Glossary of Lab Medicine Midterm UCSD SSPPS

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Negative predictive value definition?
Fraction of negatives which are correct. =(true negatives)/(true negatives + false negatives)
Postive predictive value definition?
Fraction of positives which are correct. =(true positives)/(true positives + false positives)
Reference range definition?
Inner 95% of values in a given population (usually disease free for the value)
Sensitivity definition?
Ability to detect true positive = (true positives)/(true pos + false neg)
Specificity definition?
Ability to detect true negatives. = (true neg)/(true neg + false pos)
Definition (and significance for lab tests) of hemolysis, lipemia, and icterus?
Hemolysis is blood cell lysis (deeper red blood). Lipemia is lipids in blood (milky white). Ichterus is bilirubin in blood (greenish). Each of these can interfere with common lab values
Effect of hemolysis on serum Na? K? ALT? folates?
Lowers Na (since there is very little Na intracellurly), but increases K substantially, ALT (transaminases), and folates
Effect of barbiturates on bilirubin levels?
Decrease bilirubin, because barbiturates induce glucuronyl transferase
Effect of liver-toxic drugs on bilirubin?
Liver toxic drugs like APAP increase bilirubin
Effect of opiates on amylase levels?
Opiates increase serum amylase because they constrict sphincter of oddi
Effect of quinidine on digoxin levels?
Substantial increase due to release from muscle tissue and decreased renal clearance
Factors that contribute to intraindividual variation in lab tests?
Circadian rhythms, hydration, activity, stress, posture (hemoconcentration), food intake
What is serum, as opposed to plasma?
Serum is clotted plasma
What is problem with applicability of reference ranges in many hospitals?
They apply to adults, but not children, so must keep this in mind.
In general, what type of lab values are higher in children and neonates compared to adults?
Values that result from immature liver & kidneys, high bone and muscle turnover, and high stress
In general, what type of lab values are lower in children/neonates than in adults?
Values that result from high respiration (crying), immature liver and pancreas, low muscle mass, and immature immune system
Higher or lower in kids? AlkPhos (ALP)
Higher due to high bone turnover
Higher or lower in kids? Ammonia
Higher due to less urea processing in immature liver
Higher or lower in kids? Osmolality
Lower, reason?
Higher or lower in kids? IgA, IgM, IgE
Lower due to immature immune system
Higher or lower in kids? Glucose
Lower due to immature liver lacking glycogen stores
Higher or lower in kids? AST
Higher (due to immature liver?)
Higher or lower in kids? Copper
Lower due to binding to a particular liver protein
Higher or lower in kids? Creatinine
Lower due to low muscle mass
Higher or lower in kids? bilirubin
Higher due to inability to conjugate as well with immature liver
Higher or lower in kids? Creatinine kinase (CK)
Higher due to high muscle turnover
Higher or lower in kids? Cholesterol
Lower due to lack of cholesterol in diet and also immature liver to synthesize it
Higher or lower in kids? Potassium
Higher (reason?)
Higher or lower in kids? GGT
Higher (something about immature liver?)
Higher or lower in kids? Amylase
Lower due to immature pancreas
Higher or lower in kids? Albumin
Lower due to lower synthesis by immature liver
Higher or lower in kids? Thyroid stimulating hormone (TSH)
Higher due to high level of stress stimulating thyroid hormones
Higher or lower in kids? Thyroxine (T4)
Higher due to stress-induced stimulation of thyroid
Higher or lower in kids? Bicarb
Lower due to high respiration (blow off CO2) and immature kidneys
Higher or lower in kids? Haptoglobulin
Lower (immature liver?)
What are false positives?
Values that fall outside the inner 95% distribution (either high or low), but which are healthy
What are false negatives?
Values that fall within the inner 95%, but which actually come from a person with the particular disease
How do sensitivity and specificity affect each other?
One goes up, the other goes down.
What is positive predictive value (PPV or PV+)?
How reliable the detection of a disease is using a certain test. It is the true positives divided by all positives (both true and false)
What is predictive value negative (NPV or PV-)?
The fraction of negative tests that are true. So, true negatives devided by all negatives (true and false)
How does prevalance of a disease affect the specificity, sensitivity, PPV, NPV?
prevalence is proportional to strength of predictive value, but has no effect on sensitivity or specificity.
How to know if a particular patient’s lab value has changed significantly?
If it has changed more than 3 times the standard deviation of the assay, then you can be 95% confident that the value has changed significantly
Difference between random analytic variation and systematic error?
Random analytic variation is inevitable, and all points will fall in gaussian distribution. Systematic error is when a new variable is introduced like a clogged tube, deteriorated reagent, etc..
How to know whether an erroneous value is due to systematic error or random variation?
