Monday 04/06/2020
Nephrotic Syndrome:
Occurs when the glomeruli are damaged and lets protein pass into the urine (>3.5g of urine excreted per day).
One of those protein is albumin which leads to peripheral/periorbital edema.
Causes:
1) Minimal change disease: most common cause in children. (viral syndrome, allergies, Hodgkin disease). Loss of negative charge of membrane promotes proteinuria.
2) Membrane nephropathy: most common cause in Caucasian males > 40 y/o.
3) Focal segmental glomerulosclerosis. Most common in Africans and Hispanic. (on the test these pl take HIV/ Heroin and have HTN).
Secondary cause:
1) Diabetes mellitus most common secondary cause in adults. Or another systemic disease.
Signs/ Symptoms:
1) Hyperlipidemia and fatty casts (Maltese cross-shaped fat bodies) Frothy urine
2) Proteinuria/hypoalbuminemia (>3.5g) à peripheral/periorbital edema (mc in children) worse in AM
3) Hypercoagulable state à loses antithrombin III protein as well à DVT
Diagnosis:
1) UA à initial test
Microscopy à fatty casts (Maltese cross-shaped fat bodies).
2) 24hr urine protein >3.5g/day à gold standard. Albumin: Creatinine ration
3) Definite diagnosis (rarely used) à renal biopsy.
Management:
1) Glucocorticoids à first line for MINIMAL CHANGE DISEASE.
2) Edema reductionà diuretics
3) ACEi/ ARBs à reduce proteinuria.
4) Statin therapy à for hyperlipidemia.
Nephritic syndrome (acute glomerulonephritis).
Occurs when immune-mediated inflammation damages the glomerular basement membrane à leading to protein + RBC leakage in the urine.
Causes:
1) Berger’s Disease (IgA nephropathy)à MC cause of glomerulonephritis. Affects young kids after URI/GI infection. Abnormal IgA which are released from respiratory and GI form in the body and then immune system forms IgG which forms a complex and gets stuck in kidney. Leads to overproduction of IgA.
2) Post infectionà MC due to group A streptococcus after skin impetigo.
Classically its young kids with facial edema after strep with scanty, cola-colored/dark urine.
3) Rapid Progressive Glomerulonephritis à rapid progression to end stage renal failure. You will see crescent formation in biopsy.
Signs/Symptoms:
1) Hematuria and red blood cell casts (cola/tea colored urine).
2) Proteinuria (<3g) à peripheral/periorbital edema
3) HTN
4) Oliguria (small urine amount).
5) Azotemia à Increase BUN/Creatine
Diagnosis:
1) UA à hematuria, RBC casts, proteinuria.
2) Definite diagnosis (rarely used) à renal biopsy (where you will see crescent-shaped cells).
Management:
1) Usually a self-limiting drug. For edema use a loop-diuretics and treat HTN
2) IgA nephropathy or proteinuria à ACEi +/- corticosteroids
3) Post streptococcal infection à Antibiotics and supportive + cyclophosphamide
4) Rapid progressive glomerulonephritis à Cyclophosphamide + corticosteroid.
MIXED NEPHROTIC + NEPHRITIC à HEMATURIA + PROTEINURIA (>3.5g)
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Wednesday 04/08/2020
Paradoxical Embolism:
Paradoxical Embolism refers to an embolus which is carried from the venous side of the circulation to the arterial side or vice versa. Usually it begins with the dislodgment of a venous thrombus that courses its way into systemic circulation via an intracardiac shunt or pulmonary arteriovenous malformation.
Patent foramen ovale (PFO) is a left to right shunt. However, Valsalva maneuvers such as coughing, squatting, can increase right atrial pressure leading to a shunt reversal, resulting in the transferring of potential thrombi into the systemic circulation.
Atrial septal defects (ASD) are congenital defects that vary in size and location. ASDs lead to a left to right shunt as well as a fixed split S2 on cardiac exam, however reversal in flow can reverse the shunt. ASDs accounts about 14% of the cases for paradoxical embolism.
Ventricular septal defects commonly result in left to right shunts, however certain conditions that increase right atrial pressure like Eisenmenger syndrome can reverse the shunt, allowing for paradoxical embolism.
Pulmonary arteriovenous malformations are usually hereditary and are a pathological connection between the pulmonary arteries to the pulmonary veins returning to the left atrium. This leads to a permanent right to left shunt.
Ischemic stroke is the most common complication of paradoxical embolism.
DVT: so usually a dislodged DVT will most likely settle in the pulmonary arteries causing a pulmonary embolism. However, a DVT in the presence of an intracardiac shunt can paradoxically cause an embolism in branches of the aorta. For example DVT gets dislodged and enters the right atrium where an increase in right atrial pressure during a Valsalva maneuver can force the emboli through the patent foramen oval or atrial septal defect and into the left atrium where it will travel to the left ventricle, and out through the aorta where it can occlude coronary, cerebral, renal, mesenteric, or peripheral arteries. Based on the occluded artery you can have symptoms such as: neurological deficits, chest pain, abdominal pain, or a cold limb.
Diagnosis:
Diagnosis of paradoxical embolism is that of exclusion, and other common causes of stroke should be ruled out first. EKG should be performed to assess for atrial fibrillation.
We usually also use Transthoracic echocardiogram (TTE) with color-flow Doppler to evaluate any potential intracardiac shunts which as we talked before, can increase the probability of a paradoxical embolism.
Treatment:
Treatment is to correct underlying problem such as Patent foramen ovale, septal and ventricular defect. Usually those are fixed at birth surgically.
Medical therapy is comprised of antithrombotic therapy, which includes aspirin, or Plavix (clopidogrel) as monotherapy or taken in combination with warfarin for the prevention of thrombotic events.
Source: https://www.ncbi.nlm.nih.gov/books/NBK470196/
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Friday 04/10/2020
Lyme Disease:
Overview:
Lyme disease in a vector-borne illness in the U.S and usually caused by infection with the spirochete Borrelia burgdorferi. Most of the cases in the U.S occur in southern New England, southeastern New York, New Jersey, eastern Pennsylvania, eastern Maryland and Delaware. Most of the cases of Lyme disease come from children ages 5-10 years old and the number is almost twice as high as the incidence among adults. However, most Lyme disease cases are resolved with appropriate treatment and care.
Clinical Presentation:
Clinical presentation of Lyme disease is classified into 3 stages: early localized disease, early disseminated disease and late disease. In the early localized disease, erythema migrants appears at the site of the tick bite in about a week or so. Initially the lesion will appear as red macule but then expand to a large, annular erythematous target lesion in the next few days. This lesion is usually asymptomatic but can sometimes be pruritic or painful. In the early disseminated stage, we start to see cranial nerve palsies, especially facial nerve palsy, and meningitis. There are also common reports of systemic symptoms such as fever, headache, fatigue and myalgia related to this stage. In the late stage of Lyme disease, which is uncommon in the U.S we start to see arthritis which is usually monoarticular and affects primarily the knee. Encephalitis, encephalopathy, and polyneuropathy can also be some other symptoms of late stage Lyme disease.
Diagnosis:
Labs: CBC, ESR, CRP, LFT’s
EKG
ELISA: Sensitivity 94%, specificity 97% in patients lacking erythema migrans.
We also have to keep in mind that 50% of patients with early infection can have a false-negative result but if you are still suspicious of Lyme disease, you can have titers obtained in 6 weeks.
If ELISA is positive – Western blot is a confirmatory test.
Treatment:
If patient only have Lyme disease with no complications and mild symptoms you can start them on doxycycline 100mg BIDx14 days.
If patient start to develop neurological symptoms or lyme meningitis then you can place them on ceftriaxone 2g IV QD for 12 days.
If patient develops lyme carditis then you can still use ceftriaxone 2g QD for 14 days and admit them to continue cardiac monitoring.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652387/
PPP by Dwayne A. Williams
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