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1. AA my internal medicine > 6. Nephrology > Flashcards

6. Nephrology Flashcards

1
Q

Definition of acute kidney injury ?

A
  • A rapid decline in renal function, with an increase in serum creatinine level (a relative increase of 50% or an absolute increase of 0.5 to 1.0 mg/dL)
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2
Q

Acute renal failure (ARF) ?

A

The creatinine may be normal despite a markedly reduced glomerular filtration rate (GFR) in the early stages of acute kidney injury (AKI) due to the time it takes for creatinine to accumulate in the body.

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3
Q

RIFLE criteria ?

A
  • Classification severity of acute kidney injury.
  1. RISK:
    - 1.5x increase in Cr.
    - GFR decreased by 25%.
    - Urine output: <0.5 mL/kg?hr for 6 hrs.
  2. INJURY:
    - 2x increase in Cr.
    - GFR decreased by 50%.
    - Urine output: <0.5 mL/kg/hr for 12 hrs.
  3. FAILURE:
    - 3x increase in Cr.
    - GFR decreased by 75%.
    - Urine output: <0.5 mL/kg/hr for 24 hrs. or anuria for 12 hrs.
  4. LOSS:
    - Complete loss of kidney function (i.e. requiring dialysis) for more than 4 wks.
  5. ESRD:
    - Complete loss of kidney function (i.e. requiring dialysis) for more than 3 months.
  • Svereity (stage 1-3).
  • Outcome (4 and 5)
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4
Q

The most common cause of death in AKI ?

A

Infections (75%).

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5
Q

Types of AKI ?

A
  • Prerenal AKI (decrease in renal blood flow 60% of cases)
  • Intrinsic AKI. (40%)
  • Psotrenal AKI. (5%)
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6
Q

Prerenal AKI causes ?

A
  • Most common cause of AKI; potentially reversible.
  • Hypovolemia (dehydration, excessive diuretic use, vomiting, diarrhea, burns, hemorrhage)
  • CHF. (less blood will be send to the tissues)
  • Hypotension.
  • Renal arterial obstruction.
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7
Q

Diagnostic Approach in AKI ?

A
  • hx and PE.
  1. To determine the duration of renal failure. A baseline Cr level provides this info.
  2. To determine whether AKI is due to prerenal, intrarenal, or postrenal.
  3. Medication review.
  4. Urinalysis.
  5. Urine chemistry (FENa, osmmolality, urine Na+, urine Cr)
  6. Renal US ( to rule out obstruction)
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8
Q

How to know whether AKI is due to prerenal, intrarenal, or postrenal ?

A
  • This is done via combination of H&P and labs findings:
  • Signs of volume depletion and CHF suggest a prerenal etiology.
  • Signs of an allergic reaction (rash) suggest acute interstitial nephritis (an intrinsic renal etiology).
  • A suprapubic mass, BPH, or bladder dysfunction suggests a postrenal etiology.
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9
Q

Medication causes Intrarenal AKI ?

A
  1. Acute tubular necrosis ->
    - Aminoglycosides.
    - Heavy metals (leads).
    - Myoglobin (damaged muscle).
    - Ethylene glycol. (anti-freeze)
    - Uric acid
    - Radiocontrast dye.
  2. Acute Interstitial AKI -> (type I and IV hypersensitivity)
    - NSAIDs.
    - Penicillin.
    - Diuretics.
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10
Q

Prerenal AKI ?

  • Urinalysis:
  • BUN/Cr ratio:
  • FENa:
  • Urine osmolality:
  • Urine sodium:
A
  • Urinalysis: hyaline cast
  • BUN/Cr ratio: >20:1
  • FENa: <1%
  • Urine osmolality: >500 mOsm
  • Urine sodium: <20
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11
Q

Intrinsic AKI ?

  • Urinalysis:
  • BUN/Cr ratio:
  • FENa:
  • Urine osmolality:
  • Urine sodium:
A
  • Urinalysis: abnormal.
  • BUN/Cr ratio: <20:1
  • FENa: >2-3%
  • Urine osmolality: 250-300 mOsm.
  • Urine sodium: >40
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12
Q

Acute tubular necrosis urine sediment findings ?

A
  • Full brownish pigment, granular casts with epithelial cells.
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13
Q

Intrinsic AKI causes ?

