Patho electrolytes and diseases Flashcards
distinguish between extracellular and intracelluar fluid compartments in terms of water + electrolytes
understand critical components of fluid shift—-tonicity and osmolality
understand neurohumoral responses to maintain water balance
discuss clinical presentation of both hypovolemia and hypervolemia
total body weight of water in:
- males
- females
- infants
males=60
females=50
infants=75-90
what is 2/3 of total body water
ICF
what is 1/3 of total body water
ECF
what is inside ECF
plasma and interstitial fluid
plasma components
WBC and platelets and flotting factors
serum?
=plasma-clotting factors
main ECF electrolyte and ICF electrolyte
ECF= NA+ ICF= K+
CA2+ mainly found ECF or ICF
ECF
Cl- found mainly ECF or ICF
ECF
what has the most impact on serum osmolarity?
Na+
because water follows salt
define osmolarity
-water moves from ____ to ____ areas of osmolarity
osmotic [ ] of a solution expressed as total number of solute particles/Liter of fluid—- h20 moves from areas of low to high osmolarity
–>osmolarity in plasma (ECF) is too high— water moves from inside the cell to the plasma to lower osmolarity— this shrinks cell
what happens to water movement when:
1) plasma osmolarity too high ?
2) serum osmolarity too low
1) AKA too many solutes in the plasma— so water leaves the cell and moves OUT— causng cell to shrink
2) AKA inside the cell is too much solute– so water moves INTO cell—causing it to swell
define osmolality
estimate of [ ] of dissolved particles (Na**, glucose, urea, Cl, K) in the plasma relative to plasma water—> osmoles of solute/kg solvent
what is normal serum osmolality
280-295 mOsmol/kg
what dictates the transfer of water through membranes
osmolality
define tonicity
[ ] of particular solutes that causes a shift b/w compartments
free water movement depends on?
tonicity
what are effective soluts
glucose and urea
ECF is determined primarily by?
total amount of osmotically active particles (NA) relative to water in the ECF
osmotic gradient is required for?
water to move b/w ICF and ECF
osmotic pressure is?
pressure that must be applied to solution to prevent flow of water
changes in osmolality cause the cell to
shrink or swell
which hormone tightly regulates serum osmolarity
ADH aka vasopressin
-comes from posterior pituitary
if serum osmolarity rises… what happens
- ADH released–>causing water retention by the kidneys
- sense thirst and incr intake water
- all of this LOWERS serum osmolarity
what happens when serum osmolarity decreases
ADH is decreased/inhibited–>natriuresis–>diuresis
list two non-osmotic stimuli
- decreased effective circulating volume——-ex CHF and cirrhosis
- carotid sinus baroreceptor discharge—>mechano-receptor sensory neurons in vasculature detect changes in circulation volume
sympathetic stimulation effect on NA+
causes retention of NA
where are the high pressure baroreceptors and their roles
carotids and aortic arch
- respond quickly to changes in arterial circulation to maintain pressure
- overfilling leads to natriuresis
- underfilling leads to symp activation–>retention of NA+
where are the low-pressure baroreceptors and their roles
major veins, left ventricle, right atrium
- protect against low ECF volume—-effect renal response to low volume
- ventricles and atria release natriuretic peptides
what do the renal afferent glomerular arterioles release in response to keep effective arterial blood volume
renin
list two examples of how ECF volume and tissue perfusion do not always change in the same direction
CHF with edema
cirrhosis with ascites
*****both disorders have increased ECF volume and reduced tissue perfusion due to low cardiac output (CHF) or vasodilation (cirrhosis)
most potent stimulus for thirst is
- other stimuli?
