Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
315 Cards in this Set
- Front
- Back
|
What cytokine made by macrophages in inflammation elicits production of acute phase reactants by the liver?
|
IL-6
|
|
|
negative APR:
APR: |
Albumin, prealbumin, RBP, transferrin
C3, MBP, CRP, a-1-at, a2mg, ceruloplasmin, fibrinogen, F8, haptoglobin, SAA, fibronectin... |
|
|
What is the fastest migrating protein on SPEP?
|
Prealbumin = transthyretin
Rarely seen as such small quantities |
|
|
What is the amyloid precursor protein in senile cardiac amyloidosis?
|
prealbumin
|
|
|
half life of albumin? prealbumin?
|
alb: 17d
prealb: 2d |
|
|
Name 2 causes of truly elevated prealbumin
fake elevation? |
chronic alcohol; corticosteroid therapy
falsely elevated in heparin therapy: alters beta-lipoprotein (LDL) such that it migrates in the prealbumin range |
|
|
hallmark of CSF-PEP?
|
sharp prealbumin band. crosses BBB & is actively secreted.
also: double transferrin peak (beta region). BBB transports transferrin but modifies some to Tau protein |
|
|
What migrates to the prealbumin region?
|
prealbumin / transthyretin
RBP (retinol binding protein - Vit A) |
|
|
what regions INCREASE in inflammation?
decrease? |
a1 : a1at (and orosomucoid = a1-acid-gp)
a2: haptoglobin, ceruloplasmin gamma1: gamma globulins gamma2: CRP decreased: albumin, prealbumin, transferrin (beta1) |
|
|
the greatest decreases in serum albumin are seen in?
|
protein-losing conditions (nephrotic syndrome)
|
|
|
classic pattern in nephrosis
|
low albumin
high a2 (a2macroglobulin) low gamma globulin |
|
|
normal spep.
where is the "origin" located? Which is the anode & which is the cathode? |
origin in located in the gamma region
the anode is on the left, it is + charged, and most proteins are - charged the cathode is on the right and is - charged, gamma globulins are weakly negative so they don't move far from the application site |
|
|
What is the most common defect in HyperIgM Syndrome?
|
defect in a Th2 cell protein (CD40 ligand). The disorder causes immunodeficiencies, including a higher than normal susceptibility to various types of infections.
Can't class switch! |
|
|
What are the 2 most obvious bands that are present in PLASMA but not SERUM?
|
Prothrombin (alpha 1 region)
Fibrinogen (Beta-gamma region)(can misinterpret as an M protein) (Ethanol can precipitate this out in vitro!) |
|
|
beta-gamma bridging is the hallmark of?
|
cirrhosis
|
|
|
Features of tubular proteinura UPEP?
glomerular? |
Tubular - weak albumin band, strong a1, b. impaired tubular reabsorption
glom - Strong albumin band, strong a1, b. Very large and very small proteins are conserved in the kidney |
|
|
Type I cryoglobulins
|
monoclonal. myeloma or waldenstroms
|
|
|
Type 2 cryo
|
monoclonal IgM (RF activity - anti-IgG)
AND polyclonal IgG most common |
|
|
Type 3 cryo
|
mixture 2 polyclonal
|
|
|
#1 cause of mixed cryoglobulinemia (types 2 & 3)
|
HCV
|
|
|
clinical sx of cryoglobulinemia?
Most common renal finding? |
PURPURA (leukocytoclastic vasculitis)
arthralgia HSG LAD anemia sensorineural deficits glomerulonephritis MPGN2 |
|
|
what cardiac marker rises the most compared to normal, following an MI?
What cardiac marker stays elevated the longest following an MI? |
Troponins. 50x normal levels. Most assays measure cardiac troponin I, though there's not much difference with T.
Troponins. Up to 10 days. |
|
|
What conditions can show a "flipped" LDH ratio, where LDH1 > LDH2?
|
Hemolysis, AMI, renal infarct
..since LDH1 is found in RBCs, heart, and kidney |
|
|
What is LDH-6 and what does it mean in terms of prognosis?
|
LDH6 is not a true isoenzyme of LDH but a mimic that is seen predominantly in alcohol use and indicates hepatic vascular insufficiency in the setting of shock
BAD px |
|
|
What is macro-CK-2?
|
aka mitochondrial CK
a normal variant of CK that is found in mitochondria, however its presence is a BAD finding and is usually seen in advanced disseminated malignancies |
|
|
What is macro-CK-1?
|
An Ig-CK complex that is not cleared readily from the circulation and persists. Autoimmune. Can lead to a chronically elevated CK level, but has no other clinical significance.
|
|
|
AST:ALT in EtOH?
viral hepatitis? |
>2
<1 |
|
|
what is the Regan isoenzyme?
|
form of placental alkaline phosphatase seen in 5% pts with carcinoma
|
|
|
What is the affect of heparin on ALT & AST?
Renal failure? |
Heparin can INCREASE these
Renal failure DECREASES them (cause is unknown) |
|
|
acid phosphatase found most in?
|
RBCs, prostate, bone
|
|
|
How to tell RBC acid phosphatase from others?
|
RