Damjanov Flashcards
Define precision/reliability of a test
Determined by repeating the same test on the same sample
Define accuracy of a test
Reflectts how close measured value is to the true value
Define specificity; sensivity
True negative: [TN/(TN + FP)] x 100;
True positive: [Tp/(TP + FN)] x 100
Define positive and negative predictive value; define EFFICIENCY!
Pos: [TP/(TP + FP)] x 100;
Neg: [TN/(TN + FN)] x 100;
[(TP + TN)/(TP + TN + FP + FN)] x 100
What is the most important electrolyte in the ECV? ICV?
Na; K
For Na, list the percentages where it’s distributed, what makes up the exchangeable sodium, and what the serum concentration of Na normally is
50% in ECF, 40% in bone, 10% inside cells;
made up by all Na in EC and IC fluid and approx 50% in bone;
135-145 mmol/L
How is most Na excreted? Where else is it lost? How is sodium controlled?
Through the urine; some lost in feces and sweat;
- Thirst (osmoreceptors in hypothalamus can increase osmolality of plasma if too much sodium ingested or water lost)
- ADH (if water lost and osmolality increases, ADH stimulates water reabsorption of water in kidney; depletion of intravascular volume can stimulate thirst and ADH)
- Aldosterone: Lose ECV, affects GFR; renin released from juxtaglomerular apparatus, and through RAA aldosterone promotes Na and K/H exchange in distal renal tubules
- ANP: stimulates kidneys to increase Na excretion in urine
What are the three main physiologic processes Na participates in?
- Acid-base balance: binds to anions like phos, chloride, bicarb
- Cell membrane polarity: sodium helps contribute to formation of electric charges across cell membranes; ATPase helps move it out of cell
- Osmolality of body fluids: essential for body fluid osmolality maintenance; if ECF slightly increased, osmoreceptors stimulated, and thirst, ADH release, and water reabsorption in kidneys initiated
Calc serum osmolality; what is an osmolality gap?
Serum osmolality = 2 x Na + (glucose/18) + (BUN/2.8);
measured and observed osmolality discrepancy, usually caused by something like alcohol or ethylene glycol in blood
Define hyponatremia; what are the two types? List them!
DISRS vs. GRD
Serum osmolality < 136 mmol/L;
1. Dilutional
A. Increased water intake (polydipsia, infusion)
B. SIADH
C. Reduced water excretion (heart failure, hepatorenal syndrome, renal disease)
D. Shift of water to ECV (diabetes, multiple myeloma, hyperlipidemia)
E. Hypoproteinemia (cirrhosis, malnutrition, nephrotic syndrome)
2. Depletion
A. GI loss (vomiting, diarrhea, GI fistula, ileus)
B. Renal loss (salt wasting, diuretics, osmotic diuresis, Addison’s disease)
C. Dermal loss (burns)
What are the four broad reasons for why hyponatremia occurs? How should treatment of hyponatremia be directed?
- Increased total body H2O
- Relative increase of H2O in ECV
- Reduced total body salt and water (Na > H2O)
- Increased total body H2O and salt (H2O > Na);
Correction of Na-H2O balance and the hyponatremia causes
How is hypernatremia defined? What are the body’s compensations? What can cause hypernatremia? (4 major categories)
> 150 mmol/L; increased water intake or water conservation through kidneys, and ADH release;
1. Decreased intake of H20 (Lack of drinking water, unconscious)
2. Increased loss of H2O
A. Kidney (diabetes mellitus, insipidus, nephrogenic diabetes insipidus)
B. Skin (sweating)
C. GI (diarrhea)
3. Retention of Na (Conn’s and Cushing’s, corticosteroids)
4. Infusion of Na (Medical: Na2CO3)
Symptoms of hypernatremia? TOIRCAM, HTRL
Thirsty, oliguria, irritability, restlessness, confusion, agitation, muscle weakness;
hypotension, tachycardia, renal failure due to hypoperfusion, lethargic
What is the major anion of plasma and interstitial fluids? Reference range for chloride? When would its metabolism differ from Na?