A
  • Tubular diseases (ATN): can be caused by ischemia (most common), nephrotoxins.
  • Glomerular disease (acute glomerulonerphritis): for example, Goodpasture syndrome, Wegener granulomatosis, poststreptococcal GN, lupus.
  • Vascular disease: for example, renal artery occulsion, TTP, HUS.
  • Interstitial disease. (allergic interstitial nephritis, often due to hypersensitivity reaction to medication)
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14
Q

The 3 basic tests for postrenal failure ?

A
  • PE: palpate the bladder.
  • US: look for obstruction, hydronephrosis.
  • Catheter: look for large volume of urine.
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15
Q

Postrenal AKI causes ?

A
  • Urethral obstruction. (2ndary to enlarged prostate (BPH) is the most common cause).
  • Obstruction of solitary kidney.
  • Nephrolithiasis.
  • Obstructing neaplasms (bladder, cervix, prostate, and so on)
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16
Q

RBC casts in ureine sediment indicates ?

A

Glomerular disease.

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17
Q

WBC casts in ureine sediment indicates ?

A

Renal parenchymal inflammation “ acute interstitial nephritis “

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18
Q

Fatty casts in ureine sediment indicates ?

A

Nephrotic syndrome

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19
Q

What are the nosy common mortal complications in early phase of AKI ?

A
  • Hyperkalemic cardiac arrest.

- Pulmonary edema.

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20
Q

Chronic Kidney Disease is ?

A

Defined as either:
- Decreased kidney function (GFR<60 mL/min)
OR
- Kidney damage (structural or functional abnormalities).
for at least 3 months.

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21
Q

Causes of Chronic Kidney Diseases ?

A
    • Diabetes. (most common 30%).
    • HTN (25%)
  • Chronic GN.
  • Interstitial nephritis, PCKD.
  • any cause of AKI may lead to CKD if prolonged and/or treatment is delayed.
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22
Q

NUTRITIONAL THERAPY in Chronic kidney diseases ?

A
  • WATER RESTRICTION
  • intake depends on daily urine output.
  • SODIUM RESTRICTION:
  • depends on the degree of hypertension and edema
  • salt substitutes should not be used because they contain KCl
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23
Q

life-threatening complications in CKD ?

A
  • Hyperkalemia: check ECG (although it K can be high without ecg changes)
  • Pulmonary edema (2ndary to volume overload) (look for recent weight gain).
  • Infections
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24
Q

Absolute Indications for Dialysis ?

A
  • Acidosis: significant, intractable metabolic acidosis.
  • Electrolytes: severe, persistent hyperkalemia.
  • Intoxications: methanol, ethylene glycol, lithium, aspirin.
  • Overload: hypervolemia not managed by other means.
  • Uremia (severe): based on clinical presentation NOT labs values.
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25
Q

Symptoms of uremia ?

A
  • Nausea and vomiting.
  • Lethargy/detrioration in mental status, encephalopathy, seizures.
  • Pericarditis.
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26
Q

Dialyzable Substances ?

A
  • Salicylic acid.
  • Lithium.
  • Ethylene glycol.
  • Magnesium-containing laxatives.
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27
Q

Complications of Hemodialysis during dialysis ?

A
  • Hypotension. “most frequent”
  • Arrhythmias.
  • Exsanguination.
  • Seizures.
  • Fever.
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28
Q

Complications of Hemodialysis between treatments ?

A
  • Hyper/Hypotension.
  • Edema.
  • Pulmonary edema.
  • Hyperkalemia.
  • Bleeding,
  • Clotting access.
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29
Q

Long term Complications of Hemodialysis ?

A
  • Hyperparathyroidism.
  • CHF.
  • AV access failure.
  • Pulmonary edema.
  • Neuropathy.
  • Anemia.
  • GI bleeding.
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30
Q

Kt/V ?

A
  • Kt/V is the preferred method for measuring the dialysis
    dose.
  • Kt/V is defined as the dialyzer clearance of urea (K) multiplied by the duration of the dialysis treatment (t, in minutes) divided by the volume of distribution of urea in the body (V, in mL), which is approximately equal to the total body water, corrected for volume lost during ultrafiltration .
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31
Q

Absolute contraindications of Peritoneal Dialysis ?

A
  1. Peritoneal fibrosis and adhesion following intraabdominal operation.
  2. Inflammatory gut diseases.
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32
Q

AZOTEMIA def ?

A

A pathologic increase in urea and other nitrogenous substances in the blood.

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33
Q

UREMIA def ?

A

Systemic manifestation of severe persistent decrease in renal function.

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34
Q

AKIN Criteria?

