Pance Prep MCQ: ELE Imbalances & Acid Base
What are the 3 buckets (causes) of hyperchloremic (non-AG) metabolic acidosis?
GI loss of bicarbonate (diarrhea) Renal loss of bicarb (RTA) Chloride intoxication
What is the pathophysiology of Type I Distal RTA?
H+ Excretion problem 2/2 impairment of H/K ATPase---> H stays in body and K moves out of cell and normally the opposite occurs. You can also have problems with AE1 transporter and get less HCO3- (leaves into urine) and Cl- gets higher in blood to maintain anionic balance. Hyperchloremic (Non-AG) Metabolic Acidosis and Hypokalemia w/ a higher urine pH since you are holding onto H in blood rather than the urine like usual. also losing bicarb so you can't fix the acidosis and Cl- is increasing
Acidity= HCO3-/CO2 A=B/C An alteration in pH can only result from a change in bicarb or carbon dioxide blood levels. What changes in metabolic vs respiratory disorders?
HCO3- change in metabolic (matches the change in pH) CO2 change in respiratory (change is opp. to pH change)
What are some causes of Type II Proximal RTA?
Multiple Myeloma (Buzzword) Acetazolamide Amyloidosis Fanconi Syndrome
When would you use the colloid IV solution: Hetastarch?
NEVER Bad Complications: Hypersensitivity rxns Bleeding complications Renal Failure
If a loop diuretic like Lasix doesn't increase k+ excretion or urinary output, what other method could you try?
Kayexalate to bind the K in exchange for Na, sorbital is added bc the polystyrene can cause constipation, can cause diarrhea in some patients Use after you have done things like: insulin + gluc, calcium gluconate, albuterol, D5W + sodium bicarb, lasix, etc.
What is the benefit of LR vs NS?
LR poses less risk for Cl issues like hyperchloremic acidosis that can cause AKI w/ NS Has K--so good for a hypokalemic patient Osmolarity of LR is even closer to plasma osm compared to NS Especially great for LARGE VOLUME resuscitation (ie, trauma, profuse bleeding--better than NS)
What is the equation for urine anion gap?
Na + K -Cl Cations-Chloride (anion)
What is the formula for a serum anion gap?
Na - (Cl + HCO3) Cations-anions--> anion gap The anion gap is the # of unmeasured anions (ie, albumin)
How should you treat Type II Proximal RTA (hyperchloremic metabolic acidosis 2/2 impaired HCO3- reabsorption that leads to net excess of H)?
Large amounts of HCO3 BC most of the HCO3 will bc excreted in the urine, exacerbates hypokalemia, mixture of Na and K salts is preferred Thiazides: may decrease the HCO3 required but can aggravate hypokalemia
For hypovolemic hypotonic hyponatremia 2/2 diuretics (renal) or bleeding/diarrhea (extrarenal) how would you treat the patient?
Need to increase volume status Need to increaseNa levels? Normal Saline IV volume expansion decreases the hypovolemic stimulus for ADH and taking away ADH means less water reabsorption which will help increase the plasma tonicity
Would you get hyperventilation or hypoventilation w/ a metabolic acidosis?
You compensate for the acidemia by blowing off CO2 to try to lower the acid level so you get hyperventilation.
What are the 2 main bicarbonate handling sites in the nephron?
Proximal tubule: reabsorbs filtered HCO3- Distal tubule: excretes to replace bicarbonate consumed buffering the daily acid load
Which HIV med can cause Type II Proximal RTA?
Tenofovir
Which drugs would worsen sicca in a Sjogren's patient?
antidepressants antihhistamines diuretics narcoleptics
For hypervolemic hypotonic hyponatremia such as in volume overload (CHF, cirrhosis, etc.) how would you treat the patient?
Water and Sodium Restriction Decrease water bc its collecting in interstitial space, usually causing edema or free water going to cells Diuretics for some of these patients Sodium restriction bc it makes the edema worse
A negative AG in which the Na + K < Cl means that there is a high amount of NH4 in the urine. This should make you think about processes like???
diarrhea Normal: our bodies should be producing NH4+ to offset the acidosis and get rid of protons
Why do you see decreased deep tendon reflexes in hyperparathyroidism?
hypercalcemia (high Ca) levels
How can you treat hypokalemia?
40meq KCL in 100mL Half Normal Saline (.45%) infusion over 4h You want to corrrect hypokalemia SLOWLY so as not to disrupt the membrane potential and cause arrhythmias or drastic cell shifts of K
Normal blood pH range
7.35 to 7.45 THINK 7.4
At what infusion rate of hypotonic IV fluid should you correct hypernatremia?
<0.5 mEq/L/H to prevent cerebral edema
What antibodies would you find in Sjogren's syndrome? What is the Schirmer test?
ANA +AntiSS-A (Ro) +AntiSS-B (La) +RF Schirmer Test: decreased tear production
What things cause potassium to shift into the blood from the cells?
Acidosis Exercise Hyperosmolarity
Now that you have addressed the most serious issue in your patient with Type I dRTA (the HYPOKALEMIA), the next item to address is the HCMA-Hyperchloremic Metabolic Acidosis. What do you do now?
Add Sodium Bicarbonate to the Half NS (.45%) You admin a small amount of bicarb to correct the acidosis
What are some causes of metabolic alkalosis?
Loss of Acid, Increased HCO3 Vomiting Endocrinopathies (Cushing's, & Conn's) Licorice Diuretics Excess Base
Low HCO3, High H pH <7.4
Metabolic Acidosis
High HCO3, Low H pH >7.4
Metabolic Alkalosis
In a normal anion gap, ______ (ele) make up most of the anion level. In a high anion gap, _______ make up most of the anion level.
Cl makes up most of the anion gap if it is normal (loss of HCO3 & CL accumulates to replace it & maintain ionic balance) other anions (unmeasured, added) make up most of the anion gap if it is increased (addition of acid, you have an excess of something, accumulation of organic acids, more cations in relation to anions so bigger gap between # of cations vs anions than usual)
What would be the point of administering Lasix (loop diuretic) to a hyperkalemic patient who had metabolic acidosis 2/2 lactic acid build up 2/2 sepsis?
Could do a trial of furosemide (Lasix) to see if the patient can urinate K_ from the body.
When would you use the colloid IV fluid Albumin 25%?
For tx of volume overload ESRD patients to maintain volume during dialysis volume restricted patients (CHF) Tx for Ascites
What are some of the unmeasured anions in blood?
Sulfate Phosphate Lactate Ketoacids Albumin
Normal blood CO2 level
35-45 THINK 40
Hypernatremia >145 Usually d/t free water loss rather than sodium gain. 6 D's of Hypernatremia: the MC causes are:
1) Docs--Iatrogenic 2) Diarrhea 3) Dehydration 4) Diuresis 5) Diabetes Insipidus 6) Disease (kidney, SCD, etc.) Things that make you lose water--> makes your sodium concentration relatively high in plasma d/t the water loss.
What are the 3 types of hypotonic hyponatremia that you can have? NOTE: All 3 exhibit increased free water (found inside cells w/o Na) overhydration. If you had decreased free water you would be dehydrated (less water inside cells). The 3 are different in regards to volume status (extracellular fluid + Na) NOT hydration status (free water is same=increased in all 3=overhydration).
1) Hypervolemic -high Na + ECF water, mainly in intersitial space (ie, edema) -increased free water (inside cells) STATES of VOLUME OVERLOAD: CHF, Nephrotic Syndrome, Cirrhois 2) Hypovolemic -low Na + ECF water -increased free water (inside cells) (bc volume deplete in vessels, water in cells, increased ADH d/t hypovolemia, increased thrist makes worse) RENAL OR EXTRAREANL CAUSE Diuretics, ACEI, Aldosterone Insuff. Diarrhea, Bleeding, Sweating 3) Isovolemic -normal Na + water in EC space -Increased free water (inside cells) SIADH, Adrenal insuff, hypothyroidis, primary polydipsia
Hypokalemia: <3.5 mEq/L What are 4 categories/causes of hypokalemia?
1) Increased urinary/GI Losses (MC) RTA Type I or II, Diarrhea, Vomiting, Diuretics 2) Inadequate Intake (Rare) 3) Increased intracellular shifts Metabolic Alkalosis, Insulin 4) Hypomagnesemia
Which fluids are good for IV bolus/volume resuscitation therapy? (3)
1) NS (0.9%) 2) LR 3) Colloids-Albumin
The 2 main types/etiology categories of hypernatremia are?
1) free water loss (MC) (hypovolemic, with high relative Na conc-hypertonic) 2) hypertonic sodium gain (LC) (no change in volume status--euvolemic, but hypertonic due to added sodium)
Normal AG
12-18 THINK 12
Why do you see metabolic alkalosis and hypokalemia in Cushing's Syndrome?