95% of controlled test results should fall within 2 standard deviations, and about 1/20 outside of 2 standard deviations, but within 3. If it is random, then the next series of control tests should return to 95% within 2SDs, but if outside still, then it’s a systematic error
How does intracellular location of a cardiac marker affect it’s utility as a marker?
Cytosolic components rach blood faster than structural components
Why does size matter for cardiac markers?
Smaller reach bloodstream faster than large
Besides size and intracelluar location, what other parameter is important for use as a cardiac marker?
Tissue specificity.
What is the time frame for appearance in the blood of the three major cardiac markers following an MI?
First myoglobin (MG), peaks at 6-9 hrs, elevated for 1 day. Then CK-MB, peaks at 18-36 hrs, elevated for 3 days at 2-3x normal. Then TnI and TnT, which peak at 24-36 hrs, and stay elevated for 14-20 days.
What is considered diagnostic of acute, evolving, or recent MI?
Rise and fall of Tn or CKMB plus one of the following: ischemic sxs, Q waves, ECG changes (ST), coronary intervention like angioplasty. Alternatively, pathological findings of MI
Which cardiac marker is most tissue specific?
TnI and TnT
What additional value besides indication of MI, do TnI and TnT have?
Even if no MI, if slightly elevated, it is prognostic of future cardiac event
What about TnC?
It is in both smooth and cardiac muscle, so not specific
Differences between TnI and TnT? High in any other condition?
There is only one assay for TnT, so less variability between labs. Also, TnT is elevated in 60% of end stage renal disease, but not due to MI, but predictive of future cardiac events
Which form of CK is predominate in heart?
CKMM (the same as skeletal muscle). However, there is more CKMB in the heart than any other tissue (about 20% of all CK in heart is CKMB). CKBB is on other tissues, and not used as a cardiac marker
What is relationship between creatine, creatinine, and phosphocreatine?
Creatine can either become phosphocreatine (via CK), or spontaneously degrade into creatinine. Creatinine is produced at a rate of about 1-2% of muscle mass per day.
Since high CKMB can be due to skeletal muscle damage, how can CKMB be used more reliably to test for MI?
By using the CK index. It is (CKMB ng/mL)/(total CK activity U/L) x 100. A high index and high CKMB means cardiac damage. A high CKMB, but low index means skeletal muscle damage.
How to interpret values for CKMB and CK index?
Index below 2.5 is normal, above 2.5 is abnormal (suggests cardiac damage). CKMB below 10 is normal, above 10 is abnormal, and depending on index, represents either cardiac damage or skeletal muscle damage
Other reasons for increased CKMB besides MI?
Anything that damages skeletal or cardiac muscle. Such as: myocarditis, muscle trauma, muscular dystrophy, shock, cardiac surgery, surgery, severe anemia, coronary insufficiency, myopathy, drug-induced rhabdomyolysis
how to distinguish between high CKMB levels caused by MI or muscle disease by tracking changes over time?
Take levels three times in 24 hrs to pinpoint peak. A peak in first 48 hrs is more specific for MI, but muscle disease levels usually plateau
How is myoglobin used to diagnose MI?
If patient arrives within several hours of chest pain, myoglobin is taken on admission and 90 minutes later. If it rises at least 25%, then “diagnostic” of MI, but needs to be confirmed using Tn or CKMB
Drug therapy for MI?
Thrombolytics, antiplatelet/anticoagulation, beta-blockers, vasodilators (nitrates), analgesics (if not relieved by nitroglycerin), O2, antiarrhythmics, stool softeners, angioplasty
What is BNP marker used for?
BNP is a ventricle-specific natriuretic peptide used as a marker for CHF. Pro-BNP is released, then cleaved into active BNP and NT-pro-BNP. They are measured using antibodies to those markers. Levels correlate with severity of CHF
How do cholesterol and FAs get sbsorbed, and what steps follow to get to LDL?
Absorbed into gut, made into chylomicrons with B-48, lose a little triglyceride, and FFAs taken up by adipose and muscle. Chylomicron taken up into liver, triglyceride repackaged into VLDL, sent out with ApoC-II, which activates LPL, to put fat FFAs into triglyceride and muscle. VLDL becomes IDL and then LDL where most TGs have been replaced with XOL. If LDL receptors get saturated, plasma LDL increases, gets oxidized, and taken up by macrophages→foam cells
Which lipoproteins require fasting to measure?
LDL and TGs
How can LDL be calculated if not fasting?
LDL=TC – HDL – TG/5 (as long as TG<400)
What is hemoconcentration and how can it be avoided for blood draws?
A decrease in plasma volume resulting in an increase in the concentration of red blood cells in blood. Allow pt to sit for 5 minutes before drawing blood
How often measure LDL in people?
Guidelines say q 5 yrs for everyone over 20yo
Diet as effective as drugs for lowering CHD risk?
Yes, as long as XOL lowered same amount
Guidelines for obtaining baseline XOL?