Cl; 98-106 mmol/L;
Hyperchloremic metabolic acidosis (depletion of HCO3 leads to Cl replenishment)
Hypochloremic metabolic alkalosis (Cl lost in GI tract leads to metabolic alkalosis, with anion gap filled with bicarb)
What is the principal IC cation? Where is most of it found? Reference range? What two factors regulate K excretion? What promotes K secretion into the distal tubule, and what other ion(s) can move?
K; 98% inside cells, 2% in ECF; 90% of IC K is in exchangeable IC pool, and 8% structurally bound to bone, brain cells, and RBC’s;
3.5-5;
Concentration of K in blood and GFR;
aldosterone, with reabsorption of Na
What is renal acidosis associated with? What about renal alkalosis? Excess of H favors exchange of ____ for ____? What can promote K flux across the cell membrane, and what might favor efflux of K from cells?
Hyperkalemia; hypokaelmia; Na, H;
Insulin, diabetes (due to lack of insulin
What causes hypokalemia? (4 broad categories)
- Low intake of K (starvation, anorexia nervosa, alcoholism)
- GI loss of K (vomiting, diarrhea, fistula, laxatives)
- Renal loss of K
A. Diuresis –> (diabetes, diuretics)
B. Hyperaldosteronism and Cushing’s –> (Na retention)
C. Tubular dysfunction –> (End-stage kidney) - Redistribution of K (alkalosis, insulin, familial periodic muscle paralysis)
Consequences of hypokalemia? CNGM
- Cardiac: arrythmia and abnormal cardiac contractions with ECG changes
- Neuromuscular: generalized muscle weakness and hypotonia; lethargy, depression, confusion
- GI: slow peristalsis leading to ileus or constipation
- Metabolic/renal: alkalosis and polyuria
What leads to hyperkalemia? (5 categories) A consequence of hyperkalemia and subsequent treatment?
- Excessive intake (oral supplements, infusion)
- Decreased Renal excretion (End-stage renal failure, minteralcorticoid deficiency, Addison’s, K-sparing diuretics)
- Redistribution of ICV to ECV (acidosis)
- Massive cell injury (burns, crush injury, rhabdomyolysis)
- Tumor lysis syndrome (chemo);
cardiac arrhythmias: ventricular arrhythmia and then v fib, so treat with calcium gluconate and then hypertonic glucose
Normal blood has H concentration of ______ and pH of _____; what two things account for blood’s buffering capacity? When H ions enter the urine, they are linked to ______ and ______;
40; 7.4; Hg and bicarb;
phosphate and ammonia
What does metabolic acidosis result from? How does compensation occur? What causes metabolic acidosis (two broad categories with 4 subcategories each)? DEKALS
Loss of bicarbs and increased concentration of H ion in ECF; decreased pH of arterial blood stimulates central chemoreceptors, provoking hyperventilation;
1. Acidosis with normal anion gap
A. GI loss of bicarbs (diarrhea; GI, biliary or pancreatic fistulae)
B. Renal diseases (obstructive uropaty, renal tubular acidosis, chronic pyelonephritis)
C. Hypoaldosteronism
D. Hyperalimentation
- Acidosis with normal anion gap
A. Ketoacidosis (diabetes, alcohol abuse)
B. Lactic acidosis (tissue damage and ischemia, liver insufficiency)
C. End-stage kidney disease
D. Poisoning (salicylates, ethylene glycol, methanol)
Define the anion gap; what is the normal value?
Na + K - (Cl +CO2); 10 - 20 mmol/L
Causes of metabolic alkalosis? 3 broad categories
- Gastric H loss (vomiting, gastric drainage)
- Renal H loss and HCO3 retention (hyperaldosteronism: Conn’s and Cushing’s if primary, renal hypertenion if secondary; hypokalemia: diuretics, chronic diarrhea; volume contraction (cirrhosis)
- Net gain of HCO3 (absorbable antacids: milk alkali syndrome; ingestion of bicarb: baking soda)
What is respiratory acidosis characterized by? What about respiratory alkalosis?
Retention of CO2 due to hypoventilation; hyperventilation, leading to increased loss of CO2
