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28 Cards in this Set

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conjunctiva red and swollen, with some mild lid edema

allergies, chemical irritation or infection.
Allergy: bilateral red, watery eyes, and itchiness and irritation. Discharge- mucoid and ropey. hx of hypersensitive reactions to seasonal allergens, such as pollens and molds, or to perennials such as dust mites and animal dander.

< 6y/o have bacterial than a viral infection. Both produce conjunctival redness and itching, but bacterial conjunctivitis is more likely to be bilateral and to cause a purulent exudate with eyelids crusted closed upon waking. Both viral and bacterial tend to begin in one eye, but both may spread to the other eye.
Adenovirus conjunctivitis frequently becomes bilateral and may be associated with pharyngitis and pre-auricular lymphadenopathy.

no erythema accompanying the eye swelling= inconsistent with conjunctivitis.
most common causes of bilat periorbital swelling
conjunctivitis, URI and sinusitis.

can be w/o redness as a result of inflammatory edema.
swelling usually painless and from obstruction of venous drainage from periorbital structures into veins that pass through the sinuses because the veins are partially blocked by inflamed tissues in the sinuses.
10-day duration of eye swelling would be unusual for a URI. Sinusitis or allergic rhinitis could cause more prolonged symptoms but are usually accompanied by cough or runny nose

Allergic rhinitis is possible, but is a less likely

NOT Periorbital cellulitis most often caused by pneumococcal Moraxella catarrhalis or by non-typable Hemophilus influenza.
usually unilateral and hx of a local insect bite, trauma, or infection. It may also extend from another site of infection, such as sinusitis.
nephrotic syndrome
periorbital edema and inc abd girth (hypoalbuminemia)
recent URI
fatigue w/o fever, no appetite

Periorbital edema that improves when the child is upright
Edema becomes more generalized, leading to pitting edema and ascites.
interstitial fluid accumulation rather than intravascular fluid overload (as is the case in acute glomerulonephritis)= no hypertension and severe may become hypotensive.
nonspecific symptoms of increasing tiredness and decreased appetite due to interstitial fluid accumulation
Acute glomerulonephritis
periorbital edema and inc abd girth (hypoalbuminemia) b/c intravasc fluid overload
freq follows URI
fatigue w/o fever, no appetite
periorbital swelling but no edema in children (unlike adults)
SOB (like fatigue) w/o fever
poor appettite
unlike to present this late unless new aquired cardiomyopathy
liver failure
periorbital edema and inc abd girth (hypoalbuminemia)
freq follows URI
fatigue w/o fever, no appetite
abd distention
periorbital swelling and redness (usually painless) from inflamm edema from ethmoid, maxillary, frontal sinusitis
poor appetite

nasal congestion, headache, and cough.
recent URI
abrupt periorbital swelling
accompanies by periorbital rash
would have a PMHx

may be swelling of other parts of the face as well, including the lips, tongue and other oropharyngeal structures that can compromise the airway

seasonal or perennial allergic conjunctivitis may be associated with pruritis and mucoid discharge. Often there is associated sneezing, itchy nose, and clear rhinorrhea. On exam there may be allergic shiners (dark circles under the eyes), Dennie's lines (an extra crease below the lower eyelid), and cobblestoning of the conjunctiva (fine bumps on the conjunctival mucosa).
enlarged tonsils in children
peak growth of lymphoid tissue occurs at 4 to 6 years of age, and because of frequent viral upper respiratory infections in children of this age, it is very common to see mildly enlarged tonsils. As long as there is no erythema or exudate, pharyngitis is unlikely.

strep pharyngitis (note the enlarged, red tonsils and petechiae on the soft palate).
S3 gallop
overloaded left ventricle, and would suggest congestive heart failure
why do you need a third hand to test for fluid wave?
third hand is necessary to prevent transmission of the fluid wave through adipose tissue
conditions that can cause ankle swelling
arthritis involving the ankles
systemic allergic rxn
Serum sickness- can cause arthritis or periarticular swelling, but is also associated with a urticarial rash
Henoch-Schonlein purpura- vasculitis w palpable purpuric rash of the lower extremities and abdominal pain associated with arthritis. Occasionally joint swelling or abdominal pain can precede the rash.
Minimal change disease
most common cause of the nephrotic syndrome in children, 90% < 10y/o.
fusion and diffuse effacement of the epithelial cell foot processes on electron microscopy.
nephron appears relatively normal on light microscopy.
lab studies for hypoalbuminemia
loss of albumin in the urine, or lack of production in the liver. The CBC is useful in this case as well, although it will not lead to a specific diagnosis. C3 complement level screens for hypocomplementemia, found in membranoproliferative glomerulonephritis, post-streptococcal glomerulonephritis, and SLE
proteinuria that is significant enough to warrant further diagnostic workup is defined as:
1. (30 mg/dl) on 2 random urine specimens collected one week apart if urine specific gravity is less than or equal to 1.015; or