2/2 glucocorticoid (cortisol)-induced excessive mineralocorticoid activity (cross-reactivity w/ receptors) HTN + increased aldosterone--> lose K to retain Na and water When you lose K you also lose H ALKALOSIS
Normal blood HCO3- range
22-26 THINK 24
Damage to the proximal tubule in Type II Proximal RTA, decreases the Tm (transport maximum) from ___ to the midteens. If the Tm for bicarb is only 15, for example, the serum bicarb is higher than the Tm so bicarb (leaves or enters) the urine? Eventually the loss of bicarb into the urine results in low serum HCO3 and therefore low filtered HCO3 which does what to the urine pH?
28 enters (spills into) the urine from the damaged proximal tubule Lowers urine pH
What fluid do you use for ACUTE/SEVERE, symptomatic hyponatremia (<120)?
3% NS
What is the pathophysiology like for Type IV Distal RTA?
Aldosterone plays a key role in H+ secretion by stimulating the ENac in principal cells. Low aldosterone state leads to less retetion of sodium and water and greater retention of K+ leading to hyperkalemia. H+ is also retained so you get acidosis. Na+ wasting. BUZZWORD: Diabetic Nephropathy HTN is a clue
The urine anion gap is a marker of urine ____ excretion.
Ammonium
What antifungal med can cause a non-AG (hyperchloremic) metabolic acidosis?
Amphotericin B (RTA Type I)
What happens in Sjogren's Syndrome? What is kerojunctivitis sicca? What is xerostomia?
Autoimmune disorder characterized by destruction of salivary and lacrimal glands Sicca: dry eyes 2/2 hypofunctioning lacrimal glands Xerostomia: dry mouth 2/2 hypofunctioning salivary glands
What are some common causes of Type I Distal RTA?
Autoimmune: SLE, Sjogren Hereditary Hypercalciuria Hyperparathyroidism Vitamin D Overdose Amphotercin B Lithium Topiramate
What things cause potassium to shift from the blood vessels (ECF) to inside cells?
B-agonists Insulin (K goes w/ glucose) Alkalosis
What is a complication of Type II Proximal RTA?
Bone destruction common Kidney stones rare in prox. RTA When the pH falls, bones release HCO3 as a buffer. Leads to conversion of Vit D to calcitriol which leads to hypocalcemia and secondary hyperparathyroidism.
What are some complications associated w/ Type I Distal RTA?
Bone destruction common Sones are common low pH, bone release of HCO3, phosphate as buffers to neutralize the excess hydrogen ions, results in bone destruction Bone destruction increases calcium excretion in urine and this predisposes patients to kidney stones
What are some causes of respiratory alkalosis?
CNS disease hypoxia Anxiety Mechanical Ventilator Progesterone Salicylates Sepsis Hyperventilation--blowing off CO2 rapidly trying to get O2
What is the go to IV fluid for hypernatremia tx?
D5W But an use Half NS ((.45%) too
For treatment of hypernatremia, the only appropriate fluids are those that are HYPOTONIC bc the patient already has a high concentration of solute in their blood. What are 2 fluid types you could use?
D5W or Half NS D5w is tx of choice-virtually free water Half Normal Saline (0.45%) bc it is hypotonic compared to plasma osm
Which fluids are good for volume maintenance?
D5W/Half NS (0.45%) Provides some calories from the dextrose Provides free water for insensible losses Provides some Na to promote renal function + excretion Also good post op bc you can add K to the IV if needed (prevents catobolism) Considered hypertonic fluid but great for IV maintenance therapy
What are some causes of an AG (high) metabolic acidosis?
DKA Uremia Lactic Acidosis (Sepsis) ETOH Ethylene GLycol Rhabdomyolysis Renal Faillure EXCESS of something is produced in each of these cases leading to a high Anion Gap
In hypothyroidism would you see increased or decreased DTR?
Decreased DTR
The solution by which you admin the KCL to replete K stores in hypokalemia should not contain what?
Dextrose. You want a vehicle solution that is dextrose frree to prevent transient reduction in serum K d/t enhanced endogenous insulin secretion that would be induced by dextrose. High insulin moves K into cells w/ glucose and this would make the hypokalemia worse Vehicle solution could bee half-normal saline (.45%) (good for maintenance therapy and easy to add K to)
How would Diabetes Insipidus and SIADH impact sodium levels?
Diabetes Insipidus: HYPERnatremia, losing water & not able to recapture d/t lack of ADH SIADH: HYPOnatremia, too much reasb of water, dilutes plasma sodium conc. Both are relative issues, the Na levels don't change, its the water causing the problem by diluting or concentrating!