Two measurements 1-4 weeks apart before starting therapy. ALT, AST, CK should also be obtained. Follow-up should be done 6-8 weeks following therapy initiation
How does LDL goal change with risk factors?
Normal goal is LDL<100. But, if MI or a combo of CV disease and DM, they are considered high risk and the goal is <70. If established CHD or DM, goal<100. If ≥ 2 risk factors (smoking, HTN, HDL<40, family hx, age (men≥45, women≥55)), then goal is <130. If zero or one risk factor, the goal is <160. If HDL is >60, it subtracts a risk factor
Secondary causes of hyperlipidemia?
DM, hypothyroid, obstructive liver disease, chronic renal failure, drugs (progestin, anabolic steroids, corticosteroids)
Is lifestyle changes enough for established CHD pts?
Not if LDL>130. Lifestyle cannot reduce LDL enough, so need drug therapy. Remember goal is <100
What is TLC?
Therapeutic lifestyle changes, like reduced saturated fat and XOL in diet, more plant sterols and viscous fiber, weight control, and increased physical activity
What is metabolic syndrome?
High risk for DM, CHD. Obesity, high TG, low HDL, HTN (>130/85), high fasting BG
Treatment for hyperlipidemia?
TLC for 3 months, recheck labs, then consider drugs (statin, niacin, sequestrant)
Differences between statins, sequestrants, nicotinic acid, and PPARs in changing LDL, HDL, TGs?
All reduce LDL. All increase HDL. All except sequestrants reduce TGs (same or increased).
Examples of PPARs (fibrates)?
Gemfibrozil, fenofibrate, clofibrate. They increase ApoA1, AII, and LPL, but side effects are GI distess, gallstones, myopathy, dyspepsia
Contraindications for lipid-lowering drugs?
They all are contraindicated in liver disease, except sequestrants, which are contraindicated if TG>400
Possible effect of hypothyroid on CK?
Increase 10x due to increased risk for rhabdomyolysis
Interpretation of high potassium?
Can be from cell lysis (blood or muscle)
Interaction between statins and fluconazole?
Both use CYP3A4, so any azoles shouldn’t be used with statins, or else get major rhabdomyolysis
What are LDL level classifications based on <100, 129, 159, 189, and ≥190?
Optimal, near optimal, borderline, high, very high
What anticoagulant should be used on blood collected for electrolyte analysis?
Ammonium heparinate (as opposed to EDTA, citrate, oxalate, or fluoride due to the Na and K in those). Also, some bind Ca and Mg
How do potassium values differ between serum and plasma?
Serum slightly higher due to release of K from platelets, and may be very high in thrombocythemia (high platelets)
How does storage of blood affect K and Na levels?
High K due to release from cells, and low Na due to inhibited Na/K ATPase
How does K change with hemolysis?
For every 30mg/dL increase in PLASMA Hb, K increases 0.1 mmol/L
ADH. Where made? Released by what stimulus?
Hypothalamus→ pituitary, regulated by osmolality. Retains water in collecting duct
Aldo? What does it do, how regulated?
Retains H2O, Na+, and HCO3-. Excretes K+ and H+. released by AngII due to decreased renal perfusion and hyponatremia
What is Addison’s disease?
No adrenal cortex, so no aldo and cortisol (hypoaldosteronim)
What is Conn’s disease?
How to measure anion gap?
Cations – anions = (Na + K) – (Cl + HCO3)
What does large or small anion gap mean?
High anion gap is due to acidemia. A very low anion gap can indicate hypoproteinemia
Major clinical reasons for large anion gap?
DKA, renal failure, lactic acidosis, treatment with citrate, lactate, carbenicillin, penicillin, or poisoning with ASA, salicylates, methanol (formic acid), ethylene (glycolytic and oxaclic acid), paraaldehyde (acetic acid). MEDIE = methanol, ethylene glycol, diuretics (osmotic ones), isoproterenol, ethanol
Clinical causes of very low anion gap?
Hypoalbuminemia, hemodilution (half→half), paraproteins increase positive charge
Formula for calculating serum osmolality?
1.86(Na) + (glu/18) + (SUN/2.8) + 9 This can only be used on serum since anticoagulants other than ammonium heparinate change osmolality considerably
Clinical causes of hyperosmolality?
Dehydration, hyperglycemia/DKA, diabetes insipidus, uremia (high uric acid in blood), ethanol ingestion, anticoagulants used on drawn blood
Clincal causes of hypoosmolality?
Overhydration, SIADH, psychogenic polydipsia
What’s osmol gap?
Difference between measured and calculated osmolality, which if high, might represent ethanol or something else
Causes of hypernatremia?
Dehydration, diarrhea (which can also cause hypoNa), hyperadrenalism (Cushing’s = high aldo, so high salt reabsorption), hyperaldosteronism
Causes of hyponatremia?