2. (100 mg/dl) on similarly collected urine if specific gravity is greater than or equal to 1.015.

The degree of proteinuria can be better quantified by 24-hour collection or by spot measurements of both urine protein and creatinine. In children it is difficult to obtain accurate 24-hour collections, so a urine protein: creatinine ratio is very useful.

protein:creatinine ratio:
<0.2 is normal in children older than 2 years (<0.5 is normal in 6- to 24-month-olds)
>1.0 is in a suspicious range for nephrotic syndrome
>2.5 is diagnostic for nephrotic syndrome

24-hour collection:
- Normal amount of protein excreted is less than or equal to 4 mg/m2/hour
- Abnormal: 4-40 mg/m2/hour
- Nephrotic range: Greater than or equal to 40 mg/m2/hour
Post-streptococcal glomerulonephritis (PSGN)
after a streptococcal infection of either the throat or the skin.

Pharyngitis caused by Streptococcus pyogenes classically presents with sudden onset of fever, sore throat, headache, and abdominal pain with absence of rhinorrhea, congestion, or cough.
exudative tonsillitis with palatal petechiae, strawberry tongue, tender anterior cervical lymph nodes, and sometimes an accentuation of skin lines in the flexor surfaces (Pastia's lines) and a fine papular sand-paper like rash (scarlitiniform rash). Treating strep throat with antibiotics will prevent the complication of Acute Rheumatic Fever, but it will not prevent the occurrence of PSGN.

Impetigo S. pyogenes or staphylococcal species. golden honey-colored crust. Common locations are under the nares or on insect bites or wounds. Treatment with topical or oral antibiotics will not prevent the occurrence of PSGN.

tea-colored urine, it is important to ask about recent throat and skin infections.
elevated Antistreptolysin O (ASO) titer, Streptozyme, anti-DNase B, or low C3.
benign vs significant proteinuria
Children may excrete 1+ to 2+ (30-100 mg/dL) of protein during a fever or after significant exertion, which clears after resolution of the fever or exertion. Orthostatic proteinuria is a frequent finding in adolescents and does not signify renal disease. There may be as much as 1500 mg/1.73 m2/24 hours, but protein excretion occurs when the patient is standing, not while recumbent. When the first morning urine is checked it should be negative for protein.
what else can cause proteinuria?
acute glomerularnephritis

NOT reflux or interstitial nephritis

Any disease causing inflammation of the renal parenchyma or nephritis can cause proteinuria. While acute glomerulonephritis results in varying degrees of proteinuria, red blood cells and red blood cell casts would also be present, Katie's dipstick was negative for heme.

pyelonephritis. White blood cells and white blood-cell casts would be seen with a urinary tract infection, which would cause a positive leukocyte esterase test on the dipstick.

Interstitial nephritis can be associated with red and white blood cells in the urine, but not with this massive degree of proteinuria. In children, interstitial nephritis is rare and usually caused by a medication such as Methicillin (no longer available in the United States), NSAIDs, penicillins, cephalosporins, rifampin, sulfonamides, or infection.

Vesicoureteral reflux does not cause significant proteinuria unless the patient also has significant renal parenchymal scarring.
proteinuria pysio
increased filtration of large proteins, predominantly albumin and some globulins, through the glomerular capillary wall.

There are 3 possible mechanisms for proteinuria:
1) The loss of the polyanion charge characteristic of the normal capillary wall. All layers of the glomerular filtration surface have a negative surface charge due to proteoglycans such as heparin sulfate. Therefore, loss or reduction of this charge may permit large negatively charged proteins like albumin, which previously were blocked from leaking by electrostatic forces, to leak through the membrane.

2) A shift in the capillary wall pore size in a direction permitting increased leaking of large molecules.

