Week 2 Review Flashcards
Which one of the following is a feature of nephrogenic diabetes insipidus?
Increased solute intake increases urine volume (because of inappropriate kidney response to ADH and NOT aldosterone you dumb motherfucker!!! Nephrogenic diabetes insipidus = ADH PROBLEM AND NOT A FUCKING ALDOSTERONE PROBLEM
What is diabetes insipidus?
A polyuric condition due to a failure to concentrate the urine
Can be due to a defect of VASOPRESSIN release = central DI
-should respond normally to exogenous vasopressin
Can be due to defect of collecting duct in vasopressin response = nephrogenic DI
-cannot respond normally to exogenous vasopressin
Small cell lung cancer
SIADH (syndrome of inappropriate ADH)
Secretes excessive ADH
SIADH
Small cell lung cancer
Leads to hyponatremia because too much water
Aka anti-diuresis
What can also induce excessive ADH release?
- SSRIs
- Pain
- Nausea
- Stress
What are example of edematous water disorders?
- CHF
- Liver disease
- Cirrhosis/ascites
- Nephrotic syndrome
Patients will have
High AVP, low GFR, decreased EABV and may have ongoing water intake
Which one of the following regarding urine dilution is correct?
A. Urine osmolarity at the end of DCT is typically ~300 mOsm/L
-wrong because osmolarity should be hypotonic 100-200 mOsm in DCT (asked twice)
-only time when it is 300 mOsm is at hairpin loop or collecting duct
B. Hyperkalemia increases electrolyte free water excretion
C. In the absence of ADH, the concentration of sodium in tubule lumen increases between DCT and terminal medullary CD
D. Thiazide diuretics impair ability to excrete electrolyte free water
Thiazide diuretics impair ability to excrete electrolyte free water
- because without a thiazide, sodium/Cl would be absorbed which means you can excrete electrolyte free water - but if you impair this ability, you will be excreting those above mentioned electrolytes into the water
What are we supposed to do in order to treat hyponatremic patient?
Excrete a DILUTE urine
So what are areas of kidney that can dilute the urine?
1. make sure you have isotonic ultrafiltrate
2. make sure to deliver filtrate from PT to diluting segments (DCT)
3. Diluting urine is made in DCT
4. need to suppress AVP to make sure you have dilute urine
Which one of the following is most effective in maintaining normal internal K balance?
Insulin
But why not blood pH?
-doesn’t have a consistent effect on potassium
-theoretically it has big effect but physiologically, blood pH affects so many other things that it does not consistently contribute to internal K balance
What are factors affecting internal K balance?
- plasma K concentration
- Insulin
- Catecholamines
- Aldosterone
What are factors affecting distal nephron K secretion?
- K intake and plasma K concentration
- Aldosterone
- Distal tubule Na delivery and flow
- Anions in tubular fluid
What are the three causes of hyperkalemia?
- too much in (impossible to sustain…must be transient if other factors not playing in)
- too little out
- internal shift from ICF to ECF
What are the three causes of hypokalemia?
- Too little in
- Too much out (impossible to sustain alone…must be transient if other factors not playing in)
- Internal shift from ECF to ICF
What is the emergency treatment of acute hyperkalemia?
1. treat cardiac effects (calcium) Example: calcium gluconate 2. move K from ECF into cells Example: insulin 3. Remove K from the body Example: kayexalate
Acidemia is which one of the following?
Blood pH of 7.23
How does urine excrete H+?
40 mmole of NH4+
30 mmole of Titratable acids
70 mmole of H+ per day
Titratable acid = phosphate
Why do you get tetany or muscle weakness when patient is hyperventilating?
Because patient is hypocalcemic
This is because hyperventilating causes respiratory alkalosis
Alkalosis leads to more calcium binding to albumin
This leads to a calcium deficiency
Thus treatment is stop patient from breathing so fast (smother with pillow LOL)
How do we generate bicarb?
- in proximal tubule in ammonia genesis
- every NH4+ that is made leads to 2 bicarb in blood
- alpha-intercalated cell = secretion of H+ into lumen and reabsorption of bicarb into the gut
What is anion gap?
Difference between Unmeasured anions – Unmeasured cations
Only the anions usually change
What is post-hypercapneic metabolic alkalosis?
High CO2 = bicarb is retained to compensate
If you put someone with hypercapnea on ventilator, you may get post-hypercapneic metabolic alkalosis because there still are a lot of bicarb left in body
What is the most common cause of metabolic alkalosis?
GI tract loss of H+
What sustains the maintenance phase of metabolic alkalosis?
- hyperaldosteronism
- Cl- depletion (because less Cl intracellularly means upregulation of basolateral Cl/bicarb antiport)
- Defect in bicarb secretion in beta intercalated cells
- K depletion
- upregulates H/K antiport on apical membrane of alpha inter-calated cells
- stimulates Na-H and basolateral Na/bicarb exchange in PT (so that more bicarb is reabsorbed)
- also stimulates NH3 synthesis, which as you should know, generates 2 mol of bicarb for reabsorption
Thus, given the factors that sustain metabolic alkalosis, how should you treat?
Reduction of aldosterone Intracellular repletion of Cl Intracellular repletion of K Correction of bicarb secretion in beta intercalated cells Reduce GI losses/diuretic induced losses Treat underlying disorder
Which of the following best describes this acid-base situation
pH 7.46, pCO2 26 mmHg, bicarb = 18 mmol/L
Na = 137, K = 3.8, Cl = 91, bicarb = 21, urea = 38, Cr = 1.4
Metabolic acidosis + respiratory alkalosis + high anion gap
Anion Gap = 137 – 91 – 21 = 25
What is the system for acid-base problems?
Anion gap calculation first!
Then look at pCO2 and bicarb to see what is abnormal. Then calculate expected compensation
