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STEP 2 Cardio + Renal > Renal. FMD+ renal athero + hypoalb (07-30) (1) > Flashcards

Renal. FMD+ renal athero + hypoalb (07-30) (1) Flashcards

1
Q

FMD. patients to screen.
Women age < 50 with 1 of the symtoms? 5

A

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

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2
Q

FMD. clinical presentation (2 esminiai)?

A

Resistant HTN (due to renal a. involvement)
CAROTID or VERTEBRAL artery involvement –> non specific s. such headache, tinnitus, dizziness

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3
Q

FMD. clinical presentation 2 more apart ,,main”?

A

Cerebrovascular FMD with symtpoms of brain ischemia (eg amaurosis fugax, Horner’s, TIA, stroke”

Can involve iliac, subclavian and visceral arteries

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4
Q

FMD. diagnosis? noninvasive - preferred. what?

A

Non-invasive testing preferred (CT with angiography, duplex US)

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5
Q

FMD. diagnosis? invasive - for patients with inconclusive noninvasive testing.
what?

A

catheter-based digital subtraction arteriography for patients with inconclusive noninvasive testing.

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6
Q

FMD. follow-up when?
what test/methods?

A

Medically treated patients need follow-up BP and Cr ever 3-4months.
AND
renal UG every 6-13 months.

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7
Q

FMD. in what patients?

A

90 proc women (young)

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8
Q

FMD. if internal carotid a. stenosis –> symptoms? 4

A

recurrent headaches, pulsatile tinnitus,
TIA, stroke

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9
Q

FMD. renal a. stenosis –> symptoms? 2

A

HTN, flank pain

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10
Q

FMD. examination physical? 2

A

Subauricular SYSTOLIC bruit

Abdominal bruit

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11
Q

FMD. again, what 2 diagnostics?

A

Imaging preferred: duplex UG, CTA, MRA

Catheter-based arteriography

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12
Q

FMD. treatment?

A

antihypertensives (ACEI/ARB)
PTA (percutaneous transluminal angioplasty)
Surgery (if PTA unsuccessful)

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13
Q

FMD. what is first line revascularization procedure?

A

PTA (percutaneous transluminal angioplasty) - without stent placement.

Stent spacement is reserved for arterial dissection or renal a. perforation.

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14
Q

Renal a. s.
HTN-related symptoms? 5

A

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

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15
Q

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

A

Resistant HTN (uncontrolled despite 3 drugs)

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16
Q

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

A

Malignant HTN (with end organ damage)

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17
Q

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

A

Onset of severe HTN (180/120) after 55 y/o

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18
Q

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

A

HTN with diffuse atherosclerosis

19
Q

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

…..

A

Recurrent flash pulmonary edema with severe HTN

20
Q

Renal a. s.
supportive evidence. Physical exam 2?

A

Asymetric renal size (>1,5 cm)
Abdominal bruit

21
Q

Renal a. s.
supportive evidence. Labs? 3

A

Unexplained Cr (>30 proc.) after starting ACEI/ARB

22
Q

Renal a. s.
supportive evidence. Imaging results?1

A

Unexplained atrophic kidney

23
Q

Renal a. s. what population?

A

older patients

24
Q

Renal a. s. in what patients suspect? 2

A

in all with resistant HTN and diffuse atherosclerosis

25
Q

Renal a. s. leads to what mechanism?

A

Decr. RBF –> activates RAAS –> HTN.

26
Q

Renal a. s.
Unilateral RAS. mechanism on GFR.

What happens with other kidney?

A

stenotic kidney experiences reduced RBF –> decr. GFR.

unaffected kidney compensates for this decr. in GFR.

27
Q

Renal a. s.
Bilateral RAS. mechanism on GFR.

Should we give ACEI?

A

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.

28
Q

Renal a. s.
Diagnosis? instruments

A

Renal duplex doppler US, CT, MR angiography

Captopril radionclide renal scan.

29
Q

Renal a. s.
Management - aggressive risk factors reduction (to prevent CVD). what risk factors?

A

aspirin,
optimal DM control,
hiperlipidemia control,
smoking cessation

30
Q

Renal a. s.
ACEI/ARB?
3 effects

A

Long-term nephroprotective effects

Less like to develop MI, stroke, ESRD

In conjuction with CCB, thiazides, BAB, mineralcorticoid receptors antagonists.

31
Q

Renal a. s.
Revascularization. in what patients?

A

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.

32
Q

Calciphylaxis.
Pathophysiology? 2

A

Arteriolar and soft tissue calcification

local tissue ischemia and necrosis

33
Q

Calciphylaxis. main risk factor?

A

END STAGE RENAL DISEASE

34
Q

Calciphylaxis. what other risk factor apart main?

A

Hypercalcemia, hyperphosphatemia
Hyperparathyroidism
Obesity, DM
Oral anticoagulants (warfarin)

35
Q

Calciphylaxis. clinical? 3

A

painful nodules and ulcers
Soft tissue calcification on imaging
Skin biopsy: arteriolar calcification/occlusion, subintimal fibrosis

36
Q

UW. Hypoalbuminemia.
2 etiologies?

A

Excessive albumin loss

Decreased synthesis

37
Q

UW. Hypoalbuminemia.
Excessive albumin loss? mechanisms

A

nephrotic syndrome, protein-losing enteropathy

*In case of urinary loss, hypoalbuminemia occurs when protein loss is significant (ie. +3)

38
Q

UW. Hypoalbuminemia.
Decr albumin synthesis? mechanisms

A

cirrhosis or severe malnutrition

39
Q

UW. Hypoalbuminemia.
Leads to what severe finding?

mechanism of finding?

A

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

40
Q

What is severe renal insuf?

A

GFR < 30ml

41
Q

what is normal post voidal residual urine volume?

A

<50ml in males
<150 ml in females

42
Q

what is normal post voidal residual urine in male older (>65 yo)

A

Post-void volume of 50-100 mL is generally considered normal in male patients age >65 but
considered abnormal in younger male patients

43
Q

UREA REABSORPTION DURING HYPOVOLEMIA

  1. Urea is reabsorbed by the kidneys in the setting of hypovolemia
  2. In patients taking diuretics, low fractional excretion of urea (eg, <35%) is often used as an
    indicator of decreased renal perfusion
A

.

43
Q

what is FRACTIONAL EXCRETION OF SODIUM?

A

It is the “ratio of renal sodium clearance to renal creatinine clearance”

STEP 2 Cardio + Renal (26 decks)

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