Cp - Chemistry I - Osler

Front 1

Describe Lineweaver-Burke plot

Back 1

Plot of enzyme kinetics
y-axis: 1/velocity
y-interecept: 1/Vmax
x-axis: 1/substrate concentration
x-intercept: -1/Km
(Km is the concentration of substrate that leads to half-maximal velocity; aka "Michaelis-Menton constant")

Front 2

Describe the types of inhibition in a Lineweaver-Burke plot

Back 2

Competitive inhibition: Vmax does not change. Competes with substrate for binding but can be overcome as increase substrate concentration. x-intercept changes.

Non-competitive inhibition: Vmax changes. Cannot be overcome by increasing substrate concentration. y-intercept changed; x-intercept does not.

Uncompetitive inhibition: Rare. Binds enzyme-substrate complex & stabilizes. changes BOTH x&y intercepts.

Front 3

Michaelis-Menton equation

Back 3

-Measurement of enzyme activity
-Rate of enzyme activity varies with substrate concentration, until saturated (Vmax)
-At saturation, Vmax varies only with enzyme concentration
-Km = substrate concentration at half-Vmax

Front 4

What are the units used to express enzyme activity?

Back 4

IU = amt enzyme catalyzes conversion of 1 micromole of substrate per minute

1 katal = " 1mole of substrate per sec

1IU = 16.7nanokatals

Front 5

What are the differences between ALT & AST?

Back 5

ALT: LIVER & kidney; cytoplasmic; >AST in adults

AST: heart, liver, skel m, kidney, brain, lung, pancreas; cyt & mt (80%)

Front 6

How many isoenzymes of LDH are there?

Back 6

5

LD1,2 in heart, RBCs, kidney
LD3 in lung, spleen, lymphs, panc
LD4,5: liver, skel m
(LD6 - dire finding - hepatic vasc insuff)

Front 7

Compare LDH isoenzyme concentration between serum & CSF.

Back 7

Serum: 2>1>3>4>5

CSF: 1>2>3>4>5

Front 8

What are the possible causes of serum LD1>LD2?

Elevation of LD4&5?

Elevation of LD1&5?

Back 8

MI, hemolysis, renal infarction

Liver damage, skel muscle

Acute MI + liver congestion OR chronic ETOH + liver damage + megaloblastic anemia

Front 9

Where is alkaline phosphatase produced?

Back 9

Bone (OSTEOBLASTS!), bile ducts, intestine, placenta

Marker of bone-FORMING activity
Eating can factitiously elevate alk phos up to 30%

Decreased in malnutrition

m>f

Front 10

How can we tell the source of alk phos?

Back 10

Has 4 isoenzymes by e-phoresis that have unique degrees of inactivation by heat, urea, & l-phenylalanine.

** BONE BURNS: 90% inactivation of bone alk phos with heating; 0% of placental; 50% biliary

Front 11

What is the Regan isoenzyme?

Back 11

Identical to placental alk phos; Found in 5% ppl with carcinoma

Front 12

Common clinical situation associated with mildly elevated alk phos

Back 12

Pregnancy
CHF
Hyperthyroidism
Drug (ibuprofen, acetaminophen)
anti-mitochondrial antibodies (middle aged women)

** Sensitive marker for hepatic mets

Suspect bone origin without concomitant elevation GGT or 5'nucleotidase (PAGETS, hyperPTH, osteomalacia)

Front 13

GGT source & use

Back 13

Biliary epithelial cell (v sensitive for biliary injury); also hepatocytes

Used to confirm elevated alk phos is coming from biliary tree

Also elevated with toxins (EtOH, warfarin)

Can be used as marker of alcohol consumption

M >> F
Af Am >> W

Front 14

Source & use of 5' nucleotidase

Back 14

Biliary epithelium
Highest in cholestasis
Confirms liver source of elevated alk phos
Less sens than GGT

Front 15

Source & use of ammonia

Back 15

Skel muscle & gut
Made by bacteria in gut from protein; excreted as urea by liver in urine

Hyperammonia = liver failure (inless inborn error urea metab)

Neurotoxic

*Requires fresh spec, chilled during transport, NO HEMOLYSIS

Front 16

Describe bilirubin metabolism

Back 16

Unconj = Indirect = water insol
Binds albumin --> liver --> glucuronidation to Conj (Direct) --> excretion into bile --> converted to urobilinogen by intest bacteria (some to kidney) --> colonic bact converts some to brown pigment

