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MCPHS PA Pathophys Exam 3 Renal PT II Flashcards

1
Q

What is Nephritic Syndrome?

A

Inflammation of the Kidney (sepcifically the Glomerulus)

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2
Q

What are the Symptoms of Nephritic Syndrome?

A

Inflammation of Glomeruli

HTN

Decreased GFR

Oliguria

Hematuria (Cola Urine)

Berger’s Disease (IgA Nephropathy)

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3
Q

What is Post streptococcal Glomerulonephritis (PSGN)?

A

Nephritic complication of Gram + cocci (streptococcus)

Presents with frank hematuria after 1-4 weeks and positive ant-streptolysin (ASO) titer.

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4
Q

What is the Pathogenesis of PSGN?

A

Classical complement system activation creates immune complexes that cause Hypocomplentemia and granular desposits of IgG and complement on the Glomerular Basement Membrane (GBM).

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5
Q

What are the Clinical Features of PSGN?

A

Acute Nephritic Syndrome

Edema and HTN with mild to moderate Azotemia

Gross Hematuria; smoky brown urine & some degree of proteinuria

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6
Q

What is IgA Nephropathy (Berger Disease)

A

Deposition of IgA in the mesangium post URI that causes gross Hematuria within 1-3 days.

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7
Q

What is the most common cause of recurent microscopic or gross hematuria?

A

Berger Disease (IgA Nephropathy)

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8
Q

What is the pathophysiology of Berger Disease?

A

URI causes an increase in abnormally glycosylated IgA. THis abnormally glycosylated IgA deposits in the mesangium, and may activate the alternative complement pathway (we only know it isn’t classical activation) causing Glomerular injury.

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9
Q

What are the clinical Features of Berger’s Disease?

A

Gross hematuria post URI.

Course Highly Variable.

May maintain normal Renal Function for Decades.

~25-50% - Slow progression to ESRD over period of 20 years.

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10
Q

What is one of the most common causes of Death in diabetes second only to MI?

A

Diabetic Nephropathy

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11
Q

What is Diabetic Nephropathy?

A

A series of lesions form on the glomerulus and renal vasculature eventually leading to ESRD and then death.

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12
Q

What are the 3 types of lesions encountered in Diabetic Nephropathy?

A

Glomerular

Renal Vascular

Polynephritis

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13
Q

What is the pathophysiology of Diabetic Nephropathy?

A

Early glomerular hemodynamic changes cause hyperprofusion and hyperfiltration resulting in Microalbuminuria, the earliest manifestation of Diabetic Nephropathy.

A dysfunction in the afferent arteriol dialtion due to a dysfunction in vasoconstrictive autoregulatory response contributes to increases intraglomerular pressure, and causes expansion of the messangial cell (hypertrophy) and ECM.

This causes a drop in GFR and reduction in surface area for filtration. These changes cause the glomerular basement membrane to thicken eventually leading to sclerosis which if left untreated will progress to renal failure.

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14
Q

What is Acute Tubular Injury (ATI)/ Necrosis (ATN)?

A

Either Ischemia or Nephrotoxic injury by endogenous (myoglobin, Hb) or exogenous agents (drugs, heavy metals, Radiocontrast dyes) cause tubular injury ot blockage in the nephron.

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15
Q

What is the clinical course of ATI/ATN?

A

Acute Kidney injury leads to either oliguria or anutia and decrease in GFR.

Electolyte abnormalities such as acidosis, uremia, and fluid overload.

Progress will vary depending on severity / nature of injury, and comorbidities.

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16
Q

What is the long term prognosis of ATI/ATN?

A

In the absence of treatment or dialysis PTs may die.

If a PT has preexisting CKD, complete recovery is less frequent and progression ro ESRD is common.

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17
Q

What is one of the most common diseases of the Kidney defined as inflammation affecting tubules, interstitum and renal pelvis?

A

Acute Pyelonephritis

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18
Q

What is the Etiology of Acute Pyelonephritis and UTI?

A

Gram-negative bacilli inhabitants of the GI tract (85%) eg. E. coli

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19
Q

What are the routes of infection for Pyelonephritis and UTI?

A

Hematogenous Infection (from somewhere else in the body)

Ascending Infection (most common)

20
Q

WHy are UTIs more common in Females?

A

Shorter Urethra, absence of antibacterial properties found in prostatic fluid, hormonal changes affecting adherence of bacteria to the mucosa and urethral trauma dueing sexual intercourse or combonation of the above.

21
Q

What is the progression of Pyelonephritis and UTI?

A

Colonization of the distal urethra and introitus (female)

Muiltiplication of the bacteria in the bladder

Retrograde seeding to the renal pelvis and papillae

22
Q

What are the risk factors of Pyelonephritis / UTI?

A

Female Sex

Immunosuppression

Indwelling Catheters

DM

Urinary Tract obstruction

23
Q

What mechanisms lead to Pyelonephrosis / UTI?

A

UT obstruction and urine stasis

Vesicoureteral Reflux

(Backflow of urine toward the kidneys)

Intrarenal Reflux

(expansion of the Vesicoureteral reflux into the tubules)

24
Q

What are the S/S of Pyelonephritis / UTI?