A
  • for diagnosing AKI.
  1. Time course – rapid (<48hours).
  2. Reduction in Kidney function
    - increase serum creatinine (absolute increase of >0.3mg/dl or percentage increase of > 50%)
    - decrease urine output (<0.5ml/kg/hr for> 6hours)
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35
Q

RIFLE Criteria: URINE OUTPUT ?

A
  • ANURIA: <100 mL/24 h
  • OLIGURIA: 100-400 mL/24h
  • NONOLIGURIA: : > 400 mL/24h
  • 50-60% of AKI cases are nonoliguric
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36
Q

Treatment of Potassium >6.0 mmol/L ?

A

– calcium resonium 15g QDS PO

– If septic or rising quickly treat as though K+ 6.5

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37
Q

Treatment of Potassium >6.5 mmol/L ?

A

– dextrose-insulin (50ml 50% Dextrose with 10units Actrapid insulin, IV over 5mins) Monitor BM
– calcium resonium 15g QDS PO.

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38
Q

Treatment of Potassium >7 mmol/L ?

A 
– Calcium gluconate.
– Dextrose insulin.
– Nebulised salbutamol 5mg
– IV sodium bicarbonate.
– Calcium resonium.
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39
Q

Treatment approach to hyperkalemic emergencies ?

including MOA?

A
  • Antagonism of membrane actions of potassium:
  • Calcium.
  • Drive extracellular potassium into the cells:
  • Insulin and glucose.
  • Sodium bicarbonate. (if metabolic acidosis)
  • B-2-adrenergic agonists. (salbutamol)
  • Removal of potassium from the body:
  • Loop or thiazide diuretics.
  • Cation exchange resin.
  • Dialysis. preferably if severe.
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40
Q

HYPERKALEMIA ?

A
  • Normal Potassium range is 3.5 - 5mmol/L.
  • Signs and symptoms: muscle weakness and arrhythmia (VF).
  • ECG changes:
    – Flattened P waves
    – Broad QRS complex
    – Slurring of ST segment
    – Tall tented T waves
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41
Q

HTN management in CKD ?

A
  • Diuretics
  • Ca channel blockers.
  • ACEI, ARB.
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42
Q

ANEMIA treatment in CKD ?

A
  • ERYTHROPOETHIN:
  • increases Hb and HT levels in 2-3 weeks.
  • side effect: hypertension (so its CI if we have HTN patient).
  • Iron supplements:
  • in case of low plasma ferritin (<100 ng/mL).
  • Folic acid supplements:
  • removed by dialysis.
  • necessary for RBC formation.
  • Levels should be:
    1. Hg: 11-12 g/dl.
    2. Ht: 33-36%.
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43
Q

Management of RENAL OSTEODYSTROPHY in CKD ?

A

– dietary phosphorus restriction (<1000 mg/day),
– oral P-binding agents (limit P absorption from bowel, with each meal) (e.g. calcium carbonate)
– vit. D
– increase sensitivity of Ca receptors in parathyroid glands (sensipar)
– subtotal parathyroidectomy,
– calcitriol

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44
Q

Proteinuria is?

A
  • Defined as the urinary excretion of >150mg protein/24 hrs.
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45
Q

Proteinuria classifications ?

A

A. Glomerular.
B. Tubular.
C. Overflow proteinuria.
D. Other causes of proteinuria (UTI, fever, heavy exertion/stress,CHF..etc)

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46
Q

Nephrotic syndrome ?

A
  • Proteinuria “ >3.5 mg/24 hr”
  • Hypoalbuminemia.
  • Hyperlipidemia .
  • Edema. “often initial complaint”.
  • Lipiduria.
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47
Q

Causes of Nephrotic syndrome ?

A
  • Primary glomerular disease. (50-75%):
    1. Membranous nephropathy (most common in adults 40%).
    2. Focal segmental glomerulosclerosis (FCGS) (35%).
    3. membranoproliferative GN (15%).
    4. Minimal change disease (MCD) commonest in kids 75%.
  • Systemic disease: diabetes, collagen vascular disease, SLE, RA, HSP, PAN, Wegener granulomatosis.
  • Amyloidosis, cryglobulinemia.
  • Drugs/toxins.
  • Infections.
  • Multiple myeloma.
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48
Q

Pathology of Membranous nephropathy or “MEMBRANOUS

GLOMERULONEPHRITIS” ?

A

-Inflammation of glomerular basement membrane triggered by immune complex deposits -> increased permeability, proteinuria -> nephrotic syndrome.

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49
Q

Pathology of Focal segmental glomerulosclerosis (FCGS) ?

A

▪ Histologic finding of glomerular damage, not distinct disease.
▪ Affects parts (segmental) of some (focal) glomeruli of nephron; damage, scarring → proteinuria
▪ Foot processes of podocytes damaged → plasma proteins, lipids permeate glomerular filter
▪ Proteins, lipids trapped → build up inside glomeruli → hyalinosis (hyaline/ glassy view on histology) → scar tissue (glomerulosclerosis)

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50
Q

Causes of Focal segmental glomerulosclerosis (FCGS) ?

A

▪ Primary: unknown
▪ Secondary: result of underlying cause
- Sickle cell disease, HIV, renal hyperfiltration (e.g. unilateral renal agenesis), heroin abuse
▪ Genetic forms: FSGS 1–6

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51
Q

Hematuria ?

A
  • Defined as >3 erythrocytes/HPF on urinalysis.

- Consider gross painless hematouria to be a sign of bladder or kidney cancer until proven otherwise.

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52
Q

Nephritic syndrome ?

A
  • Hematouria.
  • Oliguria.
  • Azotemia.
  • HTN.
  • Edema.
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53
Q

Pathology of Minimal change disease ?

A

▪ Type of glomerulonephritis; podocytes in glomeruli damaged by T cells cytokines
▪ Foot processes of podocytes damaged, flattened (AKA effacement) → lose function as barrier → albumin permeates, bigger proteins cannot get through (selective proteinuria)

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54
Q

MEMBRANOUS GN findings on sliver staining ?

A

“SPIKES” ON THE OUTER ASPECT OF GBM.

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55
Q

IDIOPATHIC MEMBRANOUS NEPHROPATHY ?

A

Ag: phospholipase A2receptor (PLA2R) (may be shown in a biopsy)
in patient;’s blood: anti PLA2R

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56
Q

THE ACUTE NEPHROTIC SYNDROME info about pathology ?

A

The structural abnormality shared by all nephrotic conditions or diseases with heavy proteinuria is diffuse simplification or “fusion” of the foot processes of the glomerular visceral epithelial cells.

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57
Q

THE ACUTE NEPHRITIC SYNDROME info about pathology ?

A

Diseases characterized by the acute nephritic syndrome are associated invariably with deposition of immune complexes in the more proximal layers of the glomerular capillary wall, in close proximity to the endothelial cell surfaces

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58
Q

Diffuse proliferative glomerulonephritis in a patient with recent hepatitis C infection ?

A
  • Ultrastructural details of subendothelial deposits.
  • Immune deposits are present exclusively in the subendothelial space.
  • Early formation of a second basement membrane (arrows) by the displaced endothelium has resulted in an early double contour.
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59
Q

CONDITIONS ASSOCIATED WITH DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS ?

A
  • Acute Postinfectious Glomerulonephritis:.
  • Diffuse proliferative lupus nephritis.
  • Dense Deposit Diseases early phase.
  • Essential mixed cryoglobulinemia, early phase
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60
Q

Clinical manifestation of Membranoproliferative glomerulonephritis ?
and PATTERN OF INJURY ?

A

CHRONIC nephrotic syndrome and nephritic syndrome

  1. IMMUNE DEPOSITS-MEDIATED DISEASES (glomerulonephritis)
  2. THROMBOTIC ANGIOPATHIES
  3. DEPOSITION DISEASE
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61
Q

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS ?

A

Clinical conditions that evolve with rapidly progressive decline in renal function and an active urine sediment are usually characterized by an inflammatory process that results in the formation of cellular crescents within Bowman’s space (crescents).

62
Q

Type III RPGN ?

A
  • Pauci-immune

- ANCA (+) necroticans GN

63
Q

CRESCENTIC GLOMERULONEPHRITIS types ?

AKA rapidly progressive glomerulonephritis (RPGN)

A
  • Type I, anti-GBM disease: (Goodpasture syndrome (GPS))
  • Type II, immune complex-mediated:
  • post-infectious GN, IgA nephropathy, MPGN,
    Systemic diseases (SLE, RA, H-S purpura)
  • Type III, pauci immune (ANCA-associated):
    Vasculitides (ANCA-associated): microscopic form of polyarteritis nodosa, Wegener’s granulomatosis Churg-Strauss syndrome
    Drug-induced vasculitides
64
Q

Diabetic nephropathy findings ?

A
  • 1st 3 are major histologic findings:
  • Thickened glomerular basement membrane.
  • Mesangial expansion.
  • Glomerular sclerosis
  • Kimmelstiel-wilson nodules.
  • Disruption of podocytes.
65
Q

Hepato-Renal syndrome ?

A
  • Is a life-threatening medical condition that consist of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure.
  • HRS is usually fatal unless a liver transplant is performed, although various treatments, such as dialysis, can prevent advancement of the condition.
66
Q

Absolute contraindication for renal biopsy ?

A
  • Bleeding diathesis.
  • Uncontrolled severe HTN.
  • Uncooperative patient.
  • Presence of a solitary native kidney.
67
Q

Nephritic syndrome with normal serum complement ?

A

1- IgA nephropathy.
2- Hereditary nephritis (Alport syndrome).
3- Crescentic Rapidly progressive ANCA positive GN (can also present as acute renal failure).
4- Anti-basement membrane disease (Goodpasture’s disease)
(can also present as acute renal failure).
5- Systemic vasculitis, ANCA positive. (can also present as acute renal failure).
6- Thrombotic microangiopathy.

68
Q

Nephritic Syndrome with decreased Serum Complement ?

A
  1. Membrano-proliferative GN.
  2. C3 nephropathy.
  3. Lupus nephritis
69
Q

Thrombotic Microangiopathy (TMA) gen info?

A
  • Nephritic syndrome or acute renal failure accompanied by hemolytic anemia, hemorrhages, and purpura.
  • Has multiple clinical presentations and names.
  • Most frequent presentations are TTP & HUS.
  • Many cases respond to treatment.
  • Renal biopsy confirms the diagnosis.
  • Also referred as micro-angiopathic hemolytic anemia (MAHA).
70
Q

Thrombotic Microangiopathy (TMA) clinical presentations and names ?
1- With predominantly neurologic symptoms:
2- With a domination of kidney insufficiency:
3- as complication of hypertension:
4- as complication of pregnancy:.
5- as a complication of ……………
6- as a component of ……………….

A
  • With predominantly neurologic symptoms: thrombotic thrombocytopenic purpura (TTP)
  • With a domination of kidney insufficiency: hemolytic uremic syndrome (HUS).
  • as complication of hypertension: malignant hypertension.
  • as complication of pregnancy: eclampsia.
  • as a complication of cemplement disorders (inborn or acquired).
  • as a component of scleroderma.
71
Q

Causes of acute interstitial nephritis ?

A

A. Acute allergic reaction to medications “MOST COMMON”.
B. Infection (esp. in kids). (esp. Streptococcus spp. and Legionella pneumophila.)
C. Collagen vascular diseases (eg. sarcoidosis).
D. Autoimmune disease (eg. SLE, sjögren syndrome).

72
Q

What are the classical findings of acute interstitial nephritis ?

A

Rash, fever and eosinophilia.

73
Q

MEDULLARY PYRAMIDS NECROSIS ?

A
  • Its one of the acute pylonephritis complications.
  • More common in diabetics.
  • more common in cases associated with urinary obstruction.
  • A characteristic component of analgetic nephropathy.
74
Q

What is the most common location for obstruction in Nephrolithiasis ?

A

Ureterovesical junction.

75
Q

Types of stones in Nephrolithiasis ?

A
  • Calcium stones (most common form). (80%).
  • Uric acid stones (2nd most common).
  • Struvite stones (staghorn stones).
  • Cystine stones.
76
Q

Calcium oxalate urine sediments ?

A
  • dumbbel-shaped calcium oxalate monohydrate.

- envelope-shaped calcium oxalate dihydrate.

77
Q

Struvite stones (staghorn stones) urine sediments ?

A
  • Multiple “coffin lid” magnesium ammonium phosphate crystals that form only in an alkaline urine.
78
Q

Uric acid urine sediments ?

A
  • Urine sediment loaded with uric acid crystals.
  • These crystals are pleomorphic, most often appearing as rhombic plates or rosettes.
  • They are yellow or reddish-brown and form only in an acid urine
79
Q

Cystine stones ?

A

Cystine stones only develop in patients with cystinuria (an autosomal recessive disorder) due to the poor solubility of cystine in the urine.

80
Q

Cystinuria ?

A
  • Autosomal recessive disease, defective renal transport of cystine,
    ornithine, lysine, arginine -> nephrolithiasis.
  • urine sample – hexagonal crystals.
81
Q

Cystinosis ?

A
  • A genetic lysosomal storage disease, (typically autosomal

recessive inheritance pattern).

82
Q

Pathology of Cystinosis ?

A
  • Defective transport of cystine across the lysosomal membrane, renal Fanconi syndrome, cellular accumulation of cystine -> destroys tissue ->
    • renal insufficiency.
    • hypothyroidism.
    • blindness.
83
Q

Treatment of Cystinosis ?