How to tx Type IV Distal RTA (hyperchloremic metabolic acidosis 2/2 low aldosterone, hold onto K and H, lose Na and H20).
Dietary K restriction bc patient is hyperkalemic Withdraw K retaining drugs Fluodrocortisone (combined w/ diuretics and HCO3)
Hyponatremia: <135 What are the 4 etiology categories/causes of hyponatremia?
HYPOTONIC ISSUE, TRUE: 1) Kidney can't get rid of water d/t increased ADH 2) Increased free water intake ISOTONIC, NOT TRUE: 3) Lab error/artifact 2/2 high TG or protein levels in blood HYPERTONIC, NOT TRUE: 4) Osmotically active molecules in vascular space
You should measure a urine osmolality in patients with hypernatremia. What should be on your differential if: Urine osmolality is high Urine osmolality is low
High UOsm: lots of solute in urine w/ little water, body is compensating by reabsorbing water d/t hypovolemic hypertonic state Extrarenal Fluid Loss (Diarrhea, vomiting, dehydration, etc.) Low UOsm: dilute urine, unable to compensate for hypertonic state, not absorbing water to correct Diabetes Insipidus
In hypovolemia hypotonic hyponatremia, the cause can be extrarenal or renal. How do you differentiate between the 2 with urine sodium levels?
High urine sodium levels >20 in renal cause: diuretics Low urine sodium levels <10, FeNA <1% in extrarenal causes: sweating, GI loss, dehydration--reabsorbing sodium to try to help w/ hypovolemic state and capture water
Why do you see metabolic Alkalosis in Conn's Syndrome?
Hyperaldosteronism 2/2 adrenal adenoma (secreting aldosterone) Retain Na and H20 lose K and H ALKALOSIS
Normal Anion Gap Metabolic Acidosis is also called?
Hyperchloremic Metabolic Acidosis Caused by a loss of HCO3- either from GI (diarrhea) or renally (RTA)
Hyper or Hypokalemia? nausea vomiting intestinal colic areflexia weakness flaccid paralysis arrhythmias paresthesias
Hyperkalemia For Hypokalemia you would see: fatigue muscle weakness/cramps ileus hyporeflexia paresthesias rhabdomyolysis ascending paralysis
Your patient presents with severe muscle weakness, respiratory distress, polyuria, and decreased DTR. They report recent hx of palpitations. She has been vomiting profusely for the past week. What ELE abnormality are you thinking about?
Hypokalemia In cases of severe vomiting, you lose GI HCL, this can cause metabolic alkalosis. You hold onto H+ which means you get rid of K+ in the urine leading to hypokalemia.
What is the most lifethreatening problem to be fixed first when a patient presents w/ Type I Distal RTA?
Hypokalemia It can results in arrhythmias and respiratory depression. Tx w/ bicarbonate first could worsen her hypokalemia by causing rapid shifts of K into the ICF and increased urinary K excretion.
In which ELE abnormalities would you see decreased DTRs?
Hypokalemia (low K) Hyponatremia (low Na) Hypercalcemia (high Ca) Hypermagnesemia (high Mg)
The only TRUE kind of hyponatremia is associated with INCREASED free water. Therefore it is a state of _________ (hypertonic, isotonic, hypotonic) hyponatremia.
Hypotonic
If the combined sodium and potassium levels in your urine are less than the amount of chloride, then you have a positive or negative anion gap, and what does this mean?
If the Na+ K < Cl, then you have a NEGATIVE AG. This means that there is something else not being accounted for in the measurement, the cation: AMMONIUM is present making it appear that the Cl is higher than the combined cations (Na and K) in the urine.
Which patients are most at risk for severe hypernatremia?
Impaired thirst mechanism or appropriate water intake was not possible or thirst went unrecognized: infants, elderly, debilatated patients
In Type I RTA is the urinary NH4+ low or high?
It is LOW. means that the tubular cells are not buffering the acidosis by making titratable acid like they normally would, get more alkaline urine.
What happens to the urine pH with Type II Proximal RTA?
It is initially okay and then becomes acidic
Can you use 0.9% NS to treat hypernatremia?
No!
What cholinergic drug do you prescribe to help patients with xerostomia to increase lacrimation and salivation?
Pilocarpine
What are some causes of respiratory acidosis?