** BILIRUBINURIA = CONJ HYPERBILI as unconj never in urine

Front 17

Unconjugated hyperbilirubinemia DDx

Back 17

Hemolysis
Blood shunting (cirrhosis)
R heart failure
Gilbert syndrome (not taken up into hepatocyte)
Drug(rifampin)
Crigler-Najjar (Not conjugated)
Hypothyroid

Front 18

Conjugated hyperbilirubinemia DDx

Back 18

Mechanical obstruction (PBC, PSC, stricture, stone) (CHOLESTATIC jaundice)
**>3x upper nl alk phos, elevated cholesterol, pruritis, mild elev transaminases

HEPATOCELLULAR jaundice (Not secreted: Dubin-Johnson, Hepatitis, Endotoxin/sepsis, Pregnany/Estrogen, drug-E, cyclosporine)
**>3x upper nl transaminases, nl cholesterol, no pruritis, mild elev alk phos

Front 19

Methods of bilirubin measurement

Back 19

1)Diazo-colorimetric methods: Measures conjugated; with accelerator can measure total (unconj is then estimated)

2) Direct spectrophotometry: Measures total bili; absorbance at 455 nm - that at 575 nm (hgb interference)

Front 20

What is delta-bilirubin?

Back 20

Conjugated bilirubin covalently linked to albumin. From prolonged conj hyperbili. Cannot be excreted. May persist long after correction of cause.

Front 21

How does PT measure hepatic function?

Back 21

Most coagulation factors synthesized in hepatocytes (shortest T 1/2 FVII 12 hours)

Impaired bile secretion can lead to vit K deficiency

BEST indicator of px in acute hepatic injury

Front 22

Which immunoglobulins are useful for diagnosing autoimmune hepatitis? PBC?

Back 22

ai: polyclonal IgG

PBC: polyclonal IgM

Front 23

Features of physiologic jaundice in the newborn

Back 23

DOL 2-3; pks at DOL 4-5
Does not rise at a rate greater than 5mg/dL/day

Front 24

Red flags for neonatal jaundice

Back 24

-Jaundice within first 24h
-Rising bilirubin beyond 1wk
-Persistent jaundice >10d
-Total bili > 12mg/dL
-Single-day increase >5mg/dL
-Conjugated bili > 2mg/dL

**severe: HDN, sepsis. Causes kernicterus

Front 25

Pathologic correlates of severe neonatal jaundice

Back 25

Yellowing of subthalamic nucleus, hippocampus, thalamus, globus pallidus, putamen, cerebellar nuclei, cranial nerve nuclei

Front 26

DDx neonatal hyperbilirubinemia

Back 26

1st 24h: erythroblastosis fetalis, hemorrhage, sepsis, TORCH infxn
3-7d: sepsis (UTI)
>1wk: br milk jaundice, sepsis, biliary atresia, CF, Alagille synd (congen paucity bds), neonatal hepatitis, galactosemia, inherited hemol anemia (PK def, HS, G6PD def)

Front 27

Conj vs Unconj neonatal hyperbili

Back 27

Unconj: physiologic, br milk, polycythemia, hemolysis, bowel obst, inherited (GILBERT, C-N)

Conj: Biliary obst, sepsis, TORCH, hepatis, metabolic disorders, inherited (D-J, ROTOR), TPN

Front 28

Use of phototherapy for neonatal jaundice

Back 28

Only works for UNCONJUGATED bilirubin

Use when bili > 10 before 12h, >12 at 18h, >18 at 24h

**Exchange trx when >20mg/dL

Front 29

How to test acute HCV?

Back 29

HCV RNA testing

(anti-HCV antibody only 60% sens)

Front 30

Transaminase pearls

Back 30

>1000x ULN = acute hepatic inj from ischemia or toxin (not viral)

AST > 3000 U/L = TOXIN

AST:ALT ratio >2 in toxic, ischemic, EtOH; <1 in viral

Poorly reflect degree of hepatic injury (vs PT, bili)

Front 31

Bilirubin pearls

Back 31

jaundice more common in HAV & alcoholic hepatitis > HBV, HCV; rare in kids with viral hepatitis

Bilirubin peaks after transaminases fall in all forms of acute hepatic injury

Bili > 15mg/dL indicative severe liver inj & poor px

Acute hepatic injury mimics obstruction (direct > indirect)

Front 32

How many isoenzymes of amylase?

Back 32

6
3 salivary, 3 pancreatic
Separate by electrophoresis, inhibition tests (salivary sens to inh by wheat germ lectin triticum vulgaris), antibodies

Front 33

Serum amylase in acute pancreatitis

Back 33

Rises in 2-24h, returns to nl in 2-3d.

High sens but ~70% spec

Spec of urine amylase and FEamylase is higher

Front 34

How do you calculate fractional excretion of a compound?

Back 34

Front 35

Non-pancreatic causes of high serum amylase

Back 35

(P-itis usu 250-1000; non-panc 200-500)
DKA
PUD
Cholecystitis
Ectopic preg
Salpingitis
Bowel Ischemia or Obst
Renal insuff
Opioids

(Also elevated in panc pseudocyst, IPMN)

Front 36

Lipase or amylase for acute pancreatitis?

Back 36

LIPASE

Specific for panc
Elevated for up to 14d
Less reliant on renal clearance
Not affected by triglycerides

Front 37

Limitations of amylase in dx acute pancreatitis

Back 37

Not specific
Short window
Affected by renal function
Competitive inhibition by hypertriglyceridemia

Front 38

What are the Ranson Criteria?

Back 38

Front 39

Clues to etiology of pancreatitis

Back 39

ALT>150 = gallstone (50%sens)

lipase:amylase > 5 = alcoholic (50%sens)

Triglyceride level
Ca++
Viral serology

Front 40

How do we test pancreatic exocrine function?

Back 40

Secretin-CCK (endoscopy)

Fecal fat
Fecal chymotrypsin
Fecal elastase1

Front 41

Lab evaluation of pancreatic cysts

Back 41

Front 42

Name the 3 CK isoenzymes & locations

Back 42

CK-BB: BRAIN, bladder, stomach, prostate... all tissues. Fastest on e-phoresis

CK-MM: Skel m, cardiac m. Slowest. (Serum CK is usu 100% CK-MM, from skel m)

CK-MB: cardiac m (30%), skel m (1%). In nl pts, the circulating CK-MB is from skel m.

Front 43

Types of abnormal CK

Back 43

Macro-CK: CK-Ig complex. Healthy elderly f. Migrates between MM-MB

Mitochondrial CK: Poor px; seen in pts with advanced malignancies. Migrates with MM

Front 44

CK isoenzymes & electrophoresis

Back 44

CK-BB: BRAIN, bladder, stomach, prostate... all tissues. Fastest on e-phoresis

CK-MM: Skel m, cardiac m. Slowest. (Serum CK is usu 100% CK-MM, from skel m)

CK-MB: cardiac m (30%), skel m (1%). In nl pts, the circulating CK-MB is from skel m.

Front 45

What are troponins?

Back 45

Group pf enzymes (T,I,C) that mediate actin-myosin interactions of muscle contraction.

Cardiac troponin I tested in lab. Cardiac specific (not altered in skel m injury - unlike CK-MB, myoglobin)

Immediate release with infarction (4-8h) as well as sustained release (10-14d)

Front 46

What is the most sensitive cardiac marker?

Back 46

Myoglobin.

Earliest marker of AMI.

Also the least cardiospecific.

Front 47

What are netriuretic peptides?

Back 47

Cause vasodilation & sodium excretion.

3 types: ANP, BNP (ventricular myocytes; correlates with v wall tension; rapid degradation), CNP

BNP correlates with fluid status; EXCELLENT MARKER FOR CHF

Front 48

Best markers for non-AMI acute coronary syndrome?

Back 48

BNP: predicts recurrence & higher likelihood of sudden cardiac death

Troponins: may be helpful

CK-MB, myoglobin: no role

Front 49

What is ischemia-modified albumin (IMA)?

Back 49

The amino-terminal binding site of albumin is altered in ischemic conditions. Rises in minutes, cleared in hours. Marker transient ischemia.

Front 50

Define acute myocardial infarction

Back 50

Rise & fall of CK-MB or troponin with ischemic symptoms, ECG changes, or coronary artery abnormality.

Front 51

Cardiac tests in AMI

Back 51

Troponin: Single+ highly susp; double+ better; (-) result in days excludes. If+, still need CK-MB to determine acute/resolving.

CK-MB: rise in 3-6h, pk 24h, nl in 72h. Great sens but less spec.

Myoglobin: rapid release, not spec.

Cardiac reperfusion: all markers peak EARLIER

Front 52

Cardiac enzymes in AMI. How do they change in reperfusion?

Back 52

Front 53

Methods of total protein quantification

Back 53

Nitrogen content (not commonly used)
Refractomerty (interferences)
**Colorimetry in alkaline media (Biuret) (recommended)
Coloriimetry in acid media (for globulins)
Dye binding techniques
Spectrophotometry

Front 54

Describe the technique of protein electrophoresis. What forces act on each protein?

Back 54

Movement of proteins due to electrical potential

Charge applied across solid support & fluid buffer. SS (-) charge so is drawn to + POLE (ANODE); fluid buffer drawn to - POLE (CATHODE)

2 forces act on each protein:
-ELECTROMOTIVE: Pulled toward opposite charge (usu to ANODE)
-ENDOSMOTIC: flow with the fluid buffer (toward CATHODE)

Front 55

Which force is greater on gamma globulins in electrophoresis: electromotive or endosmotic?

Back 55

Endosmotic.

Gamma globulins have a weak negative charge; the endosmotic force (toward CATHODE) outweighs the electromotive force.

Not true with most other proteins, which are more negatively charged and this driven to the + ANODE.

Front 56

What are the bands in a normal SPEP, from anode to cathode?

Back 56

Albumin (most - charge)
Alpha1
Alpha2
Beta (2pks)
Gamma (v slow movement or movement toward cathode)

Front 57

Is immunoelectrophoresis or immunofixation electrophoresis the preferred method for characterizing a monoclonal band?

Back 57

Immunofixation electrophoresis (IFE): simpler to interpret

IEP: run pt & nl serum in adjacent troughs, then run antisera, precipitation arcs form. should be symmetric.

IFE: pt serum in wells on gel, e-phoresis, antisera applied, stained.

Front 58

Immunoelectrophoresis (IEP)

Back 58

Immunofixation electrophoresis (IFE)

Front 59

What is immunotyping?

Back 59

aka immunosubtraction

used with capillary electrophoresis to identify M protein. serum incubated with antibodies; supernatants removed & e-phoresed - can see which reagents removed abnormal spike.

Front 60

What is the most abundant protein in human plasma? Function? Fetal equivalent? Half-life?

Back 60

Albumin (2/3 total plasma protein)

Carries substances; Assessment of nutritional status.

alpha-fetoprotein is fetal equivalent (but migrates to alpha-1)

t1/2 = 17days

also: serum decrements in protein-losing conditions; glycosylated >8% in diabetes; negative acute phase reactant (decreases in inflammatory conditions)

Front 61

What is bisalbuminemia?

Back 61

When a variant allotype is present, 2 peaks can be seen in the albumin band. Benign.

Front 62

What is the fastest migrating protein on SPEP? Function? Clinical utility? half-life?

Back 62

Prealbumin. Sparse though and not traditionally seen without high resolution.

Binds T3 (transthyretin), T4 (thyroxine-binding prealbumin), retinol-binding protein:vitaminA complex.

Assessment of nutritional status

t1/2 = 48h

also: rare variant with very high affinity for thyroxine (elevated total T4 in euthyroid pt); heparinzed pts may have false "prealbumin band" with altered beta-lipoprotein; elevated prealb in chr EtOH, corticosteroid use; negative acute phase reactant.

Front 63

How can you tell CSF vs serum SPEP?

Back 63

-Sharp prealbumin spike in CSF (crosses BBB & excreted by choroid plexus)

-Double Beta-band (transferrin crosses BBB & some is modified to tau protein)

Front 64

Proteins that migrate to the alpha-1 band?

Back 64

alpha-1-antitrypsin: major. inactivates proteases. ++ acute phase reactant. (DECREASED in PiZZ phenotype AAT deficiency)

alpha-1-acid glycoprotein: minor. ++ acute phase reactant.

Front 65

Proteins that migrate to the alpha-2-band?

Back 65

alpha-2-macroglobulin: elevated in liver & renal dz (lrg size not excreted well)

Ceruloplasmin: copper trx. decreased in Wilson dz. Also in hepatic failure, malnutrition, Menke synd (AR, "kinky hair synd"). Acute phase reactant (APR)

Haptoglobin: Binds free hgb (DECREASED in hemolysis = sensitive marker). APR. 2 alleles = 3 haplotypes (2-2 phenotype risk factor for CV disease in diabetics)

Front 66

Proteins that migrate to the beta-band?

Back 66

TRANSFERRIN: Transports Fe+++ (30% sat'd); INCREASED in iron def (mimics M-protein), pregnancy, estrogen thx. NEGATIVE APR. Crosses BBB (modifies some to TAU protein - double pk in CSF)

Fibrinogen (usually not in serum unless incomplete clot; straddles beta-gamma interface; present in dysfibrinogenemia, APL synd, liver dz, vit K def, heparin use)

Front 67

What migrates to the second Beta band?

