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Chemistry Pearls

Terms in this set (79)

How do you remember how the cardiac markers rise and fall?
My Tight Chest
Myoglobin
Troponin, appears in 4 to 8 hours, peaks at 1-2 days and remains elevated for 7-10 days
CKMB appears in 4 to 8 hours, peaks at 1.5-2 days, falls at 48-72 hours
What is the important wavelength to know
340 nm
CK-MB is found in cardiac and skeletal muscle
20% Cardiac and 2% skeletal
Compared to MM which is 80% of the cardiac, however, 98% of skeletal is MM

Though Troponins have replaced CKMB as the gold standard, CKMB is better at sizing the infarct
What are the three physiologic functions of natriuretic peptide hormones?
1. Natriuresis via Na+ excretion and decreased RAAS
2. Diuresis through exretion of Na and thus water
3. Vasodilation via dilatation of venous and arterial vascular beds and inhibition of ATII
What are some of the symptoms of hypocalcemia?
Neurologic, cardiovascular
Tingling sensations, muscle cramps tetany seizures coma, EKG abnormalities, and CHF
PTH
Metabolized to N-terminal and C-terminal fragments
Only the N end is active
The net effect of PTH is to INCREASE Ca in the plasma
What should be measured to evaluate Vit D status?
25 OH D

Increases intestinal CA and phosphate absorptionby stimulating intestinal production of calcium and phosphate binding proteins
How can you tell primary hyperparathyroidism from hypercalcemia of malignancy
In primary hyperparathyroidism, the calcium AND PTH will be elevated
In secondary forms like hypercalcemia of malignancy, the CA is up but the PTH is DOWN.
How does malignancy cause hypercalcemia
1. Secretion of PTH related peptide
2. Tumor production of vit D
3. Tumor is destructive to the bone
What is the differential diagnosis for hypocalcemia?
1. Hypoparathyroid
2. Pseudohypoparathyroidism, end organ resistance to PTH
3. Vit D dif, need to test vit D 25
4. Hypomagnesium AND hypermagnesium, measure urine mag
Acid Base disorders
Remember: H+ + HCO3--H2O + CO2
>Acidemia stim respiration
>Alkalemia hypoventilation to retain CO2
Kidney helps regulat via ammonium excretion to get rid of acid and ALDOSTERONE promotes Na+ resorption
What is the differential diagnosis for anion gap metabolic acidosis?
KILERS
Ketoacidosis
Ingestants including methanol, isopropyl alcohol, ethylene clycol
Lactic acidosis
Ethanol
Renal failure and rhambdomyolysis
Saliscylates (aspirin)
What is the quick and dirty way to solve acid base disorders?
Just remember a change in PCO2 by 10, normal 40, should result in an inverse change in pH of 0.08.
What are the normal values for acid base?
CO2 40
pH 7.4
HCO3 25
What is the differential diagnosis of increased urea?
1. increased production; high protein diet, GI bleed, hypercatabolism, hyperthyroidism
2. Prerenal azotemia; decreased effective circulating volume; dehydration, CHF, cirrhosis
3. Renal disease; glomerular and tubulointerstitial
What is the Jaffe method of creatinine measurement
creatinine + picrate ion --> RED derivative
the test is notorious for interferences from ascorbic acid, protein, glucose, ketoacids, and drugs
if suspect Jaffe interference, can confirm with enzymatic testing
Creatinine measurement is used for estimating index of glomerular filtration/function cause it is relatively constant and proportional to body weight
What is ddx of proteinuria?
1. glomerular; selective (albumin) or non-selective (all)
2. overflow of specific proteins such as BJ
3. Tubular cause with low molecular weight proteinuria seen in cystic renal disease, pyelo, obstructive renal disease, and interstitial nephritis
4. orthostatic
Three major categories of acute kidney injury
1. pre; decreased ECV
2. intrinsic; atn, renal ischemia, glomerulonephritis, vascular
3. post renal; urethral or bladder obstruction
What are some common causes of ATN?
Toxins! aminoglycoside amphotericin B to name a few
Keys for differentiating prerenal from ATN
1. Osmol; pre will be high (>500) and ATN will be low (<350)
2. Urine sodium; pre will be low (<20)
3. BUN:CREAT Ratio; Pre >20:1
4. UA; ATN will have casts and cells
Assuming intrinsic renal, how to differ among ATN, glomerular, and interstital
What is characteristic of ATN?
EPITHELIAL CASTS
Assuming intrinsic renal, how to differ among ATN, glomerular, and interstital
What is characteristic of GLOMERULAR?
OVAL FAT BODIES, RBC casts, and marked proteinuria
Assuming intrinsic renal, how to differ among ATN, glomerular, and interstital
What is characteristic of INTERSTITIAL?
WBC Casts
FENA calculation
FENA=[URINE SODIUMPLASMA CREAT]/[PLASMA SODIUMURINE CREAT]
Why are nephrotic syndrome people edematous?
SALT WASTING AND WATER RETENTION
What is the difference between effective circulating volume and extracellular fluid?
ECV is the portion of ECF that perfuses the tissue; ECF is all fluid outside of cells
What is the major cation of ECF?
Sodium;
Its concentration is regulated by water balance via ADH
Volume is in turn regulated by sodium via aldosterone
Calculation for osmol
OSMOL=2xNA + GLU/18 + BUN/2.8
Normal osmol is 280-296
What are some common causes of hypernatremia?
Hypernatremia, decreased water to sodium balance can be due to sodium gain and or water loss
extensive diaphoresis, fever, burns
defective renal concentration DI
What is central versus peripheral DI?
Central; decreased ADH
Peripheral; nephrogenic which is decreased response to ADH

These are separated via the H20 deprivation test
Explain how vasopressin can separate central and nephrogenic DI
Central; good response to DDAVP (vasopressin), so the problem is amount of ADH being produced and not response to it
NOTE: may not get maximal response due to renal medullary washout
Nephrogenic; Will not see a response to DDAVP
What is the differential for HYPOnatremia?
The most common cause of hypoosmolality hyponatremia is SIADH
SIADH can be due to a number of things both hypothalamic or pulmonary

Be aware of pseudohyponatremia, tip off is normal osmolality, could be hyperlipidemia, hyperproteinemia. The instrument just takes a fixed amount of fluid and measures the sodium, easy to explain why it would seem to be a lower concentration in these scenarios
What is the differential diagnosis for SIADH
1. hypothalamic; CNS infection, vascular disorders, tumor
2. Pulmonary; pneumonia, TB, respiratory failure
3. Ectopic ADH; most commonly small cell carcinoma (lung) but other NE tumors too
4. Drugs; phenothiazines, carbamazepine, bromocryptine, amytriptyline, oxytocin
Thyroid T3 and T4
T4 Thyroxine most abundant and more stable
T3 Triiodothyronine most ACTIVE
What are T3 and T4 bound to in vivo?
1. TBG: high affinity but only one binding site
2. TBPA: pre-albumin
3. ALB: low affinity
The free component is much less, BUT is the active component
Explain the resin uptake measurement of T3
Labeled T3 can either bind TBG OR resin that is infused
IF there is abundant BINDING CAPACITY then T3 binds TBG and NOT the resin; this is the case in hypothyroidism, TBG will be less saturated

In hyperthyroidism, there is more T3 bound to TBG, not many available binding sites, so the labeled T3 binds the resin instead
WHat is cushing disease and syndrome?
Cushing's syndrome is syndrome of too much ACTH
symptoms and findings: buff hump, moon face, HTN, striae, hirsutism

Cushing's disease is a pituitary adenoma causing the syndrome

Syndrome can also be caused by the adrenals; tumors, adenomas, carcinoma, or idiopathic

Syndrome can also be caused by ectopic ACTH such as seen in small cell carcinoma of the lung
How is cushing's syndrome diagnosed
Dex suppression test--with a confirmatory high dose suppression test
1. Get suppression with elevated ACTH: pituitary cause (PIT), AKA cushing syndrome
2. No suppression but elevated ACTH: Ectopic production of ACTH
3. Suppression and LOW levels of ACTH: Adrenal cause of Cushing's
Discuss adrenal insufficiency ddx and testing
Many things in ddx including primary; idiopathic and autoimmune [most common now], granulomatous disease sarcoidosis [most common in 1920s]; secondary causes such as iotrogenic, pituitary tumors and infarction

Test: ACTH stimulation test [give cosyntropin]
cosyntropin test: if adrenal insuficiency, get blunted response
Next: Metyrapone test: blocks cortisol synthesis and results in increased ACTH or cortisol precursor production [11-deoxycortisol]

If increased ACTH and low cortisol: primary adrenal insufficiency
if decreased ACTH and low cortisol: pituitary cause or tertiary
Congenital adrenal hyperplasia; what are the two key diagnoses and key laboratory findings
1: 21-hydroxylase deficiency; 90-95% of cases
>see increase in 17 hydroxyprogesterone
2: 11-B-hydroxylase; 5%
>see increaed in 11-deoxycortisol

Both disorders are characterized by virilization, female pseudohermaphrotism, salt wasting due to hypoaldosterone, hypokalemia and hypertension
What is important to remember about glucose testing?
Glucose is NOT stable in whole blood samples, get 6-8% drop per hour at room temp
Plasma more stable stable
Serum SUPERIOR
How can you tell what glucose has been running for the last 120 days?
Hemoglobin A1C
normal is 3.8-6.4%
How is DM diagnosed
Need classic symptoms
Random blood glucose >200
Fasting of >125 on more than one occasion
What is significant about DM I that isn't so with DM II
Prone to ketosis and insulin DEPENDENT
Portland protocol for tight glycemic control
Gluc to Units Insulin
<125 0
125-175 1
175-225 2
>225 3
What is the metabolic syndrome?
Abd obesity
Increased triglyceride
Decreased HDL
BP
Catecholamines
EPI-->VMA
Norepi-->VMA
DOPA-->HVA
How can one test for pheo?
Demonstration of plasma catecholamines and breakdown products in urine
Further, clonidine supression test reveals NONsupressable plasma catecholamine levels
Amenorrhea--Testosterone--
Think ovarian tumor
Amenorrhea--DHEAS--
Adrenal tumor
Amenorrhea--17-hydroxyprogesterone
21-hydroxylate dif
Amenorrhea--prolactin
prolactin secreting tumor
ALSO Consider PCOS
PCOS--what labs help?
LH and FSH with at least 2LH:FSH ratio
Prolactin is measured...
Via immunoassay
Noncompetitive
>200 it is a prolactinoma
20-100 is intermediate
NEED MULTIPLE measurements as 1 can be unreliable
Amylase S type can be elevated in...
Ruptured ectopic
Macroamylasemia
1% of population
Seen in patients with autoimmune disease, amylase bound to antibodies
High serum amylase (<5X ULN) LOW urine amylase, LOW amylase clearance ratio
Lipase
More sensitive and specific for pancreatitis
Elevated for 7 to 14 days
cleared by the kidney, elevated in renal failure
What is bioavailability?
Fraction of administered drug absorbed into the systemic circulation
F=Abs(oral)/Abs(iv)
What is typical bioavailability for PO drugs?
70%
DIscuss Free versus bound DRUGS?
Drugs commonly bind proteins in the ECV. The free drug is the relevant drug that is available to bind receptor
Decreased drug binding protein means decreased total drug and increased free drug
Volume of distribution
Hypothetical volume necessary to dilute the drug
What has a higher volume of distribution, lipid soluble or water soluble?
Lipid soluble because they distribute into all of the body fat weight
Water soluble drugs tend to stay in the blood, so low vol of distribution
PEAK BLOOD CONCENTRATION
Cp=dose/Vd
what is the total body water by %
60%
What is ICF versus ECF?
2/3 to 1/3
What component of the ECF is plasma versus interstitial fluid?
1/4 to 3/4
Which drugs must go first to the liver and then to the kidney for excretion and why?
Drugs that are highly lipid soluble, made polar so that they can be excreted via kidneys
What is phase I versus phase II reaction?
Phase I--occur in liver via cytochrome p450
Phase II--glucuronidation (morphine), glutathione conjugation (acetaminophen), and acetylation (isoniazid)
Which cytochrome p450s are important?
For drug metabolism, CYP3A4
To activate codiene, CYP2D6
What happens to patients with mutated CYP2D6?
Unable to activate codiene so they get no analygesia from it
What is significant about CYP2C9?
Increased sensitivity to Warfarin
What is first order elimination
decline in the drug level to a constant PERCENTAGE of the remaining amount per unit time.
>Half life is constant
>Most drugs, in therapeutic range, follow first order elimination; NOT SO IF DRUG IS TAKEN IN TOXIC RANGE
What is zero order elimination
Decline in the drug is a constant AMOUNT per unit of time
>alcohol
>dilantin
>theophylline
>acetaminophen
>salicylates
Briefly explain chromatography
collumn is filled with beads, drug is passed through the collumn and transit time tells what the drug is
1. The most non-polar will elute last, this is the parent compound
What factors will improve resolution in chromatography?
1. increasing the column length
2. increasing the number of particles or smaller particles
3. decreasing difference in polarity between stationary and mobile phases
Ethylene Glycol Poisoning
Antifreeze
Usually measured by gas chromatography

Increased anion gap= (Na+K)-(HCO3+Cl)
Osmol gap=measured-calculated
Calculated osmol=2(Na)+BUN/2.8+GLU/18

Calcium oxalate crystals in urine
Organophosphate poisoning tidbits
1. Common in pesticides
2. inhibit cholinesterase--stimulate acetylcholine receptors:
muscarinic (urination, miosis, salivation)
nicotinic (tachycardia, HTN, muscle cramping)

Antidote is 2-PAM (pralidoxime)

Acetylcholinesterase is present in RBCs
What is the treatment for acetaminophen overdose? What are its kinetics?
N-acetylcysteine (Mucomyst)
0 order which means you are able to clear a certain amount each hour
What is the metabolism kinetics of phenytoin?
Zero order
HIGHLY protein bound to albumin (90%); SO BEWARE IF HYPOALBUMIN
This is an indication for measuring free dilantin
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