- % change in plasma osmolality to cause thirst
hypertonicity
others: hypotension and hypovolemia
2-3% change
too much/too little ADH and the urine
too little= dilute urine with low osmolality
high adh=concentrated urine with high osmolality
renal causes of hypovolemia
SALT AND WATER
- diuretics
- diuresis: osmotic
- diursis: post-obstructive
- salt losing nephropathies –renal tubular acidosis
- genetic dz: Barter and Gitelman syndromes
- aldosterone deficiency—–Addison’s dz
JUST WATER
-diabetes insipidus–central or nephrotic
define hypovolemia
TBW reduction but NO proportional decrease in serum NA—->leads to decr ECF secondary to—–
- extra renal causes (non-renal)
- renal causes
list the causes of hypovolemia secondary to extra-renal causes
- GI LOSSES
- upper GI: vomiting, NG suction
- lower GI: diarrhea, fistula
- intestinal obstruction, pancreatitis - hemorrhage
- Muscle injury—rhabdo
- dermal losses
- burns
- sweat
- insensible losses
is dehydration the same as volume depletion
no!!
define:
- dehydration
- volume depletion
dehydration=loss of total body water—–hypertonicity
volume depletion=deficit in ECF volume
list CM for mild volume depletion
postural dizziness
thirst
weakness
list the CM for moderate volume depletion
recumbent hypotension
tachycardia
reduced urine output
BUN/CR ration > 10:1
cm for severe volume depletion
confusion oliguria hypotension clammy extremities recumbent tachycardia
Lab work for Hypovolemia
- serum
- hemoconcentration
- “renal” labs
- increased serum BUN:Cr Ratio >20
- electrolyte changes
- acid-base changes
- incr serum albumin
- incr hemoglobin and hematocrit
- urine NA+ <20
- HIGH URINE OSMOLALITY >500 with a high specific gravity for urine
treatment for hypovolemia
goal=hemodynamic stability
- treat underlying problem
- treat volume deficit
- address ongoing losses
- be aware of co-morbidities
- 0.9% NaCL 1st line– to expand ECF—- ONE LITER WILL INCR PLSAMA VOLUME BY 200 mL while the rest goes interstitially
- blood/products
* ***multiple studies show no benefit to albumin/colloids vs NSS
edema generally result of ?
EDEMA–>excess NA and expansion of ECF (hypervolemia)
- *body will retain water due do the high serum NA+
- *body will eliminate NA+— causing a low oncotic pressure, low movement and high fluid volume
patho behind hypervolemia
fluid moves out of vascular space and into the interstitium due to INCR CAPILLARY HYDRAULIC PRESSURE
hypervolemia
-tx
fix underlying problem
- restrict salt and fluids
- diuresis if volume is causing significant clinical problems–> SOB for ex
define hyponatremia
- types and exs
- which type is clinically significant?
- general causes
- general CM
- general diagnosis
- whhat happens if you correct hypoNA too fast
NA < 135 mEq/L
- losing more NA than water
- gaining more water than sodium
TYPES based on serum osmolality:
- hypotonic= serum osmolality <280
- hypertonic= >295
- isotonic= 280-295 aka normal serum osmolality
clinically significant= hypotonic hyponatremia—>hypovolemic, hypervolemic, and isovolemic
CAUSES:
- decr in serum sodium
- decr in serum sodium + water/volume—but sodium decreases MORE than water/volume
- incr in serum water/volume—which decrs [NA]
- incrs in serum water/volume and sodium—but water/volume incrs MORE than sodium
General CM= NEURO/CNS
-initially: non-specific s/s will start when NA <130—->sympotmatic N/V
<120 aka SEVERE: HA, lethargy, psychosis, seizures and coma, CEREBRAL EDEMA are causing all these severe s/s
DIAGNOSIS:
- measure serum sodium
- serum osmolality
- assess volume status
TX
*****if treated with 0.5mEq/L/hour can lead to central pontine myelinolysis (demyelination)—->leads to permanent neurologic damage
hypotonic hyponatremia
-define
-types determied by? and ex of causes
-
sodium deficient + TBW deficit–BUT the NA+ deficit is GREATER than the H2O
*serum osmolality is <280
types are determined by volume status/ECF aka if its derc, normal, incr:
Hypovolemic–>volume contraction (decr in volume) with renal or extra-renal NA loss
Isovolemic–>hypothyroidism, glucocorticoid excess and SIADH
Hypervolemic–>volume is expanded with edema—ECX: CHF, nephrotic syndrome, renal failure, cirrhosis
hypovolemic hypotonic hyponatremia
- general definition
- causes
- how to diagnose
- tx
has to be both water and salt loss BUT **decrease in TBW and LARGER decrease in [NA]
renal volume loss
- diruetics***
- ACEI
- extra-renal volume loss–>diarrhea or vomiting, burns, fever, pancreatitis
DIAGNOSIS: urine electrolytes help determine the cause (renal or extra-renal)
- urine [NA] less than 10 meq/L—>extra renal cause (sweat, stool or edema) *****this means kidneys are appropriately holding onto NA in attempt to bring it back to normal levels—which reflects the low levels of NA in urine
- GREATER than 20 meq/L means its a renal cause and NA is being lost through urine–>aka DIURETIC USE or mineralcorticoid deficinecy
TX
1. volume replacement–>NSS 0.9% IV and tx underlying cause
hypervolemic hypotonic hyponatremia
- patho
- causes
- Diagnosis
- a typical s/s?