Back 67

IgA
Complement (APR)
Some CRP
Some fibrinogen

Front 68

Proteins in the gamma region?

Back 68

- CRP: made in liver.

- immunoglobulins

Front 69

How is CRP used clinically?

Back 69

<3mg/L : normal
3-10: cellular stress
>10: active inflammation

low-level elevation predicts poor outcome after CV events as well as in healthy individuals

Front 70

What SPEP pattern is this?

Back 70

Acute inflammation

Decreased albumin
Increased alpha1 (AAT) & alpha2 (haptoglobin, ceruloplasmin); possible increased beta (complement, fibrinogen)

Front 71

What SPEP pattern is this?

Back 71

Chronic inflammation

Similar to acute (increased alpha1&2) but also increased polyclonal gamma globulins

Front 72

What SPEP pattern is this?

Back 72

alpha-1 antitrypsin deficiency

(Genotype PiZZ individuals have decreased band. This genotype has <15% normal A1AT, leading to panacinar emphysema & cirrhosis)

Front 73

What SPEP pattern is this?

Back 73

Nephrotic syndrome

Massive loss of small proteins (only albumin in minimal change dz). Leads to "dimming" of all the bands, esp albumin, with SPARING of alpha2 (large protein alpha-2 macroglobin)

Front 74

What SPEP pattern is this?

Back 74

Cirrhosis

Hallmark is beta-gamma bridging**, mainly due to increased IgA.
Also: hypoalbuminemia, blunted alpa1&2 bands.

Front 75

What SPEP pattern is this?

Back 75

Monoclonal gammopathy
aka paraproteinemia

Prominent M-SPIKE, usu in gamma but can be in beta or alpha2. Requires IFE to characterize/

DDx: plasma cell dyscrasia, Waldenstrom/LPL, CLL, AL amyloidosis

Look for cryoglobulins in pts with M-proteins

Front 76

What SPEP pattern is this?

Back 76

Hypogammaglobulinemia

10% of pts with myeloma (likely have free lt chains in urine (BenceJones).
DDx: congenital, lymphoma, nephrotic syndrome, steroids

Front 77

Which is: normal CSF? abnormal CSF? normal serum?

Back 77

Top: normal serum

Mid: abnnormal CSF (oligoclonal bands = MS)

Bottom: Normal CSF (** Prominent pre-albumin band & double transferrin/beta band **)

Front 78

How can UPEP determine source of proteinuria?

Back 78

Glomerular pattern: Very large & very small proteins retained. Thus, strong albumin, alpha1(AAT) & beta (transferrin)

Tubular pattern: Impaired tubular reabsorption of LMW proteins such as alpha1macroglobin, beta2microglobin, and light chains. Thus, weak albumin band and strong alpha1 & beta bands.

Overflow proteinuria: Usu monoclonal light chain (BenceJones); also myoglobin or hgb

Front 79

What are cryoglobulins and what types are there?

Back 79

= immunoglobulins that reversibly precipitate at low temperatures

I: monoclonal Ig assoc with MM or Waldenstrom
II: mixture monoclonal IgM & polyclonal IgG. The IgM has RF activity (anti-IgG). **Most common
III: Mixture of 2 polyclonal Ig.

Front 80

Palpable purpura, arthralgia, hepatosplenomegaly, lymphadenopathy, anemia, sensorineural deficits, glomerulonephritis. Disease?

Back 80

Mixed cryoglobulinemia (Types II&III)

DDx: HCV**, chronic infection, lymphoproliferative, SLE, liver dz. Usu females 30-50.

Vasculitis; MPGN.

EM: large subendothelial immune complex deposits.

Thx: steroids, plasmapheresis, interferon (for HCV)

Front 81

Too rapid correction of hyponatremia can lead to?

Back 81

Central pontine myelinolysis

(too slow correction can lead to cerebral edema)

Front 82

DDx hyponatremia

Back 82

SIADH (urine Na >20, euvolemia, nl renal fxn, no recent diuretics)

Pseudohyponatremia (serum osm >280: hypergly, hyperprot, hyperlipid)

+ Hypovolemia: renal: UNa>30; extrarenal: UNa<30

+Euvolemia: SIADH, psych, ADH-like drugs

+Hypervolemia: CHF, cirrhosis, nephrotic syndrome

Front 83

DDx hypokalemia

Back 83

GI loss (Uk<30/day)

Renal loss (Uk>30): diuretics, abx, RTA, mineralocorticoid excess, Cushings, CAH

Tran-cellular shifts in alkalosis, correction of DKA

Front 84

DDx hyperkalemia

Back 84

artifact (in vitro hemolysis)
acidosis
renal failure
K+ sparing diuretics (spirono)
adrenal insuff
rhabdo

Front 85

Which forms of renal tubular acidosis are NOT associated with hyperkalemia?

Back 85

I & II (low K+)

Front 86

DDx hypercalcemia

Back 86

- Primary hyperparathyroidism (inc Ca, dec Phos)
- Tertiary hyperPTH
- Malignancy
- Familial Hypocalciuric Hypercalcemia (CASR gene 3q)
- Drug (vitD)
- Hyperthyroidism, Addison
- Sarcoid
- Paget
-Milk alkali syndrome

Front 87

Which form of hyperparathyroidism is associated with DECREASED calcium?

Back 87

Secondary (peripheral resistance to PTH)

(Primary: 90% PTH adenoma; MEN1, 2A)
(Tertiary: post-renal transplant)

Front 88

What is humoral hypercalcemia of malignancy?

Back 88

Malignancy produces hypercalcemia WITHOUT bone mets

RCC, HCC, SCC, PG, islet cell tumors

PTHrp related. HIGHLY suggested when increased nephrogenous cAMP in presence of normal PTH.

Front 89

Symptoms hypercalcemia

Back 89

kidney stones
lethargy
hyporeflexia
n/v/constipation
peaked T waves on EKG

Front 90

Types of hyperPTH?

Back 90

Primary: PTH adenoma (90%), 4-gland hyperplasia (9%), ca

Secondary: Peripheral resistance to PTH; LOW CA++ (usu chronic renal failure. also Vit D def). (BROWN TUMORS OF BONE - persistent hyperPTH activates osteoclasts)

Tertiary: HyperPTH that persists post-renal transplant (autonomous PTHs)

Front 91

Elevated Ca++ and Phosphate?

Back 91

Hypervitaminosis D

(sarcoid granulomas can activate Vitamin D!)

Front 92

Sx hypercalcemia?

Back 92

Lethargy, nephrolithiasis, hyporeflexia, N, V, constip

PEAKED T WAVES EKD

Risk of pancreatitis & PUD

Long term with hyperphosphate: CALCIPHYLAXIS (Ca of vessel walls & soft tissue)

Front 93

Besides clinical history, how to distinguish cause of hypercalcemia?

Back 93

HyperPTH vs malignancy (PTHrP)

-second gen tests can detect N-terminal PTH or intact PTH (the only active forms), and can ID PTHrP

Front 94

Total CA++ vs ionized?

Back 94

50% CA++ is bound to albumin
Ionized/free is biologically active

Acidosis increases free CA++

Measuring ionized CA++ is tricky. Arterial, no air exposure, kept cool delivered rapidly...

Front 95

Sx hypocalcemia?

Back 95

neurologic excitability
muscle spasms
QT prolongation
Tetany, laryngeal spasm

Front 96

Anion gap calculation

Back 96

AG = Na - (Cl + HCO3)

Normal is < 12

Front 97

How does albumin affect the anion gap?

Back 97

Hypoalbuminemia can MASK an anion gap

Corrected AG = AG + 2.5(4-alb)

Front 98

Causes of increased anion gap:

Back 98

Methanol
Uremia
Ketoacidosis
paraldehyde
Lactic Acidosis
Ethylene glycol
Salicylate

Front 99

Osmol gap calculation

Back 99

OG = measured osms - (2Na + glu/18 + BUN/2.8)

Nl < 10

Front 100

Causes of increased osmol gap:

Back 100

with metabolic acidosis:
methanol, propylene glycol, diethylene glycol, paraldehyde, ethanol

without:
isopropyl alcohol, glycerol, sorbitol, mannitol, acetone, ethanol (sometimes)

Front 101

Compensation of HCO3 for each 1 mmHg change in pCO2:

Back 101

MAcid: 1.3
MAlk: 0.6
Resp: 0.1 acute; 0.4 chronic

Front 102

FENa calculation

Back 102

Front 103

FENa < 1%

Back 103

PRERENAL disease
Usually hypovolemia
Hepatorenal syndrome
Acute glomerulonephropathy
CHF

Front 104

FENa > 3%

Back 104

Kidney damage
(ATN or obstruction)