Overhydration, diarrhea, intestinal fistula, addison’s disease (hypoadrenalism), renal disease, salt-losing nephritis, uncontrolled diabetes in which ketoacids are lost and combined with Na, dilutional due to hyperglycemia osmotic effect in which 100mg/dL glucose lowers Na 1/6mmol/L, diuretics, SIADH
How can have hyponatremia and at same time TB Na high?
Stuff that causes water-retention (edema), such as results from renal insufficiency, CHF, hepatic cirrhosis with ascites, nephrotic syndrome, protein deficiency
What can cause hyperkalemia?
Hemolysis, tissue damage, renal impairment, shock, uncontrolled DM (tissue breakdown for calories), dehydration, Addison’s disease (adrenocortical insufficiency means no aldo to increase K excretion)
What can cause hypokalemia?
Poor nutrition, prolonged NaCl or glucose infusion, vomiting, GI fistulas, diarrhea, Lg intestine adenomas, aldosteronism, hyperadrenalism, overdose with ACTH and cortisone, familial periodic paralysis, diuretic abuse, laxative abuse
Henderson hasselbach?
pH=pKa + log (HCO3/H2CO3). H2CO3 can be estimated by 0.03 x paCO2
Causes of respiratory acidosis?
Depressed breathing, pulmonary disease, cardiac disease
How does body compensate for respiratory acidosis?
Hb and protein buffering capacity, hyperventilation, reclaim bicarb, make NH3, make phosphate, increase H/Na exchange (put more Na out of cells, and more H in)
Causes of metabolic acidosis?
Overproduction of acids (DKA, lactic acidosis), reduced H+ excretion due to lack of aldo, renal failure, decreased Na/H exchange), excessive loss of base such as by diarrhea of GI fistula
How does body compensate for metabolic alkalosis?
HCO3 buffer system, hypoventilation, decrease Na/H exchange, decrease NH3 production (NH3 is a base), decrease bicarb reclamation
Causes of respiratory alkalosis?
Increased ventilation (can be secondary to fever, high external temp, hysteria, anoxia, or early salicylate poisoning)
How compensate for respiratory alkalosis?
Decrease NH3 production, decrease Na/H exchange, decrease bicarb reclamation
Compensation for metabolic acidosis?
Reclaim bicarb, increase Na/H exchange, increase NH3 production, hyperventilation, HCO3 buffering, increase phosphate formation
Causes of hyperchloremia?
Cl compensates for bicarb changes Dyhydration, hyperchloremic acidosis, (loss of bicarb due to diarrhea or renal tubular acidosis), stimulate respiratory center (loss of CO2), high altitudes
Causes of hypochloremia?
Cl compensates for bicarb changes Overhydration, hypoventilation (CO2 retention), pulmonary disease, chronic renal disease, DKA, adrenal insufficiency (less NE/EPI, so less angII, so less aldo, and since and Na retention is stimulated by aldo, and Cl goes with Na, Cl goes down), adrenal cortex hyperactivity (aldo helps secrete K, and Cl goes with K), too much ACTH or cortisone, metabolic alkalosis, vomiting, gastric fistulas.
Three forms of Ca in the body?
Free Ca (50% ionized), protein bound (40%, usually to albumin), and complexed to small anions (10%)
Three regulators of Ca?
Vit D, PTH, calcitonin
What else need to be monitored when monitoring Ca?
Albumin, since it is highly bound
What’s phophate in the body for?
Part of high energy compounds (ATP, NADP), part o phospholipids, and phosphorylation is ubiquitous
What’s Mg in the body for, and what is common co-presentation with hypomagnesemia?
Co-factor for >300 enzymes, common with hypokalemia
Effects of PTH?
Parathyroid hormone increases serum Ca by increasing bone resorption, and decreases serum phosphate by increasing excretion. It also incrreases vit D3, and is regulated by ionized Ca levels
Effects of vit D3?
Increases serum Ca and phosphate in gut, and in presence of PTH, also increases bone resorption. It also increases resorption of Ca and phosphate in kidneys
Effects of calcitonin?
Secreted by thyroid, reduces serum Ca and phosphate by inhibiting osteoclast activity
Effect of dehydration on kidney function?
Decreased du to lower GFR
What are the 3 species of CO2 in serum?
HCO3, H2CO3, CO2 (It doesn’t include Hb-bound)
How much can HCO3 increase with pCO2 in acute vs. chronic compensation?
A change in pCO2 of 10 can increase by HCO3 acutely by 1, but chronically, by 3.5 (???)
Is serum K a good indicator of body K stores in pts with acid-base disorders?
No, because H displaces K
How are ketones aften detected?
Acetoacetate in urine
How is potassium affected in DKA, and why?