A

cysteine-leting drug cysteamine

84
Q

What is the examination of choice for the detection and localization of urinary stones ?
the most sensitive in nephrolithiasis ?

A

nonenhanced CT scanning.

85
Q

opaque stones (90%) ?

A

– calcium oxalate
– calcium phosphate
– cystine
– struvit with calcium phosphate complexes

86
Q

nonopaque stones ?

A

– uric acid

– struvit (without complexes with calcium phosphate)

87
Q

Benign renal tumors ?

A
  • Cortical (papillary) adenoma.
  • Fibroma.
  • Angiomyolipoma.
  • Oncocytoma.
88
Q

Malignant renal tumors ?

A
  • Renal cell carcinoma (RCC).

- Wilm’s tumor.

89
Q

Cortical (papillary) adenoma ?

A
  • small well-defined tumors.
  • asymptomatic.
  • are found commonly at autopsy in
    people over 40 years, the vast majority
    of whom are males.
  • They form pale yellow to gray
    subcapsular, cortical masses usually less than 2 cm in diameter.
90
Q

Renal oncocytoma ?

A
  • Benign, unifocal renal tumor that averages 5-7 cm in diameter.
  • More in females.
  • the tumors are well circumscribed and the
    cut surface has a uniform mahogany-brown
    color without foci of hemorrhage or necrosis.
91
Q

Angiomyolipoma ?

A
  • benign lesions characterized by the presence of:
    1. mature adipose tissue.
    2. smooth muscle.
    3. thick-walled blood vessels.
92
Q

Renal cell carcinoma (RCC) ?

A
  • 85% of all malignant tumors arising in kidneys.

- most common: 60-70 years.

93
Q

Renal cell carcinoma (RCC) risk factors ?

A 
– smoking
– obesity
– HT
– asbestos, petroleum products, heavy metals – CKD and acquired cystic disease
– inborn predisposition (multifocal and bilateral tumors):
• hereditary clear cell Ca
• hereditary papillary Ca
• von Hippel-Lindau syndrome
94
Q

The classic triad symptoms of RCC?

A
  • Back pain.
  • Abdominal pain.
  • Hematouria.
  • seen in
    only about 10% of patients and indicates advanced disease
95
Q

Renal cell carcinoma (RCC)

Gross morphology ?

A
  • yellowish tumor with hemorrhagic, necrotic cystic areas

* may grow into the renal vein

96
Q

Renal cell carcinoma (RCC) Microscopically ?

A
  • clear cell Ca (70-80%)
  • papillary Ca (10-15%)
  • chromophobe renal Ca (5%)
  • sarcomatoid Ca
97
Q

Nephroblastoma (Wilms tumor) ?

A

the most common renal malignancy in children and the fourth most
common childhood cancer.

98
Q

Wilms Tumor may occur as a part of a multiple malformation syndrome including ?

A

– WAGR.
– Denys-Drash.
– Beckwith-Wiedemann syndromes.

99
Q

WAGR ?

A
  • WT.
  • Aniridia.
  • Genitourinary malformations in affected 46XY males.
  • mental Retardation.
  • This is associated with deletion of the Wilm’s tumor-associated gene, WT1, located on the short arm of chromosome 11 (11p13).
100
Q

Denys-Drash syndrome ?

A
  • WT.
  • Nephropathy.
  • ambiguous genitalia in affected males.
  • DDS is due to mutation of both alleles of the WT1 gene that renders it inactive.
101
Q

Beckwith-Wiedman syndrome ?

A
  • WT.
  • Organomegaly and body overgrowth (either as gigantism or hemihypertrophy).
  • This is associated with loss of the maternal allele of a locus on 11p15 called WT2, germline duplication of paternal WT2 allele or inheritance of two paternal WT2 alleles and none from the mother.
102
Q

Clinical features of Nephroblastoma (Wilm’s Tumor) ?

A
  • the most common presentation is detection of an abdominal mass or swelling without other signs or symptoms
  • symptoms or signs that may be present include abdominal pain (30%), hematuria (12-25%), and hypertension (25%).
103
Q

Prognosis of Nephroblastoma (Wilm’s Tumor) ?

A

good outcome with early diagnosis (currently 90% long term survival)

104
Q

Simple renal cysts ?

A
  • the most common renal masses, accounting for approximately 65-70% of cases.
  • most often in patients >50 (M>F)
  • may be solitary, or multiple and bilateral.
  • typically asymptomatic.
105
Q

Autosomal recessive polycystic kidney

disease (ARPKD) ?