**water is either added or retained–diluting serum NA
- hypervolemic–>large increase in H2O and a small increase in NA+——- Water»»> Sodium—-
- edema and decr forward flow (HF) causes a decrease in circulating volume–>leads to stimulation of ADH by kidneys–>body retains more water
- decrease in circ volume also stimualtes aldosterone via RAAS–>NA+ retained–>more water retained
- *cirrhosis leads to this by pooling of blood in mesenteric veins–>decr volume perfusion—etc
CAUSES: CHF, cirrhosis, nephrotic syndrome
DIAGNOSIS
- urine [NA] will be <20 aka decreased because the kidneys are attempting to retain NA along with water (water retention»»NA retention)
- urine [NA] over 20= acute or chronic renal failure
tx
1. volume removal–>diruetics, sodium + water restriction
hypotonic isovolemic hyponatremia
- define and patho
- causes
- diagnosis
- tx
ISOVOLEMIA is in terms of the CLINICAL PRESENTATION–>the patient appears on PE not hypo or hyper volemic
but inside–>there can be slight incr in in volume but not enough to cause s/s
Excess water consumption—>aka primary polydipsia (seen in psych PTs–mental prob or SE of some drugs)
wil urinate large volumes—polyuria
BUT maintain clinical isovolemia
CAUSES
- SIADH
- hypthyroidism
- MDMA
- adrenal insufficiency
- water intoxication—aka primary polydipsia
DIAGNOSIS: is urine dilute or concentrated? if its dilute….need to disintuigsh this from DI (both cause diluted urine)
- ->DILUTE (<100 mosm/kg)
1. in DI ADH does not work or is not present–>decr intravascular volume—>increased serum [NA] ***
2. primary polydipsia–> decr or low serum [na] **** due to the massive increase in plasma volume - ->CONCENTRATED ( >100 mosm/kg)
3. SIADH–>AHD over secreted–>very concentrated urine with increased urine [na] and a high >20 serum NA
tx= water restriction and fix underlying cause
hypertonic hyponatremia
define
cause
**high plasma osmolality due to effective osmoles–aka glucose or solutes (mannitol or sucrose)
CAUSES
1. hyperglycemia–>moves water from ICF—>ECF and decreases serum NA+
–>decrease of 1.6 mmol/l of NA+ occurs for every 100mg/dl incr in glucose
or
2. mannitol infusion or sucrose
pseudohyponatremia
- define
- causes
lab artifact due to lower than normal % of body water
CAUSES:
- hypertrigs or hyperproteinemia—>both reduce water content of plasma (water is pulled out to serum) WO affecting sodium concentration—but the [NA]/unit of plasma is reduced—so if this is measured00000it will read hyponatremia
- plasma cell dyscrasias
- obstructive jaundice
major causes of SIADH
- tx
- type of electrolyte imbalance
- diagnosis
Euvolemic hyponatremia because theres too much ADH being secreted–body retains too much water—diluting serum— but clinically PT does not have edema so its EUVOLEMIC
CNS--bleeds, tumors, infections, trauma trauma malignancy drugs recent surgery HIV
DIagnosis
- urine NA >20-40 meq/L
- want to also R/O adrenal and thyroid dz
TX
-3% NSS
tx for severe hyponatremia aka <120
IV HYPERtonic saline + furosemide
-be so so so cautious about rate to avoid cerebral pontine myelinolysis
chronic symptomatic hyponatremia
- at risk for?