It is high because tissue damage shuts down Na/K ATPase, so K builds up extracellularly to buffer high H+
How is Na affected in DKA, and why?
Low because gets conjugated to ketoacids for excretion. Also, extra glucose in blood in osmotic, so blood gets diluted with extra water
How does DKA affect fluid status?
Hypovolemia due to polyuria, also leading to a decreased GFR
What is effect of insulin on K?
Stimulates K entry into cells, so if DKA pt receives insulin, give KCL too
What is a known side effect of the chemotherapeutic alkylating agent ifosfamide?
Renal tubular acidosis (can cause renal insufficiency and potentiate DKA in diabetics)
What’s isothenuria?
Urine with a fixed specific gravity (1.008 to 1.012). this indicates inability of the kidney to dilute or concentrate the urine. If urine can’t be more concentrated than specific gravity of 1.025 or 875mOsm/Kg, then can’t concentrate. If urine osmolality is always within 50mOsm/kg of plasma, then indicates isothenuria as well
How does hepatic function affect SUN?
Decreases it since most urea is produced by hepatocytes
Why urea clearance not useful?
40-70% gets reabsorbed passively in renal tubule
How does diet affect SUN?
Low protein diet, avg SUN =5, normal protein diet SUN=12, high protein diet SUN=22
SUN as an indicator of renal function?
Not a good indicator because renal function must decreae 50% before SUN increases
How much creatinine goes into urine each day?
Men 1.5g/day, women less, athletes more
How to calculate creatinine clearance (GFR) from Ucre, Scre, and BSA?
=(Ucre/Scre) x V x (1.73/BSA). V=urine flow (ml/min). Normal GFR is about 100ml/min
How well does serum cre estimate creatinine clearance with changes in renal function?
As # of nephrons begin to decrease, just small changes in serum cre represent large changes in creatinine clearance, but as disease progresses, a comparable change in serum cre will change cre clearance a lot less
How good of an estimate is creatinine clearance of GFR?
Good for healthy or slightly impaired kidneys, but overestimates for severe kidney disease due to increased proportion of urine creatinine deriving from tubular secretion instead of filtration
How to estimate GFR from age, weight, and serum creatinine?
(140-age)(weight)/(Scre x 72) If female, multiply whole thing by 0.85
What are three most common contributors to hyperosmolality?
Na, Glucose, BUN
How does SIADH affect osmolality?
urine hyperosmolality, blood hypoosmolality
What is normal SUN/creatinine ratio?
Normal ratio is about 12-20. The assay can change this based on specificity
What can increase SUN/cre ratio?
Prerenal azotemia and high protein diet can increase it to 30-35. Also, muscle wasting, or GI bleeds, trauma, and intraperitoneal extravasation of urine all can increase availability of urea. Also, increased tubular reabsorption occurs when GFR is low such as with dehydration, shock, renal disease, low C.O., postrenal obstruction, acute glomerulonephritis, nephrosclerosis
What can decrease SUN/cre ration?
Decreased urea synthesis such as chronic glomerulonephritis, starvation, hepatic insufficiency, protein deficiency. Also with decreased urea absorption due to overhydration and rapid hydration. An important case is in hemodialysis in which more urea gets removed than creatinine
What are prerenal, renal, and postrenal azotemia?
Prerenal is decreased renal blood flow (for whatever reason), renal is renal damage, and postrenal is an obstruction to flow of urine (BPH, tumor)
What is selectivity ratio for renal function?
IgG clearance/albumin clearance. If poorly selective, ratio will be low, and changes minimally with glomerulonephritis. If highly selective, ratio will be high
Similarities/differences between chronic and acute glomerulonephritis?
Acute has high SUN/cre (>20), chronic is low (<10). Both have uremia, acidosis, proteinuria, hematuria, and decreased GFR. However, chronic has hypoNa, K, Ca, PO4 (in blood), high serum alk phos (ALP), isothenuria, and cylindrical casts in urine. Acute has red cell casts.
What is macroscopic vs microscopic hematuria?
Macroscopic is red urine, microscopic is smoky urine. They are both characteristic of acute glomerulonephritis. Chronic has episodic hematuria
Lab findings for nephrotic syndrome (nephrosis)?
*Diagnostic* TRIAD (proteinuria, hypoalbuminemia, hyperipidemia), plus edema, and normal GFR and SUN/cre ratio (amounts are normal too). Hyperlipidemia is due to stimulation low oncotic pressure → VLDL production. There is also low hepatic proteins. Low urine volume, red and white cells in urine as well as granular and hyaline casts, especially with fat and oval fat bodies. Finally, thyroxine binding globulin is low, so T4 is low too, but thyroid function is normal.
Lab findings for pyelonephritis?
Normal urea, cre, uric acid (and normal SUN/cre), normal GFR. In urine: pus, microhematuria (smoky), white cell casts, bacteriuria. Leukocytosis in blood
What does an SUN/cre of >20:1 indicate?
Prerenal failure. This is because low flow in tubules allows more reabsorption time for SUN. Renal failure sometimes stays same as normal (10:1), or variable
What is the macroscopic exam of urine?
Color and turbidity
What is tested in chemical test of urine?
Specific gravity, protein, glucose, ketones, Hb (myoglobin also reacts), bile, urobilinogen
What is tested in microscopic test of urine?
Casts, mucous threads, parasites, ova, foreign bodies, # red cells, white cells, epithelial cells, bacteria, yeast, trichomonas, crystals
What protein are cell casts made of?
Tamm-Horsfall protein
What are hyaline casts?
Entirely Tamm-Horsfall protein, excreted by kidney in small amounts, seen in all renal diseases associated with benign HTN and nephrotic syndrome
What are leukocyte casts?
Formed when white blood cells cross tubular epithelium from blood. They are seen in pyelonephritis
What are red cell casts?
Seen when severe injury to glomerular basement membrane has occurred. They are reddish-orange. Associated with acute glomerulonephritis, and others
What are renal epithelial casts?
From sloughing off of tubular epithelium, indicate nephrotoxic damage or some viruses
What are granular casts?
Formed from breakdown of cellular casts and immunoglobulins, and they progress from course and granular to finely granular
What are waxy casts?
Result from progressive degerneration of cellular casts and are associated with severe chronic renal disease
What are fatty casts?
Due to leakage of lipoproteins through glomerular filtrate. Are associated with nephrotic syndrome, DM, damaged renal tubular epithelial cells
What do calcium oxalate crystals look like, and what do they indicate?
Envelopes, they are normal, esp with vit C
What do sodium urate crystals look like and what do they indicate?
Whetstone needles, common with gout
What do cystine crystals look like and what do they indicate?
Hexagons, associated with bad tubular disease (swan-neck). Can be genetic deficiency in metabolizing cystine
Possible Side effect of levaquin that we learned in our cases?
Can cause renal lesion due to hypersensitivity → immune complexes clog up glomerulus → renal failure
What considerations should be made before using tenofovir?
Renal function. If GFR<60ml/min, then no. or if Scre>1.5, then no tenofovir
Term for lack of production of stomach acid?
How do a basal gastric acid secretion test?
Fast 12 hrs, then aspirate the residual acid
Explain the pentagastrin stimulation test? And interpretation?
Synthetic pentapeptide (has four c-terminal AAs of gastrin plus alanine, to stimulate gastric acid. Pernicious anemia and some carcinomas will results in achlorhydria. Hyperacidity is seen in duodenal cancer, but there is overlap with normal values.
5 causes of hypergastrinemia?
ZE, hypersecretion by g-cells, pernicious anemia, vagotomy, chronic renal failure. Which ones increase acid? ZE and hypersecretion by G-cells. Renal failure is veriable, and anemia and vagotomy decrease acid
How to diagnose H.pylori?
Biopsy (culture ot urease test), C13 urea breath test (produces C13 CO2 via urease activity), immunoassay for IgG to H.pylori
Preferred drug therapies for H.pylori?
Triple: PPI BID plus two of either amoxicillin, clarithromycin, or metronidazole. Quadruple: PPI BID, tetracycline, bismuth and metronidazole
What’s amylorrhea, steatorrhea, and creatorrhea?
Excess starch, fat, and meat in the stool, usually due to malabsorption
Causes of malabsorption?
Pancreatic disease, ZE, liver disease (with cholestasis), intestinal disease (compromised mucosa), resin treatment
How is serum Ca affected by malabsorption?
Low due to lack of albumin to which Ca binds
How it alk phos (ALP) affected by malabsorption?
Elevated due to chronic lack of vit D and calcium which leads to osteomalacia (inadequate mineralization of bone)
How is urea nitrogen affected by malabsorption?
Low due to decreased protein absorption
How is serum XOL affected by malabsorption?
Low due to decreased absorption and decreased synthesis
How is prothrombin time affected by malabsorption?
Lengthened due to lack of clotting factors and lack of vit K
How is glucose tolerance affected by malabsorption?
Flattened due to low glucose
Disaccharidase deficiency?
Lactase, sucrase, or maltase deficiency can lead to malabsorption of carbs
Pernicious anemia?
Can’t make intrinsic factor usually due to lack of parietal cells (so no stomach acid either), so get malabsorption
Intestinal malabsorption problems?
Can be blind-loop syndrome or jejunal diverticulum, both of which lead to bacterial overgrowth. Parasites can also lead to malabsorption
How to test for carb malabsorption?
D-xylose absorption will be decreased, as will disaccharidase test. But Breath hydrogen test will increase
2 ways to test for fat malabsorption?