A
  • cystic dilations of the renal collecting ducts and congenital hepatic fibrosis.
  • ARPKD is caused by mutations in the PKD1 gene that encodes for fibrocystin (also referred to as polyductin).
  • Progressive renal failure occurs in most patients.
106
Q

Autosomal dominant Polycystic Kidney Disease (DPKD) ?

A
  • the most common genetic cause of chronic kidney disease.
  • main characteristics:
  • large multicystic kidneys,
  • liver cysts,
  • berry aneurysm
107
Q

main clinical features of Autosomal dominant Polycystic Kidney Disease (DPKD) ?

A
  • hematuria
  • flank pain
  • UTI
  • renal stones
  • Hypertension
108
Q

Autosomal dominant PKD (ADPKD) is caused by mutations of ?

A
  • Either PKD1 (gene product: polycystin 1) or PKD2 (gene product: polycystin 2) genes.
  • PKD1 mutations are more common and cause more severe disease than PKD2 mutations.
109
Q

Medullary sponge kidney (MSK) ?

A
  • is a congenital disorder characterized by malformation of the terminal collecting ducts in the pericalyceal region of the renal pyramids.
  • usually asymptomatic.
110
Q

What is the most valuable laboratory diagnostic test for UTI ?

A

Pyuria

  • The most accurate method for assessing pyuria is to examine an unspun voided midstream urine specimen with a hemocytometer; an abnormal result is ≥10 leukocytes/microL.
111
Q

Recurrent UTI ?

A

Recurrent UTI- ≥2 infections in six months or ≥3 infections in one year. Recurrent UTIs -young, healthy women with anatomically and physiologically normal urinary tracts

112
Q

Drug absorption in patient with CKD can be affected by ?

A

Edema of mucus membrane.

113
Q

A 30-year-old man complaining of chest pain, shortness of breath, and back pain during hemodialysis. Lab test reveal rapidly falling hematocrit, hyperkalemia and pink color of the plasma in a centrifuge specimens. The most likely diagnosis is?

A

Hemolysis

114
Q

Indicate the pathogen that is most common cause of peritonitis in patients undergoing continuous peritoneal dialysis?

A

Gram-positive bacteria

115
Q

Which of glomerulopathies typically manifests with erytrocyturia ?

A

IgG nephropathy

116
Q

Treatment of calcium stone disease with hypercalcinuria consist of ?

A
  • High fluid intake.
  • Thiazide diuretics, potassium citrate, low-protein and low-sodium diet.
  • Avoid avoid dietary calcium restriction !
additional info
- what was written above for idiopathic hypercalciuria.
* primary hyperparathyroidism:
– surgery
– avoid thiazide diuretic
117
Q

Urinary alkalinization is indicated in ?

A

Cystine and uric acid nephrolithiasis.

118
Q

Clinical manifestations of Diabetic nephropathy ?

A
  • Renal insufficiency.
  • Nephrotic syndrome.
  • HTN.
  • it usually accompanied by microangiopathic changes in other organs.
119
Q

macroalbuminuria is present ?

A

albumin excretion >300mg.

120
Q

microalbuminuria is present ?

A

albumin excretion 30-300 mg

121
Q

Minimal change disease characteristically produces ultrastructural changes in which renal glomerular element ?

A

Epithelium (podocytes)

122
Q

A kidney biopsy specimens that shows subendothelial granular electron-dense deposits is characteristic of which disease ?

A

SLE

123
Q

Mercury posioning causes which condition in the kidney ?

A

Acute tubular necrosis (ATN)

124
Q

Malakoplakia of the renal pelvis occurs following infection by which organism ?

A

E. Coli

125
Q

An immunoflurescence stained kidney specimen from a patient with poststreptococcal glomerulonephritis is likely to show ?

A

Granular deposits of immunoglobulin G (IgG)

126
Q

Renal cell carcinoma (RCC) common symptoms ?

A
  • The classic histopathology is that of clear cell carcinoma.
  • The combination of hematuria, flank pain, and flank mass is found in only 10% of patients and indication of severe disease.
  • affected pts may present with polycythemia and erythrocytosis.
127
Q

Postinfectious Glomerulonephritis ?

A
  • The disease follows infection with gr A strep.
  • Large subepithelial immune-type deposits are seen by electron microscopy.
  • The histologic picture is that of diffuse proliferative glomerulonephritis.
  • Clinical picture is acute nephritis.
  • there was an old question (all true except )
128
Q

Goodpasture’s syndrome ?

