Renal physiology session 2 Flashcards
Size of molecules that can be filtered through glomerulus
Molecules less than 20 angstroms are freely filtered
More than 42 angstroms are not filtered
How does damage to the glomerular glycocalyx increase susceptibility to proteinuria
Glycocalyx covering on the glomerulus endothelium creates a barrier of negative charges that disrupt a proteins ability to diffuse across it
When the barrier is destroyed, more proteins and larger proteins are able to move across
Urinary excretion equation
Amount filtered - amount reabsorbed + amount secreted
Tubular reabsorption equation
Glomerular filtration - urinary excretion+amount secreted
Filtration fraction
Usually about 20% of RPF
FF=GFR/RPF
GFR is directly proportional to renal clearance if
Substance must be freely filterable in the glomeruli
Substance must be neither reabsorbed nor secreted by the renal tubules
Substance must not be synthesized, broken down or accumulated by the kidney
Substance must be physiologically inert
Examples of substances that meet the requirements for GFR=Renal clearance
Inulin - freely filtered, neither reabsorbed nor secreted
GFR= (Uinulin)(V)/P(inulin)
Creatinine is the same way (except about 10% of the creatinine in urine is secreted)
Sympathetic effect on arterioles, JG cells and tubular epithelial cells
Vasoconstriction (mostly afferent arteriole) via a1 adrenergic receptors
Renin release from JG cells via B1 adrenergic receptors
Na-K ATPase increased activity (increased reabsorption of Na) via a1 adrenergic receptors
Know the receptors
Ultrafiltration coefficient equation
Kf = Hydraulic conductivity (permeability of endothelium) X Surface area
GFR equation using Kf
GFR = Kf x Puf (capillary ultrafiltration pressure)
Capillary ultrafiltration pressure equation
Add/subtract glomerular/bowmans capsule forces
Acidosis/alkalosis pH levels
Acidosis- less than 7.35
Alkalosis- greater than 7.45
Arterial HCO3 level
24
Increases in HCO3 will increase pH
Arterial CO2 level
40
Increased CO2 decreases pH
Factors increasing H+ secretion
Primary: Decrease in plasma HCO3 (decreased pH) Increase in partial pressure of arterial CO2 Secondary: Increase in filtered load of HCO3 Decrease in ECF volume Increase in angiotensin II Increase in aldosterone Hypokalemia
Factors decreasing H+ secretion
Primary: Increase in plasma HCO3 Decrease in partial pressure of arterial CO2 Secondary: Decrease in filtered load of HCO3 Increase in ECF volume Decrease in aldosterone Hyperkalemia
What are the main molecules that buffer the H+ from bicarbonate in the urine
NH3 and PO4-
a-intercalated vs b-intercalated cells
a-intercalated cells secrete H+ and reabsorb HCO3
b-intercalated cells reabsorb H+ and secrete HCO3-
Net acid excretion equation
NAE= [(Urine NH x V) + (Urine TA(PO salts) x V) - (Urine HCO3 x V)]
Renal tubular acidosis type I
Impaired distal collecting duct H+ secretion Very low bicarbonate <15 or usually <10 Urine pH greater than 5.5 Severe acidosis Plasma K+ usually low Caused by autoimmune disorders
Renal tubular acidosis type II
Impaired proximal HCO3 reabsorption
Plasma HPO3 12-20
Low plasma K+
Caused by Fanconi syndrome, multiple myeloma, drugs
Renal tubular acidosis type IV
Lack of aldosterone or failure of kidney to respond to it
HCO3 >17
High plasma K+
Caused by drugs
High serum anion gap means
Anion gap greater than ~16
There are other solutes in plasma (alcohols, lactic acidosis, ketoacidosis)
Osmolal gaps
Should be 0
If greater than 0 it is due to unmeasured osmotic particles such as NH4
If less than 75 it could be renal tubular acidosis
If 200-300 it could be chronic severe metabolic acidosis
Urine anion gap
Becomes negative in metabolic acidosis due to HCO3 loss in diarrhea since excretion of unmeasured NH4+ increases significantly during generation of new bicarbonate
In renal tubular acidosis, NH4 excretion is decreased due to the inability to generate new bicarbonate, so value can remain positive despite acidosis
Causes of respiratory acidosis (acute)
CANS CNS depression (opioids) Airway obstruction Neuromuscular disorders Severe pneumonia, embolism, edema
Causes of chronic respiratory acidosis
COPD
Anything chronic leading to impaired ventilation
Normal adjustments in HCO3 after increases in CO2 in acute vs chronic
pCO2 increases by 10, HCO3 should increase by 1 (acute) or 3.5 (chronic)
pCO2 decreases by 10, HCO3 should decrease by 2 (acute) or 5 (chronic)
Causes of acute respiratory alkalosis
CHAMPS CNS disease- hyperventilation Hypoxia Anxiety Mechanical ventilators Progesterone Salicylates/sepsis
Carpopedal spasm
Can be caused by respiratory alkalosis due to hypocalcemia from Ca being driven into cells in exchange for H+
Compensation vs correction of metabolic acidosis
Compensation is respiratory- hyperventilation to decrease CO2
Correction is increasing bicarbonate regeneration in the kidney
HAGMA causes
GOLDMARK Glycols Oxoproline (from acetaminophen toxicity) L-lactate D-lactate Methanol Aspirin Renal failure Ketoacidosis
NAGMA causes
HARDUPS Hyperalimentation Acetazolamide Renal tubular acidosis* Diarrhea* Uretosigmoid fistula (colon wastes HCO3) Posthypocapnea Spironolactone
Determining what PaCO2 should be, given HCO3
PaCO2 = 1.5 x [(HCO3) + (8+/-2)]
If PaCO2 is not the expected number, it is a mixed acid base disorder
Metabolic alkalosis causes
CLEVER PD Contraction Licorice Endocrine (Conn, cushing syndrome) Vomiting Excess alkali Refeeding alkalosis (eating after long starvation) Post-hypercapnia Diuretics
Chloride responsive vs resistant metabolic alkalosis
Chloride responsive: vomiting, diuretics, diarrhea
Spot urine Cl should be less than 10 since kidney should be conserving chloride
Treat with saline
Chloride resistant: Hyperaldosteronism resulting in increased H and K excretion in exchange for reabsorption of Na
Spot urine Cl greater than 20 despite fact kidney should be conserving Cl
Need to treat cause of H+ loss to treat
