Quiz 2 Flashcards

1
Q

Major indications for dialysis?

A

ARF, CRF (creatinine clearance < 8ml/min), anuria

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2
Q

What are the 2 major forms of dialysis?

A

Peritoneal (intracorporeal) and hemodialysis and hemofiltration (extracorporal).

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3
Q

What do both of the 2 major forms of dialysis do?

A

Replace function of glomeruli with a semi-permeable membrane.

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4
Q

Do you generally use peritoneal dialysis or hemodialysis first?

A

Generally peritoneal before hemodialysis.

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5
Q

What are the 3 types of peritoneal dialysis?

A
  1. CAPD (continuous ambulatory peritoneal dialysis)
  2. CCPD (continuous cyclic peritoneal dialysis)
  3. IPD (intermittent peritoneal dialysis)
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6
Q

Benefits of peritoneal dialysis over hemodialysis?

A
  1. Greatly reduced protein losses
  2. Much better control of K+ and phosphorous levels
  3. Rarely need water and sodium restriction because 2 L per d removed in the peritoneal fluid
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7
Q

Causes of structural changes in diabetic nephropathy?

A
  1. Glycosylation of proteins damage GBM (thickening)
  2. Hemodynamic changes –> glomerular hypertrophy (sclerosis)
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8
Q

Result of structural changes dt diabetic nephropathy?

A

Structural and functional changes to GBM dt hyperglycemia –> inc GBM collagen type IV, inc fibronectin, inc reactive oxidative species, increased circulating AGEs (normally excreted in urine)

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9
Q

How to monitor diabetic nephropathy?

A
  • Microalbumin (random am sample or 24 hr collection)
  • HbA1c levels (measuring glycated hemoglobin—average level of glucose an RBC has been exposed to in its 120 day life-cycle)
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10
Q

Microalbumin normal and abnormal ranges?

A

Normal: 0-30 mg/dL

Microalbuminuria: 30 - 300 mg/dL

Macroalbuminuria: >300 mg/dL

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11
Q

Target lab values for diabetes management?

A
  • A1C ≤6.5%
  • FPG <110 mg/dl
  • Blood pressure < 130/80mmHg
  • Lipids: LDL <100, HDL: >40 mg/dl men, >50 mg/dl women, TG: <150 mg/dl
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12
Q

Definition of hypertensive nephropathy and nephrosclerosis? Major cause?

A

Narrowing of the arteries that carry blood to the kidney. MC cause is atherosclerosis.

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13
Q

Hypertensive nephropathy/nephrosclerosis pathogenesis?

A

Reduced blood flow causes affected kidney(s) to secrete renin, retain NaCl and H2O⇒inc BP Hypersecretion of renin also caused by sodium depletion, hemorrhage, shock, CHF, renal artery stenosis

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14
Q

Treatment and management of hypertensive nephropathy/nephrosclerosis?

A
  1. Control BP with meds: diuretics, beta-blockers, Ca channel blockers, ACEis, ARBs. (ACEIs most effective in both managing HTN and slower progression of renal disease in African Americans)
  2. Percutaneous transluminal angioplasty (insertion of a stent)
  3. Surgical reconstruction of damaged artery
  4. Surgical bypass of renal arteries in cases of fibromuscular hyperplasia
  5. Treat atherosclerosis: guggal, garlic, EFAs, B vits
  6. Vascular protectants: bioflavonoids, vaccinium
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15
Q

What is nephroptosis?

A
  • Kidney drops >5cm upon moving from supine to standing position.
  • Theorized to be due to lack of perirenal fat and fascial support. Also pts have longer than normal renal vascular pedicle.
  • More common in females 5-10:1, young and thin, more common on right side.
  • 64% of those with fibromuscular dysplasia of renal artery have nephroptosis.
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16
Q

S/sxs of nephroptosis:

A

Severe abdominal, costovertebral, flank pain and vomiting when moving into upright position.

17
Q

What is a Dietl crisis and why does it occur?

A

Dietl Crisis: severe colicky flank pain, nausea, vomiting, chills, tachycardia, oliguria, hematuria and proteinuria. Occurs d/t nephroptosis.

18
Q

What are renal cysts?

A

Epithelium-lined cavities filled with fluid or semi-solid material, developing from tubular elements.

19
Q

Tell me all about simple or solitary cysts.

A
  • 65-70% of all renal masses usu found incidentally, often located in outer cortex and contain fluid consistent with an ultrafiltrate of plasma.
  • Usu asymptomatic, but may become infected, or if large may block ureter and cause hydronephrosis.
  • Average size: 10cm.
20
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A
  • Most common hereditary dz in US.
  • Bilaterally enlarged kidneys with multiple cysts of various sizes.
  • 1:400-1000 persons, 6000 new cases/yr.
  • Symptoms appear >40 yo.
  • 50% may also have hepatic, pancreatic, splenic or CNS arachnoid cysts.
  • Most patients have normal kidney function until 4th decade.
21
Q

Cystogenic process of ADPKD?

A
  • Mutation in renal tubule cell causes cellular division until cysts develop.
  • As cysts enlarge, they destroy anatomy and cause progressive functional impairment, may get infected, bleed, etc.
22
Q

Dx of ADPKD?

A
  • 15-39 yo: at least 3 cysts in both kidneys
  • 40-59 yo: at least 2 cysts
  • AND (for all): positive FHx
23
Q

S/sxs of ADPKD?

A
  • Pain over both kidneys due to infection, obstruction, hemorrhage, “drag” from heaviness.
  • Gross hematuria HTN (retinopathy)
  • Nocturia
  • Palpable, nodular kidney
  • Renal insufficiency: HA, N+V, weight loss
  • If infected: fever, chills, tender kidney(s)
24
Q

Labs in ADPKD?

A
  • Inc erythropoietin, leading to inc HGB and HCT
  • Anemia from blood loss
  • Proteinuria, hematuria, possibly pyuria and bacteriuria
  • Progressive uremia from renal insufficiency (BUN and creatinine)
25
Q

Imaging in ADPKD?

A
  • KUB—enlarged renal shadows up to 5X size
  • CT—95% accurate for dx, can detect cysts from 0.5cm
  • US—can detect cysts from 1-1.5cm (Most cost effective, usu start here)
  • MRI can differentiate Renal Cell Carcinoma (RCC) from cysts
26
Q

ADPKD naturopathic tx?

A
  1. Low protein diet - 0.5-0.75 g/kg/d
  2. Force fluids to 3000 ml or more per day (to suppress plasma vasopressin)
  3. Restrict caffeine
  4. Flax oil
  5. Reasonable physical activity - avoid strenuous activity or contact sports
  6. Treat uremia, stones, infection when present
  7. Screen for and treat HTN. Recommended ACE inhibitors, Angiotensin II receptor antagonist blockers
  8. Poss tx: dialysis, renal transplantation, cystic decompression (for pain)
  9. Constitutional HP: tumors, cystic—Baryta carb, Calc carb, Phos
  10. Constitutional hydro
  11. Conventional drug trials: somatostatin, everolimus (mTOR inhibitor)
27
Q

MC type of benign renal tumor?

A

Renal Adenoma.
Most common. Small, well-differentiated glandular tumors of renal cortex. Asymptomatic and usually identified at autopsy. Some can metastasize.

28
Q

Adenocarcinoma or Renal Cell Carcinoma (RCC or RCA) risk factors?

A
  • Cigarette smoking
  • Chronic analgesic use
  • ADPKD
  • Obesity
  • Toxin exposure (Cd, Pb, asbestos, PAHs)
  • Coffee
  • Animal fat diet
  • Dialysis, hysterectomy, contrast IVU, Von Hippel-Landau dz
29
Q

RCC pathogenesis?

A
  • RCC originates from the proximal renal tubular epithelium in the cortex. Tumor is nodular, distorted, bulges the shape of the kidney.
30
Q

S/sxs of RCC?

A
  • “Great masquerader”
  • Classic triad: gross hematuria, flank pain, palpable abd mass
  • Fever, weight loss, HTN
  • In males: possible L varicocele from blockage of L testicular vein
  • Sx of metastasis: dyspnea, cough (lung), seizure (brain), bone pain
31
Q

How does RCC spread?

A
  • Direct invasion through the renal capsule into adjacent structures, or;
  • Direct extension into the renal vein.
32
Q

Where does RCC most commonly metastasize to?

A
  • Metastasizes via lymph and blood vessels, most commonly the lung
  • Also bone, regional nodes, adrenal gland, brain, opposite kidney, adjacent organs, subcutaneous tissue.
  • 25-30% of patients have metastatic disease at presentation.
33
Q

Nephroblastoma (Wilms’ Tumor) definition?

A
  • A mixed malignant tumor of the kidney which is seen more often in children than adults, median 3.5 yrs.
  • Abnormal proliferation of metanephric blastema cells, genetic predisposition.
34
Q

Ssx of nephroblastoma?

A

Presents as abdominal mass, abd pain, hypertension, hematuria, anemia.