Diseases Week 3 Flashcards
Uremia
Azotemia and clinical symptoms.
Sx include: Gastroenteritis, anemia, peripheral neuropathy, pruritis, pericarditis, etc.
Nephritic Syndrome
Kidney disease w/ sx of: hematuria, mild to moderate proteinuria (
Nephrotic syndrome
Defined by >3.5g proteinuria (pitting edema, sometimes hypercoaguable and immunosuppressed), edema, hyperlipidemia, lipiduria.
Acute Renal Failure
- Rapid onset azotemia
- Oliguria or anuria
- Due to glomerular (immune), tubulointerstitial (toxic ischemic), or vascular disease
Proteinuria w/o renal disease
Causes:
- Postural (orthostatic/standing) - 3-5% of young adults
- transient
- functional (heavy exercise, cold exposure, fever) –>
Glomerular pattern of proteinuria
Albumin, small globulins –> globulins reabsorbed w/ normal tubular fxn. May be in nephrotic range (
Tubular pattern:
Beta2 microglobulin –> 1-2g/day
Agenesis of the kidney
Bilateral incompatible w/ life.
Unilateral compatible w/ normal funciton –> hyperfiltration and hypertrophy often present.
Hypoplasia of kidney
Bilateral or unilateral
No scarring w/ a decreased number of renal lobes (6 or less)
Most cases are aquired (show scarring)
Ectopic kidneys
Typically just above the pelvic brim or in pelvis
Horseshoe kidney
Fusion of the lower pole (90%) to form a single horseshoe-shaped kidney.
Incidence: 1:500–>1:1000 (most common congenital abnormality)
Kidney gets trapped on Inferior mesenteric artery during ascension in development.
Increased incidence in turner’s syndrome
Danger for infx and stone formation, and mild increase in Wilm’s tumor.
Cystic Renal dysplasia
Unilateral (most common) or bilateral (most commonly tested –> ddx vs PCKD)
Gross: enlarged, multicystic and irregular
Micro: undifferentiated mesenchyme
Most cases also have lower tract abnormalities
SPORADIC DISORDER
Autosomal Dominant Polycystic Kidney Disease
ADults (Autosominal Dominant)
Heriditary, affecting 1/400-1,000 live births
Bilateral disease, involving only a portion of the kidney initially.
-renal failure in less severe)
Gross: Bilaterally enlarged kidneys (can be huge) –> bag of cysts.
Micro: Cysts w/ variable lining, normal parenchyma between cysts.
Clinical: Asymptomatic/flank pain/ hematuria/mass/htn
High anion gap acidosis
ABG: pH 15
Compensation is to get rid of CO2
PCO2 = last two digits of pH
If this is present –> calculate osmolol and delta gap.
DDX: Methanol Uremia DKA or Alcohol ketoacidosis Paraldehyde Iron (kids) or isoniazid (TB) Lactic Acidosis Ethylene Glycol Salicylates
Normal Anion Gap Acidosis (Hyperchloremic Metabolic Acidosis)
Due to loss of HCO3- from kidney or GI most common, see equal rise for loss of HCO3-
DDX: HARDUP post Hyperventilation, hyperalimentation Acid ingestion Renal Tubular Acidosis Diarrhea Ureteral and ileal diversion Pancreatic fistulas (post-op)
Metabolic Alkalosis
Primary Disturbance is increased plasma HCO3-
Compensate by hypovenilating (limited ability)
Chloride responsive (urine Cl- due to high aldosterone –> increased H+ and K+ excretion.
- Cushings
- Hyperaldosteronism (Barters)
- Secondary hyperaldosteronism (CHR, CRF)
- Bicarb injestion
Respiratory Acidosis
Primary Disturbance is increase in arterial CO2 –> compensate by elevating HCO3- by metabolic mechanisms (acute and chronic)
Causes:
- Airway obstruction
- Lung - COPD, Asthma, PTX, ifx, etc.
- CNS - Sedative/hypnotics, drugs, tumor
- Neuromuscular weakness (ALS, quadrapalegia, guillan barre)
Respiratory Alkalosis
Primary disturbance is decrease in arterial CO2 –> compensate by decreasing HCO3- (acute and chornic components)
Causes:
- Anxiety
- Aspirin and other drugs: cocaine, progesterone (pregnancy = mild respiratory alkalosis)
- Any cause of tachypnea (sepsis, fever, PE, pneumonia, hypoxia
- Alcohol withdrawal or narcotic withdrawal
- Many others
