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Renal > Week 2 > Flashcards

Week 2 Flashcards

1
Q

initiating event of sustained increase in bicarb (metabolic alkalosis)

A
  • REQUIRES CHANGE IN RENAL BICARB HANDLING–NORMAL KIDNEY HAS IMMENSE CAPACITY TO EXCRETE HCO3
  • if levels increase (over 24 hrs) in a normal person, kidney will excrete
  • Two kinds of events: volume or chloride depletion (Vomiting or NG tube, diuretic therapy, rare tubular disorders mimicking diuretic therapy) and Volume expansion (Primary mineralocorticoid excess)
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2
Q

Acid-base balance upper GIT

A
  • stomach G cells secrete H+ into lumen
  • HCO3- also generated, secreted into blood (“alkaline tide”)
  • In pancreas, HCO3 generated, secreted into lumen to neutralize pH, while H+ is returned to blood (neutralizes with HCO3 from stomach). net neutral
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3
Q

Gastric alkalosis pathogenesis

A
  • generated by GIT, maintained by kidney
  • vomiting or NG tube removes HCl and NaCl from stomach.
  • HCO3 secreted by pancreas is not neutralized by luminal H+ from stomach. reabsorbed later in GIT –> alkalosis
  • Required secondary renal event (as in all metabolic alkalosis: Vomiting –> volume depletion –> AngII –> increased # of Na/H exchangers in proximal tubule –> increased capacity to reabsorb HCO3 (via double CAn/neutralization pathway)
  • Additionally, reduced Cl- prevents distal tubule from secreting HCO3 (via HCO3/Cl exchanger)
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4
Q

Tx metabolic alkalosis

A
  • give volume and chloride. Because volume and chloride depletion is what is increasing kidney’s capacity for HCO3 reabsorption (via AngII)
  • Removes stimulus for HCO3 reabsorption and secondary aldosteronism, and restores distal tubular HCO3 secretion
  • Correct any K+ defects. DONT GIVE NORMAL SALINE b/c risk of hypokalemia. Give KCl with saline.
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5
Q

urine of pts post vomiting

A

acid! (paradoxically).

  • All filtered HCO3 is reabsorbed in PT
  • Na+ reabsorption in the DT as NaCl in exchange for K+ and H+ is now robust
  • final urine is acid but free of Na and Cl
  • paradoxical, except that kidney is prioritizing saving volume (via Na) over pH
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6
Q

diuretic-induced alkalosis pathogenesis

A
  • generated by kidney, maintained by kidney
  • downstream of diuretic, increased Na delivered to principal cells in distal nephron, absorbed by principal cell and Cl- lags in lumen (electronegative)
  • increased driving force for H+ secretion by alpha-intercalated cell –> HCO3 reabsorption into blood from intercalated cell –> alkalosis
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7
Q

mineralocorticoid excess syndrome

A
  • volume expansion, increased delivery of NaCl to distal nephron, increased Na reabsorption there and increased H+/K+ secretion
  • alkalosis similar to diuretics, but patient is volume expanded and typically hypertensive
  • typically mild metabolic alkalosis, since no volume stimulus or chloride depletion to support increased HCO3 levels
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8
Q

Dx metabolic alkalosis

A
  • Hx: vomiting, diuretics, HTN
  • Physical: volume depletion or volume excess
  • Labs: Inc Serum HCO3. Alkalemic pH - arterial blood gas
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9
Q

Hypokalemia definition and general causes

A
  • serum K < 3.5 mEq/L
  • Change in balance: Inadequate intake or increased loss (GI, Renal)
  • Redistribution: Increased entry into cells (transient only)
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10
Q

causes of hypokalemia due to redistribution

A
  • beta-2: MI, bronchodilators
  • Insulin
  • alkalosis
  • rapid cell growth
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11
Q

causes of hypokalemia due to increased K loss

A
  • stool loss: diarrhea, laxatives, villous adenoma
  • Renal: increased DT Na delivery, increased mineralocorticoids, delivery of poorly-reabsorbed anions, acid/base balance., hypomagnesemia, DIURETICS
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12
Q

Diuretic-induced hypokalemia (mechanisms, pattern, magnitude, association)

A
  • increased delivery of Na and H2O to collecting tubule where Na reabsorption creates favorable electrical gradient for K secretion
  • increased aldosterone due to diuretic-induced volume depletion
  • diuretic-induced metabolic alkalosis
  • loss of 2 weeks, then new steady state
  • magnitude proportional to diuretic dose and Na intake
  • associated with mild-moderate metabolic alkalosis
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13
Q

Hypokalemia due to excessive mineralocorticoid activity

A

WITH HTN: primary hyperaldosteronism (adrenal adenoma, bilateral adrenal hyperplasia, adrenal carcinoma), apparent mineralocorticoid excess syndrome (inherited or licorice)
WITHOUT HTN: secondary hyperaldosteronism (primary salt-wasting nephropathies)

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14
Q

Labs primary aldosteronism

A
  • unexplained hypokalemia, severe HTN, adrenal mass

- elevated plasma aldosterone and reduced plasma renin activity

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15
Q

apparent mineralocorticoid excess syndrome

A
  • deficiency in 11beta dehydrogenase so no conversion of cortisol to cortisone and cortisol has mineralocorticoid activity
  • drugs, licorice
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16
Q

Bartter’s and Gitelman’s syndromes

A
  • primary salt-wasting nephropathies
  • Bartter’s: NKCC
  • Gittelman’s: N/Cl
  • results in increased Na delivery to DCT –> hypokalemia
  • look just like people on diuretics
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17
Q

effects of hypokalemia

A
  • EKG: flattening T waves, appearance of U waves. Risk of arrhythmias
  • NM: rhabdo
  • decreased insulin
  • polyuria/polydipsia, hepatic coma
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18
Q

blood gas normal values

A

pH - 7.4
pCO2 - 40 mm Hg
HCO3 - 24 mEq/L

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19
Q

formulas for expected compensation for respiratory alkalosis

A

Acute: HCO3 decr by 2 for every drop of 10 in PCO2 (minutes)
Chronic: HCO3 decr by 5 for every drop of 10 in PCO2 (days)

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20
Q

Associated problems with respiratory alkalosis

A
  • parasthesias, numbness, tetany (due to decreased Ca)
  • dizziness, confusion (cerebral vasospasm)
  • chronically, may be asymptomatic
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21
Q

pCO2 relative to alveolar ventilation

A

PaCO2 ~ VCO2 (metabolic production) / Va (alveolar ventilation)

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22
Q

causes of respiratory alkalosis

A

pain, anxiety, fever, exercise, hypoxia, liver disease, sepsis, pregnancy, drugs, mechanical ventilation

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23
Q

Tx respiratory alkalosis

A
  • usually unnecessary

- treat the underlying problem, if needed

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24
Q

General response to respiratory alkalosis or acidosis

A

TISSUE BUFFERING FIRST (generation or consumption of bicarb), THEN RENAL ADJUSTMENT (reabsorption or excretion of bicarb)

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25
Q

formulas for expected compensation for respiratory acidosis

A

Acute: HCO3 inc 1 for every 10 pCO2 (minutes)

chronic: HCO3 inc 3.5 for every 10 pCO2 (days)
- not as drastic as compensation for alkalosis

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26
Q

associated problems with respiratory acidosis

A
  • usually clinically important
  • confusion, obtundation (opiate-like) from cerebral vasodilation –> inc ICP
  • important defense against metabolic acidosis
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27
Q

respiratory acidosis pathophys

A
  • decrease in alveolar ventilation
  • either decrease of tidal ventilation (e.g. drugs) or increase in dead space volume (e.g. pulmonary disease–asthma, COPD, etc)
28
Q

causes of respiratory acidosis

A 
Acute:
-sedative drug OD
-acute exacerbations of respiratory disease
-giving O2 to person with chronic hypercapnia
Chronic:
-emphysema
-obesity hypoventilation
-sleep apnea
Acute-on-chronic
29
Q

steps for analyzing an acid base problem

A
  • Is it acidemia or alkalemia (pH)
  • in the primary process respiratory or metabolic?
  • Is there appropriate compensation?
  • What are the possible causes
  • Dx and Tx
30
Q

normal phosphate level

A
  1. 5-4.5 mg/dL

- people on upper range of normal probably have increased risk of CVD

31
Q

metabolic effects of phosphate

A
  • bone: low levels –> resorption
  • renal: low levels –> VtD synthesis, Ca excretion
  • adequate amounts necessary for cellular energy metabolism (ATP)
32
Q

phosphate reabsorption

A
  • Tm characteristic (like glucose)

- Na/PO4 cotransporters (inducible) on luminal membrane of PT cells. Regulated by PTH and dietary PO4

33
Q

PTH and PO4 excretion

A
  • PTH –> reduced Na/PO4 transporters on PT cells –> more phosphaturea
  • increased Pi intake –> inc serum Pi –> decr serum Ca (bind together) –> incr PTH –> incr renal excretion –> normalization of serum Pi
34
Q

PO4 and vitamin D

A

-lower serum Pi –> increased renal 1,25 (OH) D synthesis –> increase GI and renal Pi absorption

35
Q

FGF-23

A
  • GF made in bone – important in bone and cartilage development
  • acts via receptor Klotho
  • acts on kidney to increase PO4 excretion (similar mechanism to PTH)
  • May act as a suppressor of vit D activation
36
Q

consequences of profound sustained hypophosphatemia with chronic depletion of total body stores

A
  • MS: myopathy, rhabdo
  • CV: arrhythmias, cardiomyopathy
  • Pulm: respiratory failure
  • neuro: delirium, seizures
  • hematologic
  • happen because utilization of glucose is dependent on inorganic Pi
37
Q

causes of hypophosphatemia

A
  • intracellular shift (usually acute and inconsequential)–carb infusions, hormonal effects, respiratory alkalosis, rapid cellular proliferation
  • Decreased absorption: malabsorption, antacids, vitamin D deficiency (–> secondary hyperPTH)
  • increased renal excretion: hyperPTH, oncogenic osteomalacia, alcoholism, genetic defects
38
Q

alcoholic patients and PO4

A
  • have to monitor carefully!

- if you give glucose, can rapidly increase demand for PO4 –> rhabdo

39
Q

hyperphosphatemia causes

A
  • massive load (tumor lysis, rhabdo, laxatives)
  • Renal failure
  • Increased tubular reabsorption, hypoPTH, tumoral calcinosis
40
Q

corrected serum Ca

A

= serum calcium + .8(4-serum albumin)

-this is because low serum albumin will lower serum calcium reading

41
Q

acid-base and Ca

A

lowering pH competes Ca off albumin so can have Sx of hypocalcemia by being alkalemic

42
Q

PTH axis

A
  • Parathyoid cell releases PTH
  • PTH acts via PTHR in bone to release Ca
  • PTH acts via PTHR in kidney to increase reabsorption of Ca and to stimulate 1,25 (OH)D, which acts in duodenum to increase reabsorption of Ca
  • Ca feeds back on parathyroid cell and kidney to inhibit these effects
43
Q

vitamin D axis

A
  • sources: made from 7-dehydrocholesterol (and UV) in skin and absorbed from diet
  • stored in adipocyte and liver, hydroxylated (25) in liver
  • kidney: under PTH and low Phos, hydroxylates (1,25)
  • 1,25-(OH)D (calcitriol) feeds back on kidney and liver
  • calcitriol increases Ca and Pi absorption in GIT, suppresses PTH, increases renal Ca reabsorption, increases osteoblast and osteoclast activity and potentiates PTH action in bone
44
Q

why do you get hyper-everything in renal failure but hypo-calcemia?

A
  • Ca2+ is only ion with regulated absorption in gut.
  • kidney responsible for making calcitriol, which activates Ca absorption in gut
  • so net is hypocalcemia even though kidney is responsible for retaining Ca
45
Q

Ca handling in nephron

A
  • parallels Na handling
  • 65% reabsorbed in PT (paracellular passive transport by solvent drag)
  • 25% in loop of henle (Paracellular driven by (+) lumen potential)
  • 10% in distal nephron (regulatory segment)
46
Q

Action of Calcium receptor in nephron

A

-in loop of henle, inhibits NKCC and RomK channel. This is because Ca reabsorption is largely paracellular driven by (+) lumen potential, so inhibiting these diminishes Ca reabsorption

47
Q

Normal calcium levels

A
  1. 8-10.3 mg/dL

- modest variations can have no Sx

48
Q

clinical Sx hypercalcemia

A
  • 80% – none
  • nonspecific
  • neuropsychiatric (depression)
  • Cardiac changes –> Vfib
  • renal: polyuria (defense against nephrolithiasis), natriuresis (due to actions of CaR in loop of Henle), nephrolithiasis, renal insufficiency
49
Q

causes of hypercalcemia

A
  • primary hyperPTH
  • malignancy – late-stage, poor prognosis
  • vit D intoxication (iatrogenic, glomerulosis)
50
Q