Pneumonia Airway obstruction Pneumothorax Pulmonary Edema CNS depession COPD Restrictive Lung Disease Can't get rid of your CO2 d/t bad lung fxn
Name the condition: a net decrease in either tubular proton secretion or bicarbonate reabsorption that leads to a non-anion gap metabolic acidosis.
Renal Tubular Acidosis
A positive AG in which the Na + K > Cl means that there isn't an extra cation present like NH4+. A positive urine AG should make you think about what kind of process?
Renal Tubular Acidosis! Suggests low urinary NH4 not upregulating renal excretion of ammonium (weak acid) to compensate for the acidosis
What is the MC case of hypokalemia?
Renal or GI loss
High CO2 PH < 7.4
Respiratory Acidosis
Low CO2 pH >7.4
Respiratory Alkalosis
What are the S/E of pilocarpine?
SLUDD-C Salivation, Lacrimation, Urination, Defecation, Digestion, Constriction of pupil
How should you treat Type I Distal RTA (hyperchloremic metabolic acidosis 2/2 impaired H secretion in distal renal tubule)?
Small amount of HCO3 K supplementation as needed
The 2 main presenting sx of hypernatremia if physiological correction mechanisms are not impaired are: Thirst Weakness & Hyperreflexia Neuro Changes: seizures, AMS Why would you see each sx?
Thirst (trying to inc H20 to correct the concentrated plasma-hypertonicity) Seizures + AMS (hypertonicity of plasma causes water to shift from brain cells--they shrink) Weakness + Hyperreflexia 2/2 brain changes + less stimulus needed to reach action potential threshold so increased DTR
In which patients should you NOT use kayexalate for hyperkalemia tx?
Those w/ GI difficulties bc it causes intestinal necrosis if used w/ soorital, so don't use in patients w/ constipation or bowel obstruction.
When would be a good time to give a patient a colloid solution such as Albumin 5%?
To Replenish Volue HYPOTENSIVE Patient to increase BP Downside: expensive
For isovolemic hyponatremia like SIADH, how do you tx the patient?
Tx the condition Fluid restriction <1.5L /d is the MAINSTAY OF SIADH TX If hyponatremia is SEVERE, then admin IV hypertonic saline (3% NS) w/ furosemide. Can also use Demeclocycline (inhibits ADH)
H+ Secretion in the Distal Tubule Low Serum K+ Urinary pH >5.3 Associated w autoimmune disorders Complication: Nephrolithiasis (high ca)
Type I Distal RTA
If you have hypokalemia and suspect a RTA process this narrows your differential down to which 2 types of RTA?
Type I Distal RTA Type II Proximal RTA Both have hypokalemia
HCO3- reabsorption in proximal tubule Low Serum K+ urinary pH starts 5.3, then decreases once serum is acidic Associated w/ multiple myeloma, amyloidosis Complication: osteomalacia, rickets (low Ca)
Type II Proximal RTA
If you see glucose in the urine and the patient is not a diabetic which kind of RTA should you expect?
Type II Proximal RTA Glucose, AA, phosphates, H20, Na, etc. are all absorbed in the proximal tubule, so if you are losing glucose this part of the tubule is probably damaged
Hypo or Hyper kalemia is common w/ Type II Distal RTA and why?
Type II RTA is associated w/ Hypokalemia. Increased bicarb loss (anion) means that sodium is entering cells and K+ (cation) leaves for balance. The increased distal flow quickly washes away secreted K. h
Aldosterone deficiency or resistance High serum K+ levels Urinary pH <5.3 associated w/ renal insufficiency, hypoaldosteronism, ACEI/ARBs
Type IV Distal RTA
Now that you have narrowed the differential to Type I or Type Ii RTA base on the presence of hypokalemia, what do you look at next?
Urine pH <5.5 (more acidic): Type II Proximal RTA bc you can't reabsorb hco3- so eventually get low serum bicarb which means low filtered bicarb and more acidic urine >6 more alkaline urine: Type I Distal RTA bc you are holding onto H (acidosis) and getting rid of K
Normally, the proximal nephron ______ (excretes/reabsorbs) HCO3-. Normally, the distal nephron ______ (excretes/reabsorbs) H+. Normally, aldosterone facilitates ______ (excretion/reabsorption) of H+ bound to ammonia in the distal tubule/collecting duct.
proximal: excretes HCO3 (helps acidify and remember than proximal is the main absorption segment of the nephron) distal secretes H (acidifies urine at the end) aldosterone promotes excretion of H and K for reabsorption of water and Na, the H is excreted bound to ammonia