A

Sudden onset of pain (at the costovertebral angle) and systemic evidence of infection such as chills, fever, nausea, malaise, and localizing urinary tract signs of dysuria, frequency, and urgency.

Urine appears Turbid (pyuria)

25
What is the prognosis of Pyelonephritis / UTI?
The disease is unilateral and does not normally lead to Renal Failure. Disease can develop into Papillary necrosis (worse prognosis)
26
What is Chronic Pyelonephritis?
Chronic tubulointerstitial inflammation and scarring involving the calyces and pelvis. An important cause of CKD
27
What are the two types of Chronic Pyelonephritis?
**_Chronic Obstructive Pyelonephritis_** Obstruction leading to infection and scarring **_Reflux Nephropathy_** *Most common cause of chronic pyelonephritis*. Result of superimposition of a UTI on congenital vasicoureteral reflux and intrarenal reflux
28
What are the clinical features of Chronic Pyelonephritis?
Gradual onset of renal insufficiency **Hypertension; asymmetrically contracted kidney** Bilateral disease leading to **Hyposthenuria** (inability to concentrate urine) manifested by polyuria and nocturia
29
What is Chronic Kidney Disease?
Final common pathway of progressive nephron loss resulting from any type of Kidney disease.
30
What is the progression of CKD?
Maladaptive nephrons become scarred and then over time sclerosed glomeruli, tubules, interstitium & vessels mark ESRD
31
What is the Clinical course of CKD?
Insidious onset Proteinuria, HTN, or azotemia Variable rate of progress Less than 30% GFR is a significant problem Stage 5 requires dialysis or transplant
32
What is Renal Artery Stenosis?
Hardening of the Renal Artery leading to secondary HTN.
33
What is the Pathogenesis of Renal Artery Stenosis?
Hypertension is caused by increased production of renin from the ischemic Kidney. (Kidney senses low BP due to stenosis, releases renin to counteract perceived low BP raises overall BP)
34
What is the clinical course of Renal Artery Stenosis?
Symptoms are similar to essential HTN Elevated plasma or renal vein renin
35
What is Adult Autosomal Dominant Polycystic Kidney Disease?
Hereditory disorder causing multiple expanding cysts of both kidneys leading to renal Parenchyma destruction and eventually renal failure. Progressive disease initially only involving a minority of nephrons but over time involving more and more.
36
What is the Pathogenesis of Adult ADPKD?
two types PKD-1 (cell-cell / cell-matrix interactions) causing Tubular Cell proliferation and abnormal ECM PKD-2 (Ca+-permeable cation channel) causing Fluid retention Makes out tubules sticky causing cysts and fluid retention (urine retention) causes them to fill.
37
What is the clinical Course of adult ADPKD?
Asymptomatic; hemorrhage or progressive dilation of the cysts lead to pain Kidney enlargement causes a dragging sensation Features of progressive CKD such as proteinuria (rarely more than 2g/day), polyuria and HTN.
38
What is Childhood Autosomal Recessive Polycystic Kidney Disease (ARPKD)?
Mutation of the PKHD1 gene causes the encoding of Fibrocystin (a membrane protein of unknown function)
39
What are the subcategories of Childhood Autosomal Recessive Polycystic Kidney Disease (ARPKD)?
Perinatal (up to 1 Week) Neonatal (1 Week - 1 Month) Infantile (1 Month - 1 Year) Juvenile (1 Year and up)
40
What is the Pathogenesis of the PKHD1 gene?
It is highly expressed in adult and fetal Kidney also in liver and pancreas
41
What is the clinical course of Childhood Autosomal Recessive Polycystic Kidney Disease (ARPKD)?
PTs develop liver cirrhosis (congenital hepatic fibrosis) In older children, hepatic disease is the predominant clinical concern, progressing to portal HTN with splenomegaly.
42
What is Urolithiasis?
These are Renal calculi / Stones. Calcium stones (70%) Triple stones or Struvite (magnesium ammonium phosphate) Uric acid stones Cysteine stones only a problem if \>6mm in size
43
What is the Pathogenesis of urolithiasis?
**Suprasaturation** (such a concentration that the substance precipitates) occurs. Either an increase in the **concentration of the stone constituents changes in Urine pH, decrease in urine volume, or the presence of bacteria** in urine can also affect supersaturation (the more substance dissolved in the urine the less of each substance that can remain dissolved).
44
What is the clinical course of Urolithiasis?
Asymptomatic or intense pain that occurs in the back and radiates downward and centrally toward the lower abdomen or groin May cause significant renal damage / infection
45
What is Renal Cell Carinoma (RCC)?
The most common malignant tumor of the kidney (3% of all newly diagnosed cancers, but 85% of renal cancer in adults)
46
What are the risk factors for RCC?
Most often found in older individuals (\>60) Cigarrettes Obesity certain chemicals
47
What is the clinical course of RCC?
Costovertebral Pain Palpable mass Hematuria Abnormal Hormone production causing Polycythemia, hypercalcemia, HTN, hepatic dysfunction, feminization or masculinization, Cushing Syndrome) Metastasize widely (lungs, bones) before S/S *Clinical Mimic*

Pathophys (4 decks)

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