Nephrology Flashcards
parasympathetic = cholinergic (use acetylecholine) what effects?
constrict pupils, constrict bronchioles (inc secretions), decrease HR, dilate BV, increase GI mvmt and salivation, bladder contraction
kidney functions
regulate BP, volume, excrete waste, regulate solute conc (Na, K, Ca, Mg), regulate extracellular pH, erythropoietin, synthesize vit D
most active secretion (to be excreted) site in kidney?
distal convoluted tubule - uric acid, K, H, drugs, foreign substances, creatinine (from muscle activity), bile salts
most reabsorption (to keep) occurs where in kidney?
proximal tubule (reabsorb organic nutrients like glucose and a.acids, most bicarb, Na (75%), Cl, 75%-90% of H20
parathyroid hormone acts on kidneys where?
distal convoluted tubule to increase Ca reabsorption
aldosterone affects
inc aldosterone –> inc Na reabsorption (in exchange for inc secretion of K + H+) in collecting duct
hyperaldosteronism sx
hypoK and metabolic alkalosis
increased antidiuretic hormone (ADH) leads to?
production of concentrated urine when hypovolemia, hyperosmolarity and inc RAAS activation in collecting duct
aldosterone and ADH act where?
collecting duct
path through nephron
afferent art / efferent art –> glom in bowman’s –> proximal convoluted –> loop of henle (thin descend, thin ascend, thick ascend) –> distal convoluted –> collecting duct
minimal change disease
80% of nephrotic syndrome in children (20 adults)
- glomerular damage causes protein loss in urine
- associated w/ viral infx, allergies (insect, NSAIDS)
acute glomerulonephritis
immunologic inflam of glomeruli causing protein and RBC leakage in urine; often after URI, GI infx or GABHS
major differences btw nephrotic and nephritic syndrome
nephrotic - proteinuria >3.5g/day
nephritic - proteinuria and hematuria (+ immune mediated)
phases of AKI
- oliguric (maintenance phase) (dec output <400ml/d, azotemia, hyperK, metabolic acidosis
- diuretic phase (inc output, hypotension, hypoK)
- recovery
mc type of AKI
prerenal (result from hypovolemia, reduced perfusion)
prerenal AKI cause
reduced renal perfusion (hypovolemia) - nephrons intact (can lead to intrinsic if not corrected)
-can also be afferent constriction (NSAIDS, IV contrast) and efferent dilation (ACEI/ARB)
postrenal AKI cause
obstruction (ex. BPH)
intrinsic AKI basic cause
direct kidney damage - nephrotoxic, cytotoxic, prolonged ischemic, inflammatory insults
-cellular cast formation - hallmark of intrinsic
types of intrinsic AKI
- acute tubular necrosis (ATN) - MC
- acute tubulointerstitial nephritis (AIN)
- Glomerular (acute glomerulonephritis - AGN)
- Vascular
acute tubular necrosis (ATN)
acute destruction/necrosis of renal tubules of nephron
- ischemic - prolonged prerenal, hypoTN, hypovolemia
- nephrotoxic - AMINOGLYCOSIDES, contrast dye, meds, crystal precipitation (gout), myoglobinuria (rhabdo), lymphoma/leukemia, bence-jones (MM)
UA signs of acute tubular necrosis
- epithelial, muddy brown +/- waxy casts (formed in damaged tubules)
- low specific gravity (unable to concentrate urine due to damaged cells)
- hyperK, inc phosphatemia
acute tubulointerstitial nephritis (AIN)
inflammatory or allergic response in interstitium (spares glom and BV)
-MC drug hypersensitivity, then infections, autoimmune
causes of vascular AKI (intrinsic)
micro: TTP, HELLP syndrome, DIC
macro: aortic aneurysm, renal artery dissection, renal artery/vein thrombosis, malignant HTN
adult polycystic kidney disease
- autosomal dominant (genes PKD1 mc or PKD2)
- formation + enlargement of kidney cysts and cysts in other organs (LIVER, spleen, pancreas)
- vasopressin stimulates cystogenesis –> ESRD
extrarenal sx of adult polycystic kidney disease
- cerebral “berry” aneurysms
- hepatic cysts
- mitral valve prolapse
- colonic diverticula
HYPOphosphatemia causes/sx
-inc urinary PO4 excretion (primary hyperparathyroid, vitamin D deficiency)
-internal PO4 redistribution (insulin can shift PO4 intracellularly)
-decreased intestinal absorption (antacids)
SX: diffuse muscle weakness, flaccid paralysis (dec ATP)
HYPERphosphatemia causes/sx
-renal failure MC (dec Ca, inc Phos, inc iPTH)
-primary hypoparathyroid (dec Ca, inc Phos, inc iPTH)
-vitamin D intoxication (inc Ca, inc Phos, dec iPTH)
SX: soft tissue calcifications, heart block
chronic kidney disease sx:
- progressive fx decline >3 mo
- proteinuria
- abnormal urine sediment, serum/urine chemistries, imaging
- inability to buffer pH, make urine, excrete nitrogenous waste
- decreased synthesis vit D / erythropoietin
pt at risk for CKD
DM, HTN, chronic NSAID use, AA/Hisp/Asian, age >60, sLE, s/p kidney transplant, fam hx
CKD staging
Normal GFR 120-130
- kidney damage w/ normal GFR >90
- GFR 89-60
- GFR 59-30
- GFR 29-15
- GFR <15 ESRD - requires dialysis or transplant if <10 or sCR >8 (<15 and >6 for DM)
Albuminiruia
A1: ACR <30 mg/g
A2: ACR 30-300
A3: ACR >300
complications of CKD
- anemia of CD (tx w/ iron and erythropoietin if persists)
- coagulopathy (platelet dysfx –> petechiae)
- renal osteodystrophy (Ca/PO4 dysregulation)
- metabolic acidosis
syndrome of inappropriate ADH (SIADH)
non-physiological excess of inc ADH from pituitary or ectopic source –> free water retention and impaired water excretion –> hypoNa and inability of kidney to dilute urine
2 normal stimuli to increase ADH secretion
HYPOvolemia or HYPERosmolarity
etiologies for SIADH
CNS: stroke (SAH) MC, head trauma, meningitis, CNS tumors, post-op, HIV
Pulm: small cell lung cancer, infx/pneumonia
Drugs: narcotics, NSAIDs, anticonvulsants, carbamazepine, cyclophosphamide, SSRIs/TCA, hydroclorothiazide, ecstasy
Endo: hypothyroid, Conn syndrome
diabetes insipidus
-ADH/vasopressin deficiency MC (posterior pituitary)
- insensitivity to ADH (nephrogenic) –>inability of kidneys to concentrate urine –> produce large amounts of dilute urine
- hyperCa, hypoK
2 normal stimuli to increase Aldosterone release
HYPOvolemia and/or HYPERkalemia
low BP –> RAAS
hypovolemia (decrease arterial volume) causes juxtaglomerular cells in kidney to release renin, activating Renin-Angiotensin-Aldosterone System –> increased aldosterone promotes Na retention
ADH vs aldosterone
ADH determines water homeostasis
Aldosterone determines Na+ homeostasis
normal serum osmolality
285 - 295
abnormal serum Na concentration is due to problems with
water control (primarily by ADH) (i.e. dehydration --> decreased free water = increased serum [Na] = hypernatremia
abnormal extracellular fluid volume size is due to problems with…
total body Na control (determines ECFV)
ECFV = interstitial fluid vol and intravascular space vol
(i.e. hypervolemia = inc total body Na)
normal serum creatinine level
1.0
hypertonic hyponatremia
NOT true hyponatremia (not assoc w/ free water)
- dilutional drop in serum [Na] due to presence of osmotically active molecules (glucose or mannitol infusion)
- hyperosmotic causes water to shift from intracellular to extracellular space
isotonic hyponatremia
NOT true hyponatremia (free water normal)
-lab artifact/error due to hypertriglyceridemia or hyperproteinemia
hypotonic hyponatremia
TRUE hyponatremia
- kidney unable to excrete free water (make dilute urine, increased ADH)
- volume status gives clue to cause (hypovolemic, euvolemic, hypervolemic)
hypovolemic hyponatremia
- decreased volume (Na + water) and increased free water
- causes: renal volume loss (diuretics/thiazides), extrarenal volume loss like bleeding, D/V
euvolemic hyponatremia
- normal volume (Na + water) and increased free water
- SIADH, hypothyroidism, adrenal insufficiency, primary polydipsia (water intox), MDMA
hypervolemic hyponatremia
- increased volume (Na + water) AND increased free water
- edematous states: CHF, nephrotic syndrome, cirrhosis
hypernatremia
MC caused by net water loss
-CNS dysfunction (shrinkage of brain cells)
hypomagnesemia common causes
malabsorption (esp alcoholics)
renal losses (diuretics)
PPIs
hypomagnesemia symptoms
inc DTR tetany hypoCa (Mg needed to make parathyroid hormone) palpitations (due to associated hypoK) prolonged PR + QT interval TORSADES
hypokalemia common causes
diuretic therapy
V/D
metabolic alkalosis
hypomagnesemia
hypokalemia symptoms
muscle weakness / rhabdo nephrogenic - polyuria dec DTR palpitations, arrhythmias T-wave flattening (early) --> prominent U wave (+/- hypomagnesemia changes)
hyperkalemia causes
- decreased renal excretion, decreased aldosterone (adrenal insufficiency)
- ACEI/ARBs, digoxin, B-blockers, NSAIDs, K sparing diuretics
- metabolic acidosis (DKA)
MC side effect of hyperparathyroidism
kidney stones (due to excess Ca)
most common solid renal tumor of childhood
Nephroblastoma, or Wilms tumor
What drug must be withheld for 48 hours after the administration of a contrast agent? (Intravascular administration of iodinated contrast media)
metformin - can result in lactic acidosis
MC cause of AKI in children
Hemolytic-Uremic Syndrome (E. coli 0157:H7 - shiga-like toxin, strep. pneumo, drug toxicity)
Hemolytic-Uremic Syndrome Triad
hemolytic anemia (schistocytes)
thrombocytopenia
renal insufficiency
renovascular HTN (renal artery stenosis)
HTN due to renal artery stenosis (1 or both) –> inc RAAS
MC cause of secondary HTN
-suspect if HTN onset <20 or >50, HTN resistant to 3 drugs, abdominal bruit or if PT DEVO AKI AFTER INITIATION OF ACEI
-etiology: atherosclerosis mc in elderly, fibromuscular dysplasia mc women <50
