/o
HTN with diffuse atherosclerosis
Recurrent flash pulmonary edema with severe HTN
Renal a. s.
….
Malignant HTN (with end organ damage)
Onset of severe HTN (180/120) after 55 y/o
HTN with diffuse atherosclerosis
Recurrent flash pulmonary edema with severe HTN
Resistant HTN (uncontrolled despite 3 drugs)
Renal a. s.
Resistant HTN (uncontrolled despite 3 drugs)
…
Onset of severe HTN (180/120) after 55 y/o
HTN with diffuse atherosclerosis
Recurrent flash pulmonary edema with severe HTN
Malignant HTN (with end organ damage)
Renal a. s.
Resistant HTN (uncontrolled despite 3 drugs)
Malignant HTN (with end organ damage)
…
HTN with diffuse atherosclerosis
Recurrent flash pulmonary edema with severe HTN
Onset of severe HTN (180/120) after 55 y/o
Renal a. s.
Resistant HTN (uncontrolled despite 3 drugs)
Malignant HTN (with end organ damage)
Onset of severe HTN (180/120) after 55 y/o
…
Recurrent flash pulmonary edema with severe HTN
HTN with diffuse atherosclerosis
Renal a. s.
Resistant HTN (uncontrolled despite 3 drugs)
Malignant HTN (with end organ damage)
Onset of severe HTN (180/120) after 55 y/o
HTN with diffuse atherosclerosis
…..
Recurrent flash pulmonary edema with severe HTN
Renal a. s.
supportive evidence. Physical exam 2?
Asymetric renal size (>1,5 cm)
Abdominal bruit
Renal a. s.
supportive evidence. Labs? 3
Unexplained Cr (>30 proc.) after starting ACEI/ARB
Renal a. s.
supportive evidence. Imaging results?1
Unexplained atrophic kidney
Renal a. s. what population?
older patients
Renal a. s. in what patients suspect? 2
in all with resistant HTN and diffuse atherosclerosis
Renal a. s. leads to what mechanism?
Decr. RBF –> activates RAAS –> HTN.
Renal a. s.
Unilateral RAS. mechanism on GFR.
What happens with other kidney?
stenotic kidney experiences reduced RBF –> decr. GFR.
unaffected kidney compensates for this decr. in GFR.
Renal a. s.
Bilateral RAS. mechanism on GFR.
Should we give ACEI?
decr. RBF –> decr. GFR –> incr. Cr (acceptable rise is < 30 proc.)
SIAIP VISUR RASO KAD IN BILATERAL CONTRAINDICATED
ACEI sometimes are contraindicated, but still can be used with close renal function monitoring due to their long-term nephroprotective effect.
Renal a. s.
Diagnosis? instruments
Renal duplex doppler US, CT, MR angiography
Captopril radionclide renal scan.
Renal a. s.
Management - aggressive risk factors reduction (to prevent CVD). what risk factors?
aspirin,
optimal DM control,
hiperlipidemia control,
smoking cessation
Renal a. s.
ACEI/ARB?
3 effects
Long-term nephroprotective effects
Less like to develop MI, stroke, ESRD
In conjuction with CCB, thiazides, BAB, mineralcorticoid receptors antagonists.
Renal a. s.
Revascularization. in what patients?
for selected patients who are intolerant or fail to achieve adequate BP control with optimal medical therapy and for those with recurrent flash pulmonary edema/refractory HF.
Calciphylaxis.
Pathophysiology? 2
Arteriolar and soft tissue calcification
local tissue ischemia and necrosis
Calciphylaxis. main risk factor?
END STAGE RENAL DISEASE
Calciphylaxis. what other risk factor apart main?
Hypercalcemia, hyperphosphatemia
Hyperparathyroidism
Obesity, DM
Oral anticoagulants (warfarin)
Calciphylaxis. clinical? 3
painful nodules and ulcers
Soft tissue calcification on imaging
Skin biopsy: arteriolar calcification/occlusion, subintimal fibrosis
UW. Hypoalbuminemia.
2 etiologies?
Excessive albumin loss
Decreased synthesis
UW. Hypoalbuminemia.
Excessive albumin loss? mechanisms
nephrotic syndrome, protein-losing enteropathy
*In case of urinary loss, hypoalbuminemia occurs when protein loss is significant (ie. +3)
UW. Hypoalbuminemia.
Decr albumin synthesis? mechanisms
cirrhosis or severe malnutrition
UW. Hypoalbuminemia.
Leads to what severe finding?
mechanism of finding?
significant peripheral edema, but does not cause pulmonary edema (usually).
alveolar capillaries have a higher permeability to albumin at baseline
(reducing oncotic pressure difference) and greater lymphatic flow than skeletal muscle,
protecting the lungs from edema
What is severe renal insuf?
GFR < 30ml
what is normal post voidal residual urine volume?
<50ml in males
<150 ml in females
what is normal post voidal residual urine in male older (>65 yo)
Post-void volume of 50-100 mL is generally considered normal in male patients age >65 but
considered abnormal in younger male patients
UREA REABSORPTION DURING HYPOVOLEMIA
- Urea is reabsorbed by the kidneys in the setting of hypovolemia
- In patients taking diuretics, low fractional excretion of urea (eg, <35%) is often used as an
indicator of decreased renal perfusion
.
what is FRACTIONAL EXCRETION OF SODIUM?
It is the “ratio of renal sodium clearance to renal creatinine clearance”
