Renal Pathophysiology Flashcards

1
Q

Which classes of drugs are potential causes of drug-induced kidney disease?

A

NSAIDs, some antibiotics, thiazide diuretics, high doses of analgesics (particularly when APAP/ASA are combined)

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2
Q

Define azotemia and what its presence indicates in regards to kidney function.

A

azotemia: elevated levels of nitrogen-containing compounds in the blood (BUN and creatinine)

indicates poor GFR due to kidney damage

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3
Q

What is uremia? How is it similar to yet different from azotemia?

A

uremia: presence of elevated nitrogen containing compound (urea rather than BUN or creatinine)

Both uremia and azotemia are caused by elevated levels of some nitrogen containing compound in the blood. Uremia, however, is often secondary to some other metabolic or endocrine disorder and involves elevated levels of urea. Often GI, CV, or neuromuscular involvement.

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4
Q

Which protein is most likely to show in the urine of a patient with renal disease? (proteinuria gets its alternate name from its frequent presence in the urine)

A

albumin (proteinuria sometimes called albuminuria)

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5
Q

Which two symptoms of renal disease are related to the failure of the kidneys to excrete excess fluid?

A

edema and circulatory congestion

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6
Q

AKI is defined as an abrupt decrease in ________ or _________.

A

GFR, creatinine clearance

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7
Q

What classification system, based on GFR and UO as measures of kidney function, is used to assess AKI?

A

RIFLE (risk, injury, failure, loss of function, end stage renal disease)

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8
Q

Describe the three ways AKI is classified according to anatomical area of injury/malfunction.

A

(1) pre-renal: decreased kidney perfusion
(2) intrinsic: structure within the kidney is damaged
(3) post-renal: obstruction present in the urinary collection system

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9
Q

What is chronic kidney disease, and how is it different from AKI?

A

Chronic kidney disease (CKD) is a progressive loss of function of kidney parenchyma that occurs over several months to years. Normal kidney structure is altered because of parenchymal fibrosis. It is most often caused by damage to the filtration units of the kidneys.

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10
Q

What are 3 disease states that can contribute to the progression of CKD if uncontrolled?

A

hyperlipidemia, hypertension, DM

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11
Q

Which form of renal replacement therapy involves perfusion of blood and dialysate on opposite sides of a semipermeable membrane?

A

hemodialysis

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12
Q

How does peritoneal dialysis work?

A

The dialysate is pumped into the highly vascularized peritoneal cavity. The peritoneal membrane acts as the semipermeable membrane. After substances are exchanged between fluids, the dialysate is pumped out of the peritoneal cavity and the process is repeated several times.

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13
Q

What substances are often used to create the osmotic gradient in peritoneal dialysis?

A

dextrose and icodextrin

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14
Q

What is the difference between primary and secondary glomerulonephritis?

A

Primary is associated with the glomerulus itself, while secondary occurs due to some other disease state (SLE, HTN, HLD, DM).

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15
Q

The pathogenesis of glomerular disease involve the ________ system.

A

immune

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16
Q

Which three antibody-mediated mechanisms of glomerular injury were discussed?

A

(1) immune complex deposition
(2) production of anti-GBM antibodies
(3) antibodies against some other glomerular antigen

17
Q

What is the main difference between nephrotic and nephritic syndrome?

A

In nephrotic syndrome, glomerular damage allows protein leakage into the urine. In nephritic syndrome, glomerular damage is more significant and RBCs escape into the urine along with proteins.

18
Q

What are the symptoms of nephrotic syndrome? (think about the pathophysiology)

A

(1) proteinuria
(2) hypoalbuminemia
(3) edema
(4) hyperlipidemia and lipiduria

Proteins escape into the urine, primarily albumin, which explains low albumin in the blood. As you lose protein, you increase the concentration of free water and other substances, like lipids.

19
Q

What are the symptoms of nephritic syndrome? (think about the pathophysiology)

A

(1) hematuria
(2) hypertension
(3) oliguria
(4) azotemia

The greater extent of glomerular damage allows blood to escape in the urine. Hypertension results from a decreased GFR due to glomerular membrane damage.

20
Q

What is APKD?

A

autosomal dominant polycystic kidney disease

21
Q

APKD arises from ___________.

A

mutations in either the PKD1 or PKD2 genes

22
Q

_________ is the only completely effective treatment for APKD.

A

kidney transplant

23
Q

What are some complications associated with APKD?

A

HTN (severely decreased GFR)
intermittent gross hematuria
urinary infection

24
Q

Autosomal recessive polycystic kidney disease results from a mutation in the _________ gene.

A

PKHD1 (fibrocystin)

25
Q

How is autosomal recessive (childhood) PKD different from autosomal dominant (adult) PKD?

A

The involve mutations of different genes. They also manifest different clinically. Childhood patients will show severe manifestations at birth, and if they survive will likely develop hepatic fibrosis. Adult patients will manifest later in life with hematuria, hypertension (decreased GFR), and urinary infections.

26
Q

What are two mechanisms by which an individual could develop acute pyelonephritis?

A

(1) bacteremic spread (aka through the blood)

(2) ascending infection through ureters

27
Q

What is the most common mechanism by which acute pyelonephritis develops?

A

an ascending infection (involves bladder infection followed by vesicoureteral reflux and intrarenal reflux)