Post Type Archives: Topics

Acute tubular necrosis (ATN) is characterized by damage to tubular epithelial cells and abrupt decline in renal function. There is the shedding of granular muddy brown casts and tubular epithelial cells into the urine. ATN is the most common cause of acute kidney injury and may cause oliguria (urine output of <400 mL/day). It is the most common cause of AKI in hospitalized patients. It is associated with high morbidity and mortality.

Bladder musculature has an important role in the storage and emptying of urine from the bladder.
Detrusor
The bladder wall contains specialized smooth muscle – known as detrusor muscle which contracts during micturition and pushes urine out of the bladder. The fibers of the detrusor muscle are arranged in multiple directions. It retains the structural integrity of the bladder when stretched. The detrusor receives innervation from both the sympathetic and parasympathetic nervous systems. It is under the control of the autonomic nervous system.
Spinal cord lesions and the bladder
The bladder has important clinical considerations when it comes to spinal cord lesions. There are two different clinical syndromes, depending on where the damage has occurred.
Spinal Cord Transection Above T12- Reflex Bladder
The afferent signals from the bladder wall are unable to reach the brain → no awareness of bladder filling → no descending control over the external urethral sphincter→ external urethral sphincter is constantly relaxed voluntary control over micturition is lost bladder empties as it fills (like newborn have spinal reflex and no voluntary control on micturition (like newborn babies).
In spinal reflex, the parasympathetic system initiates detrusor contraction in response to bladder wall stretch. The bladder automatically empties as it fills – known as the reflex bladder.
Spinal Cord Transection Below T12- Flaccid Bladder (detrusor areflexia)
Damaged parasympathetic outflow to the bladder → detrusor muscle is paralyzed and unable to contract → the bladder will fill uncontrollably → becomes abnormally distended until overflow incontinence occurs.
Detrusor Hypertrophy (myogenic bladder)
The fibers of the detrusor muscle often become hypertrophic (presenting as prominent trabeculae) to compensate for the increased workload of the bladder emptying, in cases of bladder outlet obstruction (for example in Benign prostatic hyperplasia). Eventually, these hypertrophic muscles will become fibrotic and rigid, making a weak noncompliant bladder wall.
Detrusor sphincter dyssynergia (DSD)
The human bladder has two functions—to store and empty urine. The Coordination and transition between these functions require synergy among the detrusor muscle, urinary sphincters, and the central nervous system. DSD is diagnosed via urodynamic studies in neurogenic bladder patients.
When the central neurologic pathways controlling urine storage and emptying are disrupted by injury, inflammation, degenerative process, or congenital malformation, the urinary sphincters and detrusor can lose coordination leading towards dyssynergia.
If the detrusor muscle contracts while the sphincter is contracted, there is functional bladder outlet obstruction. Detrusor sphincter dyssynergia (DSD) is the urodynamic description of this neurologically induced bladder outlet obstruction.

Hydronephrosis means dilation of renal calyx and pelvis. It occurs due to an obstruction in urine flow or vesicoureteral reflux leading towards urinary retention and stasis. The urinary tract obstruction may be sudden or insidious.

Lower urinary tract (infravesical) obstruction can be acute or chronic. The clinical features depend upon duration, etiology, and site of the obstruction

Acute obstruction 

Acute obstruction is an emergency, and obstruction should be relieved as early as possible, remember stone lodged at the bladder neck. 

Urinary retention- acute blockage causes impaired urine flow and urinary stasis. It increases hydrostatic pressure in the urinary bladder. 

Suprapubic pain- due to urinary retention and stretching of the bladder, it is excruciating pain.

Palpable bladder- the distended bladder is palpated near the lower abdomen (suprapubic area). 

Friedreich’s ataxia is the most common form of inherited ataxia. It has congenital impairment of mitochondrial function leading to cerebellar and spinal cord atrophy and neurodegeneration.

Restrictive cardiomyopathy is a primary disease of ventricular compliance. It causes impaired ventricular filling during diastole because the ventricular wall is stiffer and noncompliant. 

Causes

Idiopathic
Amyloidosis- deposition of insoluble β-pleated sheets causes stiff ventricular muscles. Some immunoglobulin light chains are directly cardiotoxic and can induce myocardial dysfunction.
Hemochromatosis- iron deposition can induce free radicle injury and fibrosis of cardiac muscles. It is most commonly associated with dilated cardiomyopathy but can also cause restrictive cardiomyopathy.
Sarcoidosis – granuloma formation, and chronic inflammatory reaction in cardiac muscles cause fibrosis and stiffening of heart muscles
Scleroderma
Post radiation fibrosis – radiation exposure is associated with free radicle formation and fibrosis.
Loffler Syndrome- It has peripheral hyper-eosinophilia, and eosinophilic tissue infiltrates. The release of eosinophil granule contents causes endocardial and myocardial necrosis. It causes the scarring, and layering of the endocardium by thrombus. The thrombus organization leads to stiffened and noncompliant ventricles.
Endomyocardial Fibrosis- there is dense diffuse fibrosis of the ventricular endocardium and subendocardium. It involves the tricuspid and mitral valves. The fibrous tissue markedly diminishes the volume and compliance. Endomyocardial fibrosis is associated with nutritional deficiencies and inflammation related to helminthic infections.
Malignancy

Hepatitis B is a virus which attacks the liver and can cause acute or chronic disease. It is associated with hepatocellular carcinoma. All Hepatitis viruses are hepatophilic viruses (they have an affinity for liver) and that is why they cause liver damage. Transmission Perinatal transmission  In highly endemic areas, hepatitis B is most commonly spread […]

Goodpasture syndrome is an anti-glomerular basement membrane (anti-GBM) disease. It is an autoimmune disease characterized by damage to the alveolar and renal glomerular basement membranes by the anti-GMB antibody. It is a pulmonary-renal syndrome.Goodpasture syndrome characteristically has -• Pulmonary hemorrhage – hemoptysis• Glomerulonephritis-hematuria• circulating anti-glomerular basement membrane antibodies

Polyhydramnios is a condition where amniotic fluid exceeds 1.5-2 litres in volume, and an amniotic fluid index (AFI) is greater than 20-25.
Etiology
Excess in amniotic fluid can be due to
Decreased resorption (decreased fetal swallowing) –
The gastrointestinal obstruction associated abnormalities like intestinal atresia, tracheoesophageal fistula, or anencephaly cause reduced swallowing of amniotic fluid by the fetus. It leads to excessive amniotic fluid in the uterine cavity.
Increased production (excess fetal urination)- Fetal polyuria, as in maternal diabetes, leads to increased amniotic fluid.

Renal tubular acidosis (RTA) is normal anion gap (hyperchloremic) metabolic acidosis in a patient with normal or almost normal renal function.
Patients with uremic acidosis (metabolic acidosis due to renal failure) have a decreased glomerular filtration rate (increased serum creatinine) and increased anion gap metabolic acidosis. Patients with renal tubular acidosis have relatively normal glomerular filtration rates and normal anion gap metabolic acidosis.