- common causes
- timing of development
- tx
s/s are less severe than acute
Develops over 72 hours or more
CAUSES:
- thiazide-induced–esp eldeyr
- Heparin induced–antagonism of aldosterone (bc it retains NA)
- Cerebral salt wasting—-neurosurgery, SAH, CA, meningitis
- Cortisol deficiency–hypothyroidism, SIADH
PT at risk for osmotic demyelination if corrcted too rapidly
TX
-no greater than 8 mEq/24 hours
steps to diagnose hyponatremia
***serum NA <135
- check serum osmo
A) LOW–>hypotonic hyponatremia (TRUE)
B) NORMAL—>lab error (incr protein, incr triglycs)
C) HIGH–>Hyperglycemia or mannitol administration - ECF VOLUME
A) LOW= hypovolemia—> where is the fluid loss coming from—->renal or extra-renal?
- UNa >20= renal loss—Diuretics (thiazides and K-sparing), ACEI, ARBs, hypoaldosteronism
- UNa <10=extra-renal loss—bleeding, burns, GI (N/V/D), Pancreatitis
- tx for all is to correct volume issue via IV NSS
B) NORMAL= ISOVOLEMIA *SIADH, POST-OP *hypothyroidism *adrenal insuff *Reset Osmostat *water intoxication---Primary polydipsia TX: water restriction
C) HIGH=HYPERVOLEMIA
*UNa <20–>CHF, Cirrhosis, Nephrosis
*UNa >20–>acute/chronic renal failure
TX: H20/salt restriction
rate to correct hyponatremia
< or equal to 0.5mEq/L/Hr to prevent demyelination
define HYPERnatremia
Na >145 mEq/L
Hypernatremia
- MCC
- patho/time line
mcc=unreplaced h20 loss -->negative water balance from: an incr in free water loss not replaced or diminished intake of water -->increase in sodium intake relative to water (not common) ETIOLOGES *Diarrhea or GI losses *diuretics *sweating *burns *fever *insensible loss *DI **** both central and nephrogenic
PATHO: sustained hyperNA seen when appropriate water intake NOT possible or impaired—>elderly, infants, debilitiated, OR the thirst mechanism impaired (hypothalamic lesion)
- HyperNA develops over time——>cells adapt—>bc cells protect themselves–>so as water moves out of cells to balance high NA in blood–>osmotically active particles move INTO CELLS to help keep water inside!
- ***but it can sometimes develop acutely—-and cells dont get time to adapt
CM for hypernatremia
- when do elderly start to show s/s
- infant s/s
NEURO—–>due to shrinkage of brain cells from dehydration—shrunk cells are more prone to rupture and cause intracranial bleeding
- thirst is MC initial s/s
- confusion
- disorientation
- fatigue
- n/v
- muscle weakness or muscle twitching
- seizures *** can be from rapid rehydration or someone administering hypertonic saline soln to fix hyponatremia
- coma
- brain damage
- resp arrest severe
*polydipsia esp for COLD WATER
elderly show s/s starting at 160mEq/L
INFANTS
- tachypnea
- muscle weakness
- restlessness
- high-pitched cry
- insomnia
- lethargy
- coma
PE for hypernatremia
DEHYDRATION
- dry mouth
- dry mucous mems
- decr skin turgor
- *tachycardia
- hypotension
how to diagnose hypernatremia
SERUM STUDIES
- serum sodium
- urine osmolarity
- serum osmolarity
- assess volume status
**nearly always assoc with hyperosmolarity
**Urine osmolality >600 and UNa <10= kidneys working properly and respond to incr [ ] NA by retaining water —extra-renal cause (sweating, or GI issue)
**urine osmolality of <600 and UNa >20= kidneys cannot retain h20—eliminate dilute urine in spite of high [NA]—renal cause (DI or osmotic diruesis)
**Isovolemic= DI and urine osmol <250
tx for hypernatremia
- Hypotonic fluids–>pure water PO, D5W, 0.45% NS, 0.2% saline
* pref route is PO or tube feeding - isotonic fluids if hypovolemic—- NSS or LR
* then switch to hypotonic fluids to correct hyponatremia once volume is repleated
**8Rapid correction (>0.5 mEq/L/hr) can result in cerebral edema
polydipsia
- define
- often seen with
- DDx
increase in urine volume >3L
-often seen with hypernatremia
DDX
- DI
- Primary polydipsia
- osmotic diuresis
**either bc they are taking too much water or cannot hold onto water
DI
- what is it
- rxplain two types
- how to tell diff b/w two types
- tx
- polyuria >3L/day and polydipsia scondary to ADH abnormality
- —leads to hypernatremia sec to water loss
*central= deficiency of ADH causes= most is idiopathic, head trauma, pituitary dz/tumors, infections, infiltrative dz (sarcoid), surgery
*nephrogenic= ADH produced by kidney is insensitive to the hormone
causes=meds like LITHIUM, amphotericin, elecr abnormalities, rarely congenital
water deprivation test + GIVE DDAVP to tell diff bw the two: urine osmolarity will stay the same in nephrogenic and will increase in central
TX
- volume replacement
- central: DDAVP
- nephrogenic: thiazides and salt restriction, amiloride for lithium pt, and NSAIDs
steps to diagnose hypernatremia
ALWAYS ASSOC WITH HYPEROSMOLARITY (step 1)
- ECF volume
A) HYPOVOLEMIC
*UNa <10 and Urine osmolarity >400–>EXTRA RENAL–>sweating, respiratory loss, N/V/D, dehydration
*UNa >20 and urine osmolarity 300-600–>RENAL LOSS–>severe hyperglycemia, diuretics
B) HYPERVOLEMIC
- hypertonic saline administration
- mineralcortcioids excess
C) ISOVOLEMIC
- Urine osmolarity <250
- DI
- reset osmostat
Hyperkalemia
-define
> 5.9 mEq/L
NORMAL= 3.5-5.0
list things that drive K+ out of cells
- metabolic acidosis
- respiratory alklalosis
- hypertonicity ** glucose and mannitol stimulate K to leave the cell——> why a DKA patient has also hyperK
- b2 adrenergic antagonists
- alpha adrenergic antags
- Glucagon **
list things that drive K+ into cell
- metabolic alkalosis
- insulin
- B2 adreenergic agonists
- alpha adrenergic agonists
- thyroid hormone
etiologies for hyperK
- decreased renal K+ excretion
* acute or chronic renal failure
* acidosis
* reduced distal Na and H20 delivery—– aka diminished blood volume - hyPOaldosteronism–>primary adrenal insuff (addison dz) OR drugs that block aldosterone (ACEI, ARBS, spironolactone,)
- MEDS:
* K+ supps
* ACEI–>block aldosterone receptors
* NSAIDs
* cyclosporine
* heparin
* bactrim
* BB
* digoxin–>
* K+ sparing diruetics—>block Na channel at the distal nephron and decrease renal K+ excretion - Tissue destruction
* Rhabdo
* burns
* tumor lysis syndrome - K+ exteacellular redistribution
* metabolic acidosis (DKA)
* insulin deficiency
* catabolic states
* mannitol
what is pseudohyperkalemia
due to hemolysis–>venipuncture esp if PT clenches first during the draw or tourniqutte left on too long
- lab error lysis of the cells
- **suspect in asympto PTs with high K+, thrombocytosis or leukocytosis and NO ECG changes
why does metabolic acidosis cause hyperK
H+ enters the ICF—> too much (+) in the cell so K+ leaves to maintain electroneutrality
list cardiac CM with hyperkalemia and ekg findings
decreases membrane potential decreases cell conduction velocity increases rate of repol **palpitations **arhythmias
***PEAKED T WAVES, incrs PR interval and widened QRS complex
list renal CM from hyperk
impairs urinary acidification—-interferes with renal NH4+ excretion and may lead to–>type IV RTA or metabolic acidosis
list skel muscle CM with hyperK
paresthesias
weakness
paralysis
resp failure
does hyperK cause seizures
no
hormonal CM from hyperk
stimulates endogenous aldosterone secretion
NOT insulin secretion
GI CM from hyperk
n/v
ileus–>paralyzes intestinal muscles
what labs would you get to R/I hyperk?
- serum K+—-> is it > 5.0
- glucose— check for hyperglycemia
- bicarb–check for acidosis
- CBC–check for hemolysis
- CK—check for rhabdo
***check for hypocalcemia– bc this can exacerabte arrythmias
tx for hyperk
- stabilize cardiac membrane
* IV Calcium gluconate (or Calcium chloride)—.CONTRAINDICATED WITH DIGOXIN TOXICITY
* does not lower K+ but protects against arrhythmias - Drive K+ back into cell:
* IV insulin with glucose
* high dose beta 2 agonists–albuterol nebs
* Bicarb if patient is acidotic
* Resin Binder–>K+ removal
* diuretics–loop and thiazides if kidney function normal
* Sodium Polysteryene sulfonate—removes K from body via bowel movement
* DIALYSIS IS FASTEST AND MOST EFFECTIVE
list indications for dialysis with a hyperK patient
- Acidosis
- Electrolytes + EKG changes
- ingestions—esp those that cause renal failure like salicylates or ethylene glycol
- overload–volume overload causing pulm edema
- Uremia
Hypokalemia
- define
- mild, mod, severe—list the numbers
- roles of K in body
- % of K excreted by kidneys and GI
K < 3.5
MILD= 3-3.5
MOD= 2.5-3.0
SEV=<2.5
ROLES OF K
- nerve conduction
- osmotic pressure
- protein synthesis
- acid-base balance
GI excretes 5-10% of K
kidneys excretes 90%
causes of hypokalemia
GI:
- diarrhea (severe)
- vomiting
- laxative use
- low K+ intake
URINARY/RENAL:
- diuretic therapy (including loops, thiaxides)
- increased mineralcorticoid activity—-hyPERaldosteronism
INCR K+ intracellular shifts:
- metabolic alkalosis—> H+ ions leave the cell in exchange for K entering cell
- meds: insulin tx, b2 agonists, chloroquine, vit B12, amphotericin
- hypothermia
- catecholamine excess
HYPOMAGNESIA—low mag opens mag-dep K+ channels—spilling K+ into the urine
-licorice
- Type 1 and Type 2 RTA
- hyperthyroidism
- genetics
Pseudohypokalemia
- K+ normal in pt but falls in the test tube
WHY?
*uptake 2nd to high number of metabolically active cells
*acute or chronic Myeloid leukemia - Increase ambient temperature
WHY?
*increases NA/K/ATPase activity which drives K+ into cell
HTN + Hypokalemia— we think?
hyperaldosteronism****
-primary
others ddx:
- congenital adrenal hyperplasia
- renal vasc htn
- genetic
- LICORICE!!!!!
hypokalemia WITHOUT HTN— we thnk?
- distal RTA (type 1)
- proximal RTA (2)
- hypomagnesemia—-etoh, diuretics,
CM of hypokalemia
HORMONAL
-glucose intolerance
MUSCULAR
- smooth muscle dysfunction
- weakness
- fatigue
- cramps
- rhabdo
RENAL
- incr ammonia production
- metabolic alkalosis
- impaired urinary [ ]
- polyuria—->nephrogenic DI
CARDIOVASCULAR
- palpitations
- arrhytmias—–Atrial tachyacrdia, sinus brady, AV blocks, junctional tachy, PVCs, VTACH, VFIB
cardiac CM for K+ <2.5
tachycardia
incr muscular irritability
-flattened t wave
cardiac arrest
EKG: depressed ST seg, decreased t wave amplitude, increased U wave amplitude
hypokalemia tx
STOP THE LOSSES
- for each decrease of 1.0 mEq/L there is a K+ deficit of approx 100 mEq/L
1. Asympto/mild–>PO K+
- SEVERE:
* SLOW IV potassium chloride (usually 10-20 mEq/L/hr)
* peripheral infusions >40 mEq/L/hr can lead to burning, sclerosis or phlebitis - if patietns dont respond– always check the mag
- montor cardiac status
*do not add glucose or sodium bicarb to solutions initially bc they cause intracellular intake of K+
Diagnosis for hypoK
- hx suggestive of intracellular shift? aka drugs?
* NO= go to step 2
* YES= tx the cause - Check spot urine potassium
*Urine K+ <20= extra-renal causes: vom, diarrhea
*urine K+ >20=
A) metabolic acidosis—>RTA or DKA
B) Normal or high serum bicarb?
C) Check BP
—>HIGH= primary hyperaldosteronism or cuhsings syndrome
—>LOW= diuretics, vom, mag depletion
