Renal Flashcards
What is the percentage of the body that is water? What may change this?
60% (42L) Percentage may vary if obese (b/c fat doesn’t have H2O)
What is the major extracellular cation?
Na
What is the major extracellular anion?
Cl (followed by HCO3)
What is the major intracellular cation?
Potassium
What is the major intracellular anion?
Phosphate
How much of total body H20 is found intracellularly vs. extracellularly? What is the breakdown within the different extracellular compartments?
Total body water - 42L Intracellularly - 60% total body water (24L) Extracellularly - 40% total body water (16L) - Interstitial Space - 28% of extracellular water (11.2L) - Plasma Space - 8% of extracellular water (3.2L) - Transcellular Space - 4% of extracellular water (1.6L)
How much of total body H20 is found intracellularly vs. extracellularly? What is the breakdown within the different extracellular compartments?
Total body water - 42L Intracellularly - 60% total body water (24L) Extracellularly - 40% total body water (16L) - Interstitial Space - 28% of extracellular water (11.2L) - Plasma Space - 8% of extracellular water (3.2L) - Transcellular Space - 4% of extracellular water (1.6L)
What is the pneumonic for retroperitoneal structures?
Suprarenal glands (adrenal glands) Aorta & IVC Duodenum (2-4 segments) Pancreas (all except tail) Ureters Colon (ascending and descending) Kidneys Esophagus (distal 2/3 or thoracic portion) Rectum
Kidneys are found at what level?
Between T12-L13
Which kidney is lower?
Right slightly lower b/c of liver above it.
Which kidney has a longer renal vein?
Left kidney b/c IVC is on the right side of the body, so has a longer path to travel.
Which kidney is most often used for living donor transplant and why?
Left kidney because the renal vein is longer.
What is the difference between the R & L gonadal veins in terms of drainage paths and what pathology can this difference lead to?
Right gonadal vein goes directly into IVC, but Left gonadal veins drains into left renal vein (which then drains into the IVC) B/c of this + angles and length of renal vein, pressure can build up and back into the gonadal vein which can cause testicular varicoceles. Bottom line: Testicular varicoceles are more common on the left than the right.
What is the path of the renal veins in relation to the aorta and renal arteries?
The renal veins pass in front of the aorta and renal arteries
Renal arteries branch from the aorta at what level?
Between L1 and L2 (just after SMA)
What is a varicocele?
A varicocele is an enlargement of the panpiniform plexus (small network of veins) found in the spermatic cord in the scrotum. It can be very painful and can decrease fertility.
What is the pathway of arterial blood from the aorta to the nephron?
aorta –> renal a. –> segmental a. –> lobar a. –> interlobar a. –> arcuate a. –> interlobular a. –> afferent a. –> glomerular capillaries! Real
What is the pathway of arterial blood from the aorta to the nephron?
aorta –> renal a. –> segmental a. –> lobar a. –> interlobar a. –> arcuate a. –> interlobular a. –> afferent a. –> glomerular capillaries! Mneumonic: All Real Sports Lovers Interests Are Interesting Always, Geez
What is the pathway of arterial blood from the aorta to the nephron?
aorta –> renal a. –> segmental a. –> lobar a. –> interlobar a. –> arcuate a. –> interlobular a. –> afferent a. –> glomerular capillaries! Mneumonic: All Real Sports Lovers Interests Are Interesting Always, Geez
Ureters pass under or over the uterine artery and ductus deferens?
Ureters pass UNDER the uterine artery and ductus deferens. Remember: “Water (ureters) under the bridge (urterine artery & vas deferens)
What can be damaged during gynecologic procedures involving ligation of uterine vessels?
The ureters may be damaged because they pass beneath the uterine vessels –> ureteral obstruction or leak. Think: ureter damage, post renal azotemia, hydronephrosis.
What is the arterial supply of the ureters?
Upper 1/3 - renal a. Mid 1/3 - gonadal + common iliac a. Distal 1/3 - internal iliac a.
Renin is released by what type of cells?
Juxtaglomerular cells (modified smooth muscle cells located in tunica media of afferent a.)
Renin is released by what type of cells?
Juxtaglomerular cells (modified smooth muscle cells located in tunica media of afferent a.)
What does renin do? What is stimulated by?
Renin helps convert angiotensin to angiotensin II to help increase BP. Stimulated by: 1) dec. in BP, 2) dec. Na levels, 3) inc. sympathetic tone
What comprises the renal corpuscle?
Glomerulas and Bowman’s space/capsule. It is the initial blood filtering component.
Kidneys send sensory input at what level? This means you can elicit that pain at what anatomical area?
Kidneys send sensory input at T10 & T11. You can elicit this pain at the costovertebral angle.
Ureters pass under or over the uterine artery and ductus deferens?
Ureters pass UNDER the uterine artery (female) and ductus deferens (male) [aka gonadal vessels]. Remember: “Water (ureters) under the bridge (urterine artery & vas deferens)
How much of total body H20 is found intracellularly vs. extracellularly? What is the breakdown within the different extracellular compartments?
Total body water - 42L Intracellularly - 60% total body water (24L) Extracellularly - 40% total body water (16L) - Interstitial Space - 28% of extracellular water (11.2L) - Plasma Space - 8% of extracellular water (3.2L) - Transcellular Space - 4% of extracellular water (1.6L)
Kidneys send sensory input at what level? This means you can elicit that pain at what anatomical area?
Kidneys send sensory input at T10 & T11. You can elicit this pain at the costovertebral angle.
What comprises the renal tubule?
Renal tubule - system that filters the filtrate (produced by renal corpuscle) = all the ducts and tubules post bowman’s space (proximal convoluted T, loop of Henle (descending + ascending), distal convoluted tubule, collecting duct (coritcal and medullary)).
List the path of the nephron.
Glomerulas Bowman’s Space/Capsule Proximal convoluted tubule Proximal straight tubule Descending portion of the loop of Henle Thin ascending portion of the loop of Henle Thick ascending portion of the loop of Henle Distal convoluted tubule Cortical collecting duct Medullary collecting duct
What sections of the nephron are in the renal cortex?
Glomeruli, Bowman’s capsule, convoluted tubules (proximal + distal), cortical collecting ducts
What section of the nephron are in the renal medulla?
Proximal straight tubule, loop of Henle, medullary collecting ducts
How much of total body H20 is found intracellularly vs. extracellularly? What is the breakdown within the different extracellular compartments?
Total body water - 42L Intracellularly - 60% total body water (24L) or 40% of total body mass Extracellularly - 40% total body water (16L) or 20% of total body mass - Interstitial Space - 28% of TBW (11.2L) or ~70% ECF - Plasma Space - 8% of TBW (3.2L) or ~ 20% ECF - Transcellular Space - 4% of TBW (1.6L) or ~10%ECF Note: First aid just talks about intersititial space and plasma (75% and 25% of ECF)
What section of the nephron are in the renal medulla?
Proximal straight tubule, loop of Henle, medullary collecting ducts
What is total body mass of an average person?
~70kg
What is the total body water in percentage, liters and weight?
TBW is 60% of body mass = ~42L = 42kg
What is the major extracellular cation?
Na Think “Banana floating in the open sea” - potassium intercellular cation, sodium extracellular cation
What is the major extracellular anion?
Cl, followed by HCO3 (used as an extracellular buffer system and as a transporter of CO2)
What is the major intracellular cation?
Potassium Think “Banana floating in the open sea” - potassium intercellular cation, sodium extracellular cation
What is the major intracellular anion?
Phosphates + Protein Maj of protein and ATP INSIDE cell
What is the total body water in percentage, liters and weight?
TBW is 60% of body mass = ~42L = 42kg
What is the extracellular and intracellular osmolarity?
Both are about 290mmOsm
When a cell is at rest is there movement of water?
No because at rest the osmolarity is about equal extracellularly and intracellularly.
When a cell is at rest is there movement of water?
No because at rest the osmolarity is about equal extracellularly and intracellularly.
Of the total body mass what percentage is TBW, ICF, and ECF?
60% TBW 40% ICF 20% ECF Remember this is of the total body mass
Of the total body mass what percentage is TBW, ICF, and ECF?
60% TBW 40% ICF 20% ECF Remember this is of the total body mass
1.38 ml/min
Answer: Higher
During shock, patients’ BP will be low –> dec renal plasma flow –> increase filtration fraction (FF = GFR/RPF).
Dec. renal plasma flow also causes the kidney to selectively dialate the Afferent a. and constrict the Efferent a. which will increase the GFR (b/c inc hydrostatic gradient [inc.Pgs]
–> increase FF.
ACE Inhibitors
With the prevention of Angiotensin II –> more Na will be lost in urine –> more water diuresis
No Angio II –> no stimulus for aldosterone release –> dec. in BP and inc. sodium and water loss.
The glomerulas has aa basement membrane fused with what?
The glomerulas’ basement membrane is fused with heparin sulfate which acts as a charge barrier for negatively charged particles causing them not to be filtered
In nephrotic syndrome this charge barrier is lost.
Podocytes stop what from entering bowman’s space?
Proteins and solutes.
What are some freely filtered solutes and why?
AA, glucose, electrolytes
B/c thy are th same size as the waste products (urea, creatanine, etc.)
Why do we adjust certain drug amounts in the elderly (think kidneys)?
As age increases kidney function decreases. Thus, renally cleared drugs will not be cleared as well in the elderly (higher plasma conc.) so we should lower doses.
In the Starling equation which items encourage plasma be filtered INTO bowman’s space?
hydrostatic pressure of the glomerulas (Pgc) and oncotic pressure in bowman’s space (πbs)
This makes sense b/c hysrostatic pressure pushes fluid out (so Pgc pushes fluid OUT of glomerulas) and oncotic pressure tries to keep fluid in (so πbs would try to keep fluid IN bowman’s space)
Remember: Net fluid movement between compartments = Kf[(Pgc - Pbs) - (πgc - πbs)]
What relation does the filtration coefficient (Kf) have to GFR and resistance?
Kf and GFR are proportional – the higher the Kf, the higher the GFR
Kf and resistance are inversely proportional – higher Kf, the lower the resistance
In the Starling forces equation, which items inhibit plasma being filtered? What does this do to GFR?
hydrostatic pressure of bowman’s space (Pbs) and oncotic pressure in glomerulas (πgc)
This makes sense b/c hysrostatic pressure pushes fluid out (so Pbs pushes fluid OUT of bowman’s space keeping it in glomerulas unfiltered) and oncotic pressure tries to keep fluid in (so πgc would try to keep fluid IN the glomerulas)
Remember: Net fluid movement between compartments = Kf[(Pgc - Pbs) - (πgc - πbs)]
What is the glomerular filtration rate?
GFR = the amount of plasma filtered through the glomerulas/minute.
When comparing renal clearance of a substance (Cx) to GFR when do you see reabsorption? Secretion? Or no net reabsorbtion or secretion?
Cx < GFR = reabsorption
Cx > GFR = nephron secretion (this would be downstream of the glomerulas b/c that is the only way a substance can enter the filtrate once filtration has occured)
C= GFR = no net reabsorbtion or secretion
Filtered load = ?
Excreted Rate = ?
Filtered load (mg/min) = GFR (mL/min) x Plasma conc(mg/mL)
Excreation Rate = urine flow rate x urine conc. of substance
Reabsorption =?
Secretion = ?
Reabsorption = filtered load - exreated rate
Secretion = excreted rate - filtered load
Remember: FL = GFR x Px
ER = V x Ux
Based on filtered load and excreation rate how can you tell whether something is being reabsorbed or secreted by/into the tubules?
FL > ER = substance is being reabsorbed by tubules
FL < ER = nephron is secreting substance into tubules
If you have constant kidney stones and need to be diuresed what diuretic do we NOT use?
Furosemide b/c it promotes Ca excretion by kidneys which could lead to more kidney stones.
Remember: Furosemide works as a diuretic by inhibiting the NKCC co transporter. Thus more ions in lumen and water will follow –> excretion of more fluid.
In the Thick Ascending loop of Henle how are Mg and Ca reabsorbed?
Paracellularly (between cells; no transporter)
K+ leak channels create the gradient that allows this to happen.
What hormone opposes PTH? Where is secreted from? What does it do? What malignancy releases this hormone?
Calcitonin.
Secreted from parafollicular C cells in the thyroid.
Decreases serum calcium levels.
Note: Medullary thyroid carcinoma releases calcitonin.
Insulin shift potassium into or out of the cells?
Insulin shifts potassium INTO the cells.
Adrenergic stimulations causes what to happen to potassium?
Adrenergic stimulation causes inc. in Na/K ATPase work –> K+ is shifted INTO the cells –> DEC. Serum K+
What stimulates potassium shift INTO cells?
Insulin
Adrenergic stimulation
Hypo-osmolarity (K+ will follow water into cells to maintain proper acid-base balance)
Alkalosis (inc. H/K exchanger)
What drug causes potassium to be shifted out of the cell? What is the mechanism?
Digatalis
B/c block Na/K ATPase –> high conc of K will build up outside of cells.
What is a normal anion gap?
8-12 mEq/L
anion gap formula?
anion gap = [Na] - ([Cl] + [HCO3])
What are some causes of high anion gap?
MUDPILES
Methanol –> formic acid
Uremia
Diabetic Ketoacidosis
Propelyne glycol
Iron tablets or Isoniazid
Lactic Acid
Ethylene Glycol –> oxalic acid
Salicylates
What are causes of metabolic acidosis with a normal anion gap (8-12mEq/L)?
HARDASS
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea (b/c Na + HCO3 are being lost in stool –> dec. HCO3 –> acidoisis)
Acetazolamide (carbonic anyhydrase inhibitor)
Spironolactone (aldosterone antagonist)
Saline infusion
What are some causes of respiratory alkalosis?
Overall hyperventilation
Causes include:
Hysteria
Hypoxemia (ie high altitude)
Salicylates (b/c inc. respiratory drive)
Tumor
PE
What is metabolic alkalosis associated with?
Associated with dehydration –> contraction alkalosis
Normally hydrated person can excrete bicarb, but dehydrated –> inc. plasma bicarb in a setting of volume contraction –> contraction alkalosis
What are some causes of metabolic alkalosis?
Vomiting (loss of HCL)
Hyperaldosteronism (inc H secretion in collecting tubule)
Antacid use (inc. H secretion)
Loop/thiazide diuretics (inc. H secretion)
What are some causes of respiratory acidosis?
Overall: Hypoventilation
Airway obstruction
Acute lung disease
Chronic lung disease
Opiods, sedatives (decrease respiratory drive)
Weakening of respiratory muscles
What are ways to treat with methanol overdose?
Ethanol treatment - competitive inhibitor
Hemodialysis
Fomepizole - inhibits alcohol dehydrogenase
What is type 1 of renal tubular acidosis?
Type 1 = “distal RTA”
Defect in ability of α intercalated cells in collecting tubule to secrete H+ –> no new HCO3 is generated –> metabolic acidosis. Urine pH = > 5.5
Associated with hypokalemia (b/c less H+ secreted so more K+ secrete to balance neg charged lumen).
Inc. risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover [ie more Ca]).
Causes: amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract.
What is type 2 renal tubular acidosis?
Type 2 = “proximal RTA”
Defect in PCT HCO3 reabsorption (alpha intercalated cells are normal) –> excretion of HCO3 in urine and subsequent metabolic acidosis.
Urine is acidified by α -intercalated cells in collecting tubule –> increased urine pH trying to balance all the HCO3 lost –> Urine pH <5.5.
Associated with hypokalemia, increased risk for hypophosphatemic rickets.
Causes: Fanconi syndrome, carbonic anhydrase inhibitors, and proximal tubular toxins such as lead or amino-glycosides,.
What is type 4 renal tubular acidosis?
Type 4 RTA = “hyPERkalemia RTA”
Hypoaldosteronism (or inability of collecting tubules to respond to aldosterone) –> reduced K and H+ secretion –> hyperkalemia –> dec. NH3 synthesis in PCT –> dec. NH4+ excretion (dec. urine pH).
SEEN MOST COMMONLY WITH DIABETIC NEPHROPATHY
Causes: Dec. aldosterone production (e.g., diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insuffi ciency) or aldosterone resistance (e.g., K+ -sparing diuretics, nephropathy due to obstruction, TMP/SMX).
Answer: C - Iron supplement
Why?
pH is low (7.28) = acidosis
HCO3 is low (19) = metabolic acidosis
Anion gap is high = look for MUDPILES option
Remember: Anion gap = ([Na] - ([Cl] + [HCO3]) = (143 - (103 +19) = 19 <– higher than 8-12mEq/L
What is the mneumonic and the disease that can cause nephritic syndrome?
RAPID M
Rapid Progressive Glomerularnephritis
Alport Syndrome
Post Streptococcal Glomerulonephritis
IgA Nephropathy
Diffuse proliferative glomerularnephritis
Membranoproliferative glomerularnephritis
Does treating a patient with acute post-streptococcal glomerulonephritis with antibiotics work?
No, because it is immune complex deposition along the basement membrane from a hypersensitivity type III.
What is the hypersensitivity reaction type III occur between in acute post-streptococcal glomerulonephritis?
Immune complexes formed between the patient’s antibodies and the bacterial antigens.
Note: Inc. anti-DNase B titers and dec. complement levels
What are the components of crescents? Name at least one disease with crescents.
Crescents are comprised of:
1) Fibrin, 2) Macrophages, 3) Plasma Protein, 4) Monocytes, 5) Glomerular parietal cells
What are some causes of Rapidly Progressive Glomerulonephritis?
1) Goodpasture’s syndrome (type II hypersensitivity) - hematuria + hemoptysis
2) Wegner’s syndrome or Granumalotosis with polyangiitis (c-ANCA)
3) Microscopic polyangiitis (p-ANCA)
What are Henoch Schloen Pupura? When is it found? What are the symptoms?
HSP - Systemic deposition of immune complexes
Seen with IgA nephropathy
Classic triad: Small vessel vasculitis with palpable purpura, arthritis, and abdominal pain
Describe Alport Syndrome.
X-linked mutation in type IV collagen –> splitting of glomerular basement membrane (which is made of type IV collagen) –> deafness, eye problems, and glomerulonephritis
Describe the 2 type of membranoproliferative glomerularnephritis.
Type 1
- subendothelial immune complex deposits
- granular deposits on IF
- Tram track appearance best seen on PAS stain
- Seen with Hep C >> Hep B, sometime idiopathic
Type 2
- intramembranous immune complex deposits or “dense deposits”
- C3 nephritic factor that stabilizes C3 convertase causing a dec. in serum C3 levels
Why is there a greater risk for thrombotic events and infxn’s with nephrotic syndromes?
B/c you’re urinating out antithrombin III and immunoglobulins
What is minimal change nephrotic syndrome triggered by?
1) Recent Infx
2) Immunization
3) Immune stimulus
4) Hodgkin’s lymphoma
What are the antibodies found in some patients with membraneous nephropathy?
Antibodies to phospholipase A2 receptor (Anti-PLA2R)
What are some causes of Membranous Nephropathy?
1) Hep B >> Hep C
2) Drugs (NSAIDs, Penicillamine)
3) Lupus
4) Solid tumors (esp elderly)
Which nephrotic syndrome responds well to steroids? Which responds poorly to steroids?
Responds well: Minimal Change
Responds Poorly: Membranous Nephropathy
Amyloidosis is found using what stain? What will it look like?
Congo Red stain –> apple green birefringence
Amyloidosis in kidney is associated with?
Multiple Myeloma
Tuberculosis
Rheumatoid arthritis
Diabetes causes diabetic nephropathy how?
High blood glucose –> nonenzymatic glycosylation of BM and efferent arterioles (glucose molecules start binding to these areas) –> BM will thicken in response and mesangial matrix will expand
What is a kimmelsteil-wilson nodule? When is it seen?
Acellular ovoid nodules in periphery of glomerulas.
Seen with diabetic nephropathy.
Diabetic Nephropathy causes what effects on the GBM and Efferent arterioles?
GBM - thickening and inc. permeability (previously blocked things can now get through it - such as albumin)
Efferent arterioles - constriction of Efferent a. –> Inc. GFR (one of the reasons diabetic patients urinate so much)
What is the other reason? B/c glucose osmotically pulls water along with it into the tubules.
What test should be ordered to screen for early diabetic nephropathy
urine microalbumin - b/c albumin will start to leak out as BM is weakened
What type of medication should you put your diabetic patient on to protect their kidneys?
ACE inhibitors
Minimal change disease (nephrotic)
What is hydronephrosis?
Atrophy of the renal tissue due to compression by the urine that cannot flow out due to an obstruction such as a kidney stone (nephrolithiasis)
Calcium PHOSPHATE precipitates at a inc or dec pH?
Calcium OXALATE precipitate at a inc or dec pH?
Calcium phosphate precipitates at an inc. pH
Calcium oxalate precipitates at a dec. pH
Uric Acid stone
RadiolUscent
What chromosome has a deletion that is associated with an increased risk of developing renal cell cancer?
Deletion of the von Hippel Lindau tumo suppresor gene on chromosome 3 –> von Hippel Lindau Syndrome –> inc. risk of developing RCC
Renal cell carcinoma
Weight loss + hematuria –> think renal cancer
New flow murmur caused by inc. viscosity of blood b/c of inc. EPO production (causing polycythemia) –> think RCC
Remember: pts usually male 50-70s; inc. risk w/ smoking & obesity.
Answer is B
This is b/c it is a THIAZIDE, which is known to cause hyperGlycemia (remember HyperGLUC), metabolic alkalosis, and low urine calcium excretion.
Low urine calcium excretion indicates that it isn’t a loop diuretic (“Loops Loose Calcium”)
Note: In this question the potassium isn’t low (it actually appears high; 3.5 - 5 is a normal value) and thiazide are known for HYPOKalmic metabolic alkalosis, just chalk it up to first aid express being crummy sometimes.