Fecal fat elevation, or C14-triolein test (which is TG that turns into CO2)
How to test for bacterial overgrowth?
C14-xylose breath test
Schilling test?
Radiolabeled B12, then detect in urine (most common) or other. If decreased, shows malabsorption
What’s celiac disease?
Gluten-sensitivity. Sxs include abdominal discomfort, diarrhea, flatulence, bloating, steatorrhea, weight loss, etc. 90% of patients have HLA-DQ2. Risk is higher if other autoimmune diseases
How can test for celiac disease?
IgA endomysial antibody (EMA) to transglutaminase, which is close to 100% sensitive and 95% specific, biopsy, or just trying a gluten-free diet. For under 3 yo, or others who cannot make IgA, should do an IgG test
Explain the sweat test for cystic fibrosis?
Most reliable test for cystic fibrosis. Sweat chloride is normally <60mmol/L, but in CF, it’s 60-120. It is done by ionophoresis with pilocarpine to induce sweating, and performed after 3 weeks of age.
How are occult blood tests done?
Use peroxidase properties of heme to produce O2 from H2O2. Menstrual blood, nose bleeds, perianal bleeding, and meat in diet can confound result. Also, salicylates, indomethacin, reserpine, colchicine, iron, steroids can cause intestinal bleeding (false positive) and vit C can counter peroxidase activity (false neg)
What’s octreotide?
Synthetic somatostatin (stop secretion of lot s of stuff including gastrin)
How are anemia and celiac disease related?
Celiac disease can cause anemia, and present the same way
What is acute pancreatitis?
Diffuse, enzymatic destruction of the pancreas
What is amylase? Why measured in serum?
Pancreatic amylase measured for panceatic damage
What is chronic pancreatitis?
Chronic inflammation of the pancreas, usually reversible
Why are serum lipase level important?
Another pancreatic enzyme (in addition to amylase) used to measure pancreatic damage
Causes of acute pancreatitis?
More frequent with age, alcholism, hyperlipidemia, biliary disease, or drug-induced (about 2%)
Less specific markers of pancreatitis (other than amylase, lipase)?
Decreased serum calcium, and increased methemalbumin, glucose, bilirubin, TGs
Amylase and diagnosis of acute pancreatitis?
If levels elevate more then 5x upper limit within hours of pain, and then decrease over 2-3 days are diagnostic of pancreatitis. But, amylase isn’t super specific, so need lipase test too. Another cause of high amylase is in ectopic pregnancy (from fallopian tubes in this case)
Shows up as high amylase in serum, but low in urine (due to being too big to be filtered). It’s a benign condition in which immunoglobulins aggregate with amylase. The only problem is that it can mess up a diagnosis of abdominal pain if urine values and lipase aren't considered too.
Pattern of lipase levels following pancreatitis?
Similar to amylase, except stay elevated for up to 2 weeks, and none shows up in urine at all due to full reabsorption.
Other conditions in which serum lipase is increased?
Carcinoma of head of pancreas, alcoholic cirrhosis, severe renal azotemia, adipose trauma, fat embolism, hyperalimentation therapy
What does urine amylase elevation mean?
It is often better than serum amylase since amylase in serum drops off quickly after pancreatitis, and it’s for differentiation of pancreatitis and macroamylasemia. It can also be high due to burns, myeloma, duodenal perforations, or extraperitoneal surgery. However, overall serum amylase test are considerd more diagnostic than urine tests
How does pancreatitis affect serum calcium?
Hypocalcemia, in part by glucagon and gastrin release stimulating calcitonin release from the thyroid, which also leads to calciuria and phosphaturia. Calcium infusions don’t help. If calcium goes below 7mg/dL, it is strongly associated with fatal outcome
How are TG levels during pancreatitis?
Elevated, causing turbidity of serum. Hyperlipidemia can also cause pancreatitis
How is plasma glucose affected by pancreatitis?
Often leads to pancreas burnout (affects endocrine pancreas too), so hyperglycemia, decreased tolerance
Diagnosis of chronic pancreatitis?
Difficult to establish, serum levels variable, maybe long standing sxs of acute
What’s felodipine?
Calcium channel blocker, for HTN
Two sources of alk phos?
Bone and liver (and many others)
How to treat acute pancreatitis?
Abx, antiinflammatories
What's AST?
Aspartate aminotranferase – detect liver damage
What’s ALT?
Alanine aminotransferase – detect liver damage
What’s direct bilirubin?
Conjugated to glucuronate (measurable)
What’s GGT?
Gamma glutamyl transferase, used to differentiate whether high alk phos is due to bone or liver. It is upregulated with cholstasis and esp. by EtOH (ordered by psych commonly)
What’s indirect bilirubin?
Unconjugated, produced from dying blood cells
Tests of hepatocellular damage?
AST, ALT, bilirubin
Test of biliary tract disease?
Alk phos, GGT, bilirubin
Describe utility of bilirubin test? What affects bilirubin levels?
Measures conjugated and total. Hemolysis lowers result. Low values have no clinical significance. Bilirubin increases with fasting, and even more with Gilbert’s syndrome (deficient glucurolnyl transferase).
Causes of high unconjugated bilirubin with normal conjugated?
Hemolysis, (Gilbert’s, Arias, Crigler-Najjar = low or no glucuronyl transferase), immature liver of newborn, cirrhosis.
Causes of high conjugated bilirubin with normal or slightly high unconjugated?
This is usually transient, and associated with cholestasis
Causes of elevation of both conjugated and unconjugated?
Hepatitis, cirrhosis, posthepatic obstruction, Dubin-Johnson (esp. with estrogen, plugs up ductules, so increase conjugated, however there is no problem conjugating, so there is an increase in conjugated unlike Gilbert’s which increases unconjugated. Rotor’s is more severe Dubin-Johnson), drug-induced cholestasis
Bilirubin in urine?
Only bilirubin in urine is conjugated (water-soluble). It shows up as yellow bubbles if >0.7. If only unconjugated bilirubin is high, then no bilirubinemia
What is utility of A/G ratio?
Liver disease can show normal levels of total protein, but albumin is low (because globulins offset it). So, a low A/G ratio is a better indicator of liver disease
What is PT time used for?
Prothrombin time indicates liver function (ability to produce clotting factors). Fibrinolysis is also increased in some hepatic disease due to lack of plasmin inhibitors
Aminoaciduria and liver disease?
Handling of AAs by the liver is impaired, so get aminoaciduria, even to the point of crystals (leucine spheres and tyrosine rosettes)
Blood ammonia and hepatitis?
High ammonia means less taken out of blood, can lead to encephalopathy
AST and ALT?
The most sensitive markers of hepatocellular damage, with ALT more sensitive, and persisting longer
Alk phos goes up when lining of biliary tract is damaged (such as blockage). The rule is if the elevation is less than 3 times normal, it is probably hepatocellular disease. If it is greater than 3 times normal, it is probably post-hepatic blockage
How to differentiate between alk phos from the bone, intestines, liver, and placenta?
Heat at 56F. Placenta is the “Regan isoenzyme”, so it is most stable. “placenta persists”, “bone burns”, “liver lives”. 10% of bone will survive, 90% of placenta will survive.
So: bone<intestine<liver<placenta.
A possible side effect of celecoxib on liver function?
Can rarely cause bilicholestasis. Also very rarely caused by lamisil (terbenifine). But of all cholestasis, 2-5% are drug-induced
What is best use for tumor markers?
Detecting recurrence and monitor therapy. They can screen populations and high-risk groups, and aid diagnosis. Used mainly in carcinoma
What’s an adenoma?
Benign epithelial tumor
What’s a sarcoma?
Connective tissue tumor (usually malignant)
What’s a carcinoma?
Malignant epithelial tumor
What’s AFP test for?
Alpha feto protein, raised in testicular cancer
What’s CA 19-9 for?
Cancer antigen 19-9. A tumor-associated glycoprotein, increased in 80% of patients with pancreatic adenocarcinoma, and rare in benign pancreatic disease
What’s CA 125 for?
Tumor marker for ovarian cancer, especially to detect residual cancer after first-line therapy
What’s CEA for?
Carcinoembryonic antigen. A tumor marker especially for colorectal cancer. It is a bad prognosis if persists with treatment. It can also indicate pancreatic, breast, cervix, uterus, ovary, bladder, lung.
Estrogen and progesterone receptors (ER and PR). What used for?
This is the only cytosolic tumor marker of the ones we learned. It is for breast tumor tissue. If ER and PR are both positive , then hormone therapy is more likely to be successful. ER positive tumors have longer disease-free periods
hCG used for?
Used to detect pregnancy, but can also be positive in trophoblastic cancers such as choriocarcinoma and hydatiform mole, but AFP is normal
What’s PAP used for?
Tumor marker positive in prostatic cancer. Especially useful in monitoring patients with confirmed prostatic cancer
What’s PSA used for?
Tumor marker for prostatic cancer, but also high in BPH. Less free PSA = increased risk for cancer due to complexing with inflammatory proteins like antichymotrypsin. So, this is useful to differentiate between prostate cancer and BPH. Gray zone is >4 and <10. >10 is probably cancer (of non-free PSA)
What’s Her2/neu?
A tumor marker for breast cancer to predict responsiveness to Herceptin (a humanized monoclonal antibody that binds to the Her/neu receptor to disable it.
What’s goserelin?
LHRH agonist, to decrease testosterone in prostate cancer
What’s bicalutamide?
A testosterone receptor blocker for prostate cancer

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