3) A change in the hemodynamic characteristics of capillary flow so there is a greater filtration of larger molecules.
hyperlipidemia along with hypoalbuminemia
low albumin and elevated lipids are due to nephrotic syndrome. With nephrotic syndrome there is a major loss of albumin in the urine due to leaking through the defective capillary basement membrane. There is evidence for increased loss of albumin due to problems with renal tubular reabsorption/metabolism and decreased synthesis of the protein in the liver. In reaction to the decreased albumin, the liver is stimulated to make lipoproteins as well as albumin, which leads to hyperlipidemia and hypercholesterolemia. There is also decreased lipid clearance from the circulation.

Lipid abnormalities are associated with atherosclerosis and increased risk of coronary artery disease in adults with persistent nephrotic syndrome. Whether lipid abnormalities are associated with accelerated atherosclerosis in childhood minimal change nephrotic syndrome is unclear. The duration of the hyperlipidemia and the concentration of high-density lipoprotein may be important. There is some evidence to suggest that relapsing and remitting nephrotic syndrome of childhood does not increase cardiovascular risks. Currently most pediatric patients with steroid-responsive nephrotic syndrome are not treated with lipid/cholesterol-lowering medications.
An increase in interstitial fluid causing anasarca will occur if there is:
- An increase in capillary hydrostatic pressure (as in congestive heart failure);
- A decrease in plasma protein concentration (as in nephrotic syndrome);
- Increased vascular permeability to proteins (as occurs in allergic reactions);
- Impaired lymphatic flow.

Some patients will present with hypovolemic shock during an exacerbation of nephrotic syndrome, requiring restoration of plasma-oncotic pressure with IV albumin. However, decreases in intravascular volume are not present in most patients studied who have nephrotic syndrome.

Intravascular hypovolemia activates volume sensors and extrarenal neurohumoral and hemodynamic mechanisms that signal the kidney to retain salt and water through increased renin-angiotensin-aldosterone, catecholamines, antidiuretic hormone and depressed natriuretic factor leading to edema.
hyonatremia in nephrotic synd
Hyponatremia in nephrotic syndrome is due to total body fluid overload caused by excessive sodium and water retention.

Pseudohyponatremia, caused by the hyperlipidemia, may also exist. This depends on how the lab measures sodium. Pseudohyponatremia will occur only if the lipids are high enough to cause the blood to have a milky appearance
thrombosis in nephrotic syndrome
even with a normal CBC, patients who have nephrotic syndrome are predisposed to venous thrombosis involving any of the large veins of the body, including the sagittal sinus and pulmonary arteries. Renal venous thrombosis is a relatively frequent complication in adults. Factors predisposing to venous thrombosis include urinary loss of proteins that inhibit coagulation (antithrombin III) or increased fibrinolysis, destabilization of platelets by hyperlipidemia, increased fibrinogen levels, and increased blood viscosity due to a rise in the hematocrit (especially if diuretics are used without albumin replacement). Intense, prolonged therapeutic use of corticosteroids, which are themselves thrombogenic
complement lvls
C3 and C4, determine if there is a secondary cause for nephrotic syndrome such as a collagen vascular disease (systemic lupus erythematosis (SLE), a primary renal disease other than minimal change disease (membranoproliferative glomerulonephritisor) or an infectious etiology such as a recent group A strep infection (post streptococcal glomerulonephritis).

decreased in secondary glomerulonephritis or nephrotic syndrome. Hepatitis B, HIV and other infectious etiologies can also cause nephrotic syndrome, but would be expected to show other abnormalities on liver enzymes and the CBC, high risk population. Normal complement levels and renal ultrasound, as well as a negative Streptozyme, help to rule out post-streptococcal glomerular disease. The Streptozyme is a combination of antibody tests to detect a recent streptococcal infection. A negative ANA helps to rule out SLE and is recommended in the evaluation of children >10 years old. Other secondary causes of nephrotic syndrome include Henoch Schoenlein Purpura or IgA nephropathy (usually associated with significant hematuria) and lymphoma (should be considered particularly if presentation incudes lymphadenopathy and/or hepatosplenomegaly).
tx nephrotic synd
IV furosemide alone is very dangerous because could lower intravascular volume to dangerously low levels, precipitating shock and increasing risk for venous thrombosis. preceded by an albumin infusion. Treatment with albumin alone could lead to pulmonary edema if the blood volume expands too rapidly. Combined use of furosemide and 25% albumin is recommended only for those children with symptomatic edema, particularly to relieve dyspnea and edema if these symptoms are causing discomfort, or, in boys, to reduce scrotal edema that may compromise testicular perfusion. The albumin infusion should be followed with 1 to 2 mg/kg of furosemide to promote diuresis. Katie also should be started on corticosteroids.

average American child's diet already contains 1.5 grams more protein than is recommended per day and would compensate for what is lost in the urine, so adding more protein to the diet is not recommended. During edema accumulation, the patient usually excretes less than 5 mEq of sodium per day. A diet of 50 mEq per day will result in the net gain of a kilogram of body water every 3 days. Current guidelines recommend sodium restriction to a level of 1500-2000 mg daily
1 and 10 years without gross hematuria and with a normal serum complement level should receive a trial of
corticosteroids because the diagnosis is most likely Minimal Change Disease

histological: glomeruli normal or with a minimal increase in mesangial cells and matrix.
3 groups: steroid responsive, relapsing or steroid-dependent and steroid resistant. Steroid-resistant patients (those who do not respond to steroids with elimination of proteinuria after 8 weeks of therapy) usually then undergo a renal biopsy.

Other indications for renal biopsy in patients with NS include:
younger than 6 months (increased chance of congenital NS);
Infants >3 months and <18 months of age with hematuria;
Children >10 years of age if the diagnosis is not a drug reaction or postinfectious glomerulonephritis;
Children with type I diabetes <10 years' duration;
Children of all ages who have hematuria and proteinuria if the mother has hematuria (Alport syndrome);
Children with Henoch-Schoenlein purpura;
Children with non-postinfectious glomerulonephritis with progressive decline in renal function and urine output;
Patients with suspected lupus nephritis with a positive ANA, elevated anti-DS DNA titer, and a decrease in C3 that persists more than 3 months;
Patients with a low serum complement at the time of initial presentation not related to acute postinfectious glomerulonephritis;
Patients with systemic lupus erythematosus with proteinuria or NS;
Evidence of chronic renal insufficiency with persistent elevation of serum urea nitrogen and creatinine.

Fortunately, more than 95% of children will respond to corticosteroid therapy, and although relapses are common, the long-term prognosis is excellent for these
repeated relapses until the disease resolves spontaneously toward the end of the 2nd decade of life,
no long-term renal damage
focal segmental glomerulonephritis (FSGS)
after minimal change disease, the next most commonly seen etiology of idiopathic nephrotic syndrome is focal segmental glomerulonephritis (FSGS), which accounts for roughly 10% of patients.
most of the glomeruli appear normal or show mesangial proliferation, while others, especially juxtamedullar glomeruli, show segmental scarring in one or more lobules. The disease frequently leads to involvement of all glomeruli, and to end-stage renal failure in most patients.
Only about 20% of patients respond to steroid or cyclophosphamide therapy. Unfortunately even with transplantation the disease may recur in the transplanted kidney. Genetic testing is currently being developed to help distinguish familial foms of FSGS, which are unlikely to respond to immunosuppressive therapy from sporadic cases, which are more likely to respond to immunosuppression.

Even less frequently seen are membranoproliferative glomerulonephritis (about 5% of idiopathic nephrotic syndrome patients) and other glomerular diseases
fever w nephrotic synd
During a nephrotic syndrome relapse with steroid use, high risk for infection.
decreased immunoglobulin levels, edema fluid acting as a culture medium, protein deficiency, decreased leukocyte bactericidal activity, immunosuppression from steroids, decreased splenic perfusion due to hypovolemia, and urinary loss of a complement factor (properdin factor B) that opsonizes certain bacteria.

Spontaneous peritonitis is one of the most frequent complications, with an insidious presentation of fever and minimal other findings,
Untreated it can lead to overwhelming sepsis and death, especially while the patient is on steroids.

Streptococcus pneumoniae is the most common pathogen causing peritonitis, but gram-negative bacteria can also be found. Pneumonia, cellulitis, and urinary tract infections are other common infectious complications of nephrotic syndrome.

cultures of blood and peritoneal fluid), and early treatment with broad spectrum antibiotics to cover gram-positive and gram-negative organisms
polyvalent pneumococcal vaccine and two doses of varicella vaccine, and influenza vaccine annually.