Tx hypercalcemia

A
  • enhance renal Ca excretion with isotonic saline +/- loop diuretic (if volume replete)
  • suppress osteoclastic bone resorption with bisphosphonates/calcitonin
  • hemodialysis
51
Q

approach to hypocalcemia

A
  • correct for albumin!
  • impaired mobilization from bone (hypoPTH, vit D deficiency)
  • tissue or vascular accumulation through calcium complexation
52
Q

Sx hypocalcemia

A
  • usually s sign
  • depression, altered mental status
  • prolonged QT
53
Q

Mg handling along nephron

A
  • only 70% filtered
  • unlike other ions, only 10-15% absorbed proximally
  • most reabsorbed in loop of Henle (paracellular reabsorption driven by electrochemical gradient). Mg regulates it’s own absorption via CaR (integrates Ca and Mg signals and regulates Na, Mg, Ca absorption)
54
Q

hypermagnesemia clinically

A

-not rare, but often not important
-Causes: renal insufficiency, Mg infusion (Tx of exlampsia and preexlampsia), oral ingestion, magnesium enemas.
Sx: loss of deep tendon reflexes, cardiac, other NM, cardiac arrest at very high levels

55
Q

hypomagnesemia clinically

A
  • common in hospitalized/ICU pts
  • GI losses: diarrhea, malabsorption, PPIs
  • Renal: diuretics and nephrotoxins, volume expansion, alchol
  • drugs: aminoglycosides, cisplatinum, calcineurin inhibitors, pentamidine
  • Sx: NM weakness, can progress to tetany. hypokalemia. hypocalcemia, arrhythmias
56
Q

nephrolithiasis clinical

A
  • renal colic. worse pain ever.
  • hematuria
  • fever implies concomitant infection and risk of sepsis
  • renal failure is unusual.
  • spontaneous passage is the rule (90%)
57
Q

metabolic vs anatomic activity of stones

A
  • metabolic activity = stone growth

- anatomic activity = movement of stone

58
Q

activity product and stone inhibitors

A
  • activity product = [Ca]*[Phos]
  • most of us are in “metastable region”: above saturation point, but below product formation ratio (due to presence of stone inhibitors like Citrate and proteins)
59
Q

Risk factors for calcium stones

A
  • increased crystalloid: hypercalciuria (PTH), hyperoxaluria (genetic, hyperabsorption), low urine volume
  • increased promotors: hyperuricosuria, alkaline urine pH (calcium phosphate), acid urine pH (uric acid)
  • Decreased inhibitors: hypocitruturia (acidosis, K depletion, renal insufficiency)
60
Q

diet and hypercalciuria

A
  • actually a lot more to do with Na and Ca
  • very few people are eating too much Ca and no benefit to Ca restriction
  • Na inhibits reabsorption of Ca in PT –> stone formation
61
Q

risk factors for uric acid stones

A
  • persistently acid urine, often due to defect in urinary ammonia production. highly associated with insulin resistance and metabolic syndrome. (uric acid much less soluble than urate and more prevalent at acid pH)
  • fewer (20%) hyperuricosuria
62
Q

infection stones

A
  • most severe form of nephrolithiasis: sepsis, perinephric abscess, renal failure.
  • recurrent UTI, neurogenic bladder, other anatomic abnormality
  • weird infection
  • can form staghorn stones
63
Q

Cystine stones

A
  • rare
  • inherited defect in renal tubular amino acid reabsorption
  • hexagonal crystals
  • can form staghorn stones
  • Tx: high fluids (4L/d!)
64
Q

Tx calcium stones

A
  • diet (Na restriction), fluids
  • thiazide diuretics with Na restriction: anticalciuric action in PT
  • potassium citrate: increases urine citrate (Ca stones), increases urine pH (uric acid stones)
65
Q

acidosis and calcium excretion

A
  • acidosis –> increased turnover of Ca channel in DT, which is sensitive to pH
  • -> increased Calciuria –> increased risk of stones
66
Q

metabolic syndrome and stone formation

A

big risk factor! especially for uric acid stones because of failure of ammoniagenesis

Renal (5 decks)

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