A
  • Patients present with hemoptysis and hematuria.
  • Death occurs due to uremia and pulmonary hemorrage.
  • Electron microscopy shows an absence of electron-dense deposits.
  • Immunofluorescence reveals linear deposits of IgG in the glomeruli.
  • there was an old question (all true except )
129
Q

immunoflurescence stained kidney specimen from a patient with Poststreptococcal glomerulonephritis (PSGN) are likely to show deposits of ?

A
  1. Immunoglobulin.
  2. Fibrin.
  3. Complement.
130
Q

Condition leads to hydronephrosis ?

A
  1. Prostatic hypertrophy.
  2. Pelvic tumor.
  3. Renal calculi.
  • was a question except (chronic vein thrombosis)
131
Q

Asymptomatic bacteriuria ?

A

Significant (>10(5)) bacteria count in the urine culture in individuals with no clinical or laboratory signs of UTI.

132
Q

Is the major cause of anemia in chronic kidney disease is?

A

Erythropoietin deficiency.

133
Q

The most common type of chronic GN in the world?

A

IgG neohropathy.

134
Q

Typical biochemical findings associated with end-stage renal disease are ?

A
  • Increase PTH.
  • Decrease calcium.
  • Increase PO4-
  • Decrease 1,25 (OH) vit D3
  • Renal osteodystrophy
135
Q

Percentage of HTN presentation in patient with kidney failure ?

A

80-90%

136
Q

Pure red-cell aplasia is caused by ?

A

Anti-erythropoietin antibodies.

137
Q

Which organism constitute the most common cause of urinary tract infection?

A

E. coli

138
Q

What are the typical components of dialysis fluid ?

A

Sodium, potassium, bicarbonates, ultra pure water, calcium, chloride, glucose.

139
Q

Patient with chronic kidney disease what is the main alternative route of potassium excretion?

A

GI tract.

140
Q

first line treatment regimen of acute and uncomplicated cystitis in young women ?

A

Fosfomycin

141
Q

Indicate the dysfunctions of the renal tubules in fanconi syndrome ?

A
  • glycosuria
  • aminoaciduria
  • phosphaturia
  • proximal renal tubular acidosis
142
Q

ANGIONEPHROSCLEROSIS ?

A

A phenomenon secondary to long-lasting, poorly controled arterial hypertension and renal tissue aging

143
Q

Biochemical risk factors associated with calcium stone formation ?

A
  1. Hypercalciuria.
  2. Hyperoxaluria.
  3. hypocitraturia. “citrate is important inhibitor of calcium oxlate stone formation”
  4. A persistently alkaline urine pH.
  5. Low urine vloume.
144
Q

Q: dialysis disequilibrium syndrome (DDS) ?

A
  • caused due to water movement into the brain leading cerebral edema
  • severe DDS can be reversed by rising the plasma osmolality with infusion of hypertonic fluid
  • symptoms of this syndrome are self-limited and usually disappear within several hours
  • early findings include headache nausea restlessness and ….

WRONG: Usually progress Tacoma and death.

145
Q

Q: dialysis related amyloidosis ?

A
  • eventually develops in all patients who have been haemodialyzed for more than 13 years
  • beta-2-microglobulin is major protein found in amyloid deposits
  • mostly affects musculoskeletal system
  • ””"”all of the above
146
Q

Q: analgesic nephropathy ?

A
  • associated with chronic use of analgesics
  • promotes urinary tract tumors
  • chronic interstitial nephritis

all of the above

147
Q 
the most common cause of secondary membranous glomerulonephritis?
A. infection with hepatitis C virus
B. lymphoproliferative cnacer
C. bacterial infection
D. SLE
A

A. infection with hepatitis C virus

148
Q

Asymptomatic bacteriuria

Whom to treat ?

A
  • Pregnancy (beta-lactams,nitrofurantoin, fosfomycin).
  • Urologic intervention.
  • Renal transplant recipents.
149
Q

Asymptomatic bacteriuria

Whom not to treat ?

A
  • Nonpregnant premenopausal women,
  • Diabetics,
  • The elderly (in community and in health care facilities),
  • Nursing home residents,
  • Patients with spinal cord injury,
  • Patients with indwelling urethral catheters,
150
Q

The diagnosis of acute cystitis in young woman should be based on?

A
  • Clinical symptoms (dysuria, polyuria, suprapubic pain).
  • Result of urinalysis.
  • Result of urine culture - bacteriuria 10(3).

1. AA my internal medicine (9 decks)

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