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NURS 234 - Intro to Patho > Disorders of the Kidney > Flashcards

Disorders of the Kidney Flashcards

1
Q

oligohyrdaminos

A

Infants born with congenital kidney disorders result from low levels of amniotic fluid (AF) during fetal development

Nonfunctional kidneys or outflow obstruction of urine from the kidneys in infants causes the amount of amniotic fluid to be small.

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2
Q

agenesis

A

is when one or both of the kidneys do not develop

Unilateral is survivable. Bilateral is not

Facial features: the eyes are widely separated and have epicanthic folds, the ears are set low, the nose is broad and flat, chin is receding

Previously called Potter syndrome

The most life threatening component of this syndrome is - no amniotic fluid to cushion fetus.

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3
Q

renal hypoplasia

A

is when kidneys do not develop to normal size
and contain fewer lobes

may be bilateral or unilateral

some cases number of nephrons is reduced, nephrons are larger as the kidneys work harder to compensate, thus increasing risk for glomerular disease

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4
Q

renal dysplasia

A

is an abnormality where cells are malformed during embryonic development (differentation) and cause tubules to form cysts (cystic dysplasia)

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5
Q

ectopic kidneys

A

kidneys lie outside normal position

kinking of ureters and obstruction of of urinary flow may occur

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6
Q

horseshoe kidneys

A

kidneys (upper and lower poles of the two kidneys are fused)

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7
Q

Autosomal Dominant Polycystic Kidney Disease

ADPKD

A

Etiology and Pathogenesis

  • Cysts arise in segments of the renal tubules from a few epithelial cells
  • High proliferation rate of epithelial cells lining the cysts
  • Defective basement membrane - underlying abnormal epithelium allows for dilation and cyst formation
  • Cysts detach and grow
  • Compression causing loss of renal tissue functioning

Clinical Manifestations

  • Asymptomatic early and if cysts are small
  • Pain
  • Gross hematuria from bleeding into a cyst
  • Infection
  • Hypertension - compression of intrenal blood vessels
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8
Q

Autosomal Recessive Polycystic Kidney Disease

A
  • Cystic dilation of cortical and medullary collecting tubules
  • Smooth kidney surface
  • Fibrocystin - gene product responsible for regulation of cell proliferation

Clinical Manifestions

  • Bilateral flank masses
  • Restriction of lung growth (very large kidneys)
  • Liver fibrosis and portal hypertension - diminished blood flow to liver
  • Potter faces
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9
Q

Nephronophthisis - Medullary Cystic - Disease Complex - NPHP

A

Etiology and Pathogenesis

  • Onset in childhood
  • Small kidneys and cysts
  • Distal tubule membrane disruption
  • Chronic and progressive tubular atrophy

Clinical Manifestations

  • polyuria
  • polydispia
  • enuresis (bed wetting)
  • salt wasting
  • growth retardation
  • progressive renal insufficiency
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10
Q

Simple and Acquired Cysts

A 
Etiology and Pathogenesis:
-Common in older adults 
-Single or multiple 
-Unilateral or bilateral
<1 cm, but can grow larger

Clinical Manifestations

  • Most asymptomatic
  • In symptomatic: flank pain, hematuria, infection, HTN
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11
Q

Hydronephrosis

A

Urine filled dilation of the renal pelvis and calices associated with progressive atrophy of the kidney due to obstruction of urine outflow

Etiology and Pathogenesis:

Obstructed outflow of urine
Acute or insidious onset
May occur at any level in urinary tract 
Leads to infection or stone formation
Leads to anuria (failure to produce urine) and renal failure

Clinical Manifestations

  • Unilateral may remain silent
  • Pain
  • Bilateral see oliguria (less urine)
  • Inability to concentrate urine,
  • Polyuria (too much urine) and nocturia
  • Hypertension
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12
Q

Renal calculi (Kidney stones) Nephrolithiasis

A

Polycrystalline structures (formation of crystals that can grow) that kidney normally excretes

Etiology

  • Supersaturated urine
  • Nucleus present
  • Deficiency of inhibitors for stone formation

Types of Stones

  • Calcium
  • Struvite
  • Uric acid
  • Cystine

Clinical Manifestations

  • Pain
  • Renal Colic Pain
  • Non-colicky pain
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13
Q

Urinary Tract Infections

A

Asymptomatic bacteriuria, symptomatic infections,

cystisis (lower UTI)
pyelonephritis (upper UTI)
-Upper UTIs more serious than lower UTIs

Etiology
Ecoli (common cause in lower UTIs)
Washout phenomenon (urine from the bladder washes out urethra)
Seen more in woman due to anatomy
Urinary obstruction, reflux or neurogenic disorders
-Sexually active
-Pregnant
-Post-menopausal and elderly women
-Diabetes
Indwelling catheter

Manifesations
-Neonates: fever, hypothermia, apnea, poor skin perfusion, abdominal distension, diarrhea, lethargy (signs of sepsis)

Older infants: feeding problems, failure to thrive, fever, vomiting, diarrhea

Children: fever is a common sign, frequency, dysuria

Adults: frequently no fever, frequency, dysuria, burning with urination lower abdominal or back pain, cloudy, foul smelling urine

Older adults: Often neurological change is first sign,

Asymptomatic or vague symptoms, anorexia, confusion, fatigue, weakness

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14
Q

Disorders of Glomerular function

A

Inflammatory process that involves the glomerular structures and induces glomerular cellular injury

Causative agents

  • non-immunologic (infection, hypertension, drugs chemicals)
  • immunologic (antibodies trying to attach to antigen)
  • hereditary (rare)
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15
Q

Disorders of Glomerular function

Cellular changes can be

A
  • Diffuse
  • Focal
  • Segmental
  • Mesangial
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16
Q

Effects of Glomerular Disease

A

too much allowed through or too little goes through = depends on the disease

17
Q

Manifesations

A

-Elevated BUN (blood urea nitrogen)
-Sudden insidious
onset of hypertension
-Proteinuria (loss of proteins in blood)
-Edema
-Decreased GFR leads to elevated plasma creatinine and urea (more waste)
-Glomerular capillary blood flow triggers mechanisms to increase BP
-Increased glomerular capillary permeability results in loss of plasma proteins
-Resulting hypoalbuminemia encourages plasma fluid to stay in interstitial spaces leading to edema.

18
Q

Acute Nephritic Syndrome

A

Etiology

  • Acute inflammatory process that occludes (blocks) the glomerular capillary lumen and damages the capillary wall.
  • Characterized by decreased GFR

Clinical Manifestations

  • Hematuria (cola colored urine)
  • Proteinura (varies)
  • Nitrogen waste buid up
  • Oliguria
  • HTN
  • Edema
19
Q

Acute Postinfectious Glomerulonephritis

A

Etiology:

  • Occurs after infection with a certain strains of streptococcus (Group A Beta Hemolytic strep) 7-12 days after strep throat or other viruses
  • Hypercellularity: infiltration of leukocytes (neutrophils and monocytes)
  • Proliferation of endothelial and mesangial cells
Manifestations:
Oliguria
Proteinuria
Hematuria (increased capillary wall permeability)
Edema
Hypertension
20
Q

Rapidly Progressive Glomerulonephritis

A

Etiology:

  • Rapid decline in GFR
  • Focal and segmental proliferation of the glomerular cells
  • Monocytes and macrophages recruited along with destruction of Bowman’s capsule

Manifestations
Rapid progression often within matter of months
Can progress to acute renal failure and death if untreated

21
Q

Goodpasture syndrome

A
  • Uncommon and aggressive form of glomerulonephritis
  • Antibodies attack parts of glomerular basement membrane (GMB) and cross react with pulmonary alveolar basement membrane (affect kidneys and lungs - membranes share an antigen)
  • Produce the syndrome of pulmonary hemorrhage associated with renal failure
  • Caused by influenza, exposure to hydrocarbons
22
Q

Nephrotic Syndrome

A

Etiology

  • May be primary disorder (more common in children)
  • Or secondary disorder (more common in adults) to systemic diseases such as diabetes, SLE, or amyloidosis
  • Characterized by increased glomerular permeability
  • At risk for thrombotic complications
  • At risk for atherosclerosis
  • Increase risk of infections

Manifestations

  • Massive proteinura
  • Hypoalbuminemia
  • Lipduria
  • Hyperlipidemia
  • Hallmark is generalized Edema
  • Initially dependent body parts, then becomes generalized as disease progresses
  • Dyspnea (pulmonary edema)
23
Q

Asymptomatic Hematuria or Proteinuria

Immunoglobulin A Nephropathy - Berger disease

A
  • IgA immune complexes in mesangium (sit in extracellular fluid in glomeruli) of glomerulus lead to inflamation
  • Most common cause of glomerular nephritis in Asians
  • Onset usually in 20s and 30s
  • Hematuria and mild proteinuria
24
Q

Alport Syndrome - Hereditary

A

Hereditary defect in glomerular basement membrane

  • X linked boys more severe (due to only one x chromosome)
  • hematuria and chronic renal failure
25
Q

Hypertensive Glomerular Disease

A

mild to moderate HTN causes sclerotic changes to the renal arterioles and small arteries. Usually bilateral. Most prevalent in blacks

26
Q

Diabetic Glomerulosclerosis

A

-Mechanism of change uncertain
-Effects of basement membrane and mesangial matrix
Increased GFR associated with microalbuminuria

27
Q

Acute pyelonephritis

A

Etiology
Acute infection of the renal pelvis interstitium around the cells
Ascending route of infection through the lower urinary tract is most common. Infection can also occur through the blood
Outflow obstruction - vesicoureteral reflux (ascending infection)

Manifestations 
chills 
fever malaise
HA, backpain, tenderness over costovertebral angle
Dysuria
Frequent urination
uirne urgency
28
Q

Chronic Pyelnephritis

A

Etiology
Persistent or recurring episodes of acute pyelonphritis that leads to scarring
Reflux is most common cause
Risk of chronic pyelonephritis increase in individuals with renal infections and some type of obstructive pathologic condition
HTN can contribute to progression of disease

Manifestations
Insidious onset
Inability to concentrate urine due to loss of tubular function
Polyuria, nocturia, mild proteinuria

29
Q

azotemia

A

is a medical condition characterized by abnormally high levels of nitrogen containing compounds in the blood such as urea, creatinine

30
Q

When kidneys fail

A

less waste is removed

unable to regulate fluid, electrolyte and pH balance

31
Q

Acute Kidney Injury (AKI)

A

Rapid deterioration in renal function characterized by progressive azotemia
GFR is reduced = reduced excretion of nitrogenous wastes and fluid-electrolyte imbalances
Often asymptomatic

32
Q

Types of AKI

A

based on where injury occurs

NURS 234 - Intro to Patho (4 decks)

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