Renal Flashcards
Pronephros vs. Mesonephros vs. Metanephros
1st: Pronephros = to wk 4, then degenerates
2nd : Mesonephros = 1st trimester. => adult Male genital system
*“ureteric bud” (caudal end) => ureters, pelvises, calices, collecting ducts
3rd: Metanephros = permanent, => adult kidney
Fetus w/ oligohydramnios (can’t pee)
=> consecuences, causes
= “Potter Sequence”
Causes: ARPKD, posterior urethral valves, bilat. renal agenesis
Consequences: Limb and facial deformities, pulmonary hypOplasia (= cause of death)
1 site of obstruction of urinary tract in fetus
= Ureteropelvic junction,
* Last to canalize => failure -> hydronephrosis
Renin-Ang-Aldosterone signal molecs & actions
- Renin (from JG cells in kidney) -> Angiotensinogen to Angiotensin I
- Ang I –> Ang II via ACE (Angiotensin Converting Enzyme)
- Ang II => systemic effects:
a) vasoconstrict (AT1 Rs), b) constrict eff. arterioles
c) stimulate aldosterone & ADH, d) increase Na/K exchange in PCT
e) stimulate thirst @ hypothalamus
signal molecs that respond to low blood volume:
- Angiotensin II
- ADH (=> insert aquaporins in renal collecting duct to retain H2O)
- Aldosterone (=> insert more Na+ channels in principle cell to retain Na & H2O, & increase K+ excretion “BK” channels)
* ANP responds to HIGH volume in heart atria => regulates RAAS*
components of Juxtaglomerular Apparatus
- JG cells: modified sm. muscle on aff. arteriole => secrete renin
(when low NaCl delivery to DCT, low renal BP, or B1 stim.) - Macula Densa: on distal conv. tubule, sense low NaCl
Effect of ANP on kidney
(secreted from atria of heart when HIGH pressure/volume)
increase GFR & Na filtration @ distal tubule
=> Na+ & volume loss
(opposes Renin/Ang/Aldosterone)
Effect of PTH on kidney
secreted when:
low plasma [Ca2+], high plasma [PO4—], or low 1,25-(OH)2 VitD
=> decrease PO4 resorption (PCT), increase Ca resorption at DCT, and increase 1,25-OH2 vitD activation
Angiotensin II vs. ANP
BOTH increase GFR, but
ANP: no compensatory Na resorption => net volume loss
Ang II: w/ compensatory Na resorption => net maintenance of renal BF (& NO volume loss)
Electrolyte changes associated with Aldosterone activity
bc aldosterone increases Na resorption at collecting duct,
=> increased K+ and H+ excretion
(may become hypoKalemic or alkalotic)
Causes of K+ shift OUT of CELL
- Digitalis ==> hypERkalemia
- hyperOsmolarity
- Insulin deficiency
- Lysis of cells
- Acidosis
- Beta-adrenergic antagonist
Causes of K+ shift INto CELL
==> hypOkalemia
- hypO-osmolarity
- Insulin presence (increases Na/K ATPase)
- Alkalosis
- Beta-adrenergic AGonist (also increases Na/K ATPase)
Signs/symptoms of Na+ imbalance (High or Low)
Both: stupor/coma
High Na+: irritability
Low Na+: nausea, malaise
Signs/Symptoms of K+ imbalance (High or Low)
Both: arrhythmias, mm weakness
High K+: Wide QRS complex & peaked T waves
Low K+: U waves on ECG & flattened T waves
Signs/Symptoms of Ca2+ imbalance (High or Low)
High Ca2+: “stones, bones (pain), groans (abdom. pain), & psychiatric overtones” (anxiety, altered mental status)
Low Ca2+: tetany, seizures
Signs/Symptoms of Mg2+ imbalance (High or Low)
High Mg2+: decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa2+
Low: tetany, arrhythmias
Signs/Symptoms of PO4(3-) imbalance (High or Low)
High: kidney stones, metastatic calcifications, hypoCa2+
Low: bone loss, osteomalacia
Calculation for Anion Gap
Anion gap = Na+ - (Cl- + HCO3-)
- normal = 8-12
Calculation for respiratory compensation in metabolic acidosis
PaCO2 = 1.5([HCO3-]) + 8 +/-2
- if PCO2 is:
a) MORE than predicted, = COMBINED met. acidosis & resp. acidosis
b) LESS than predicted, = MIXED met. acidosis & resp. ALKalosis
3 types of RTA (Renal Tubular Acidosis 1, 2, & 4)
(normal anion gap metabolic acidosis)
Type 1: “distal” = can’t excrete H+ => urine pH >5.5, hypoK+
Type 2: “proximal” = can’t reabsorb HCO3- => urine pH poor NH3 synth => poor buffer ability, very acidic urine.
Type 1 RTA
“Distal” = can’t excrete H+
=> urine pH >5.5, hypoK+
*Assoc. w/ Sjogrens & Amphotericin B
Type 2 RTA
“Proximal” = can’t reabsorb HCO3-
=> urine pH s anemia, mult. myeloma, carb.anhydrase Is
Type 4 RTA
“HyperK+” = hypoAldo or no response to aldosterone
=> poor NH3 synth. = poor buffer ability, very acidic urine.
*assoc. w/ Diabetes, adrenal insuff., ACE Is
Kidney stones that occur in ACIDIC environment:
vs. alkaline
LOW pH (acidic) #1: Calcium oxalate, 2. uric acid, 3. cysteine (hexagonal)
Basic (high pH):
Ca-phosphate, Struvite (NH3-Mg-PO4, *from urease+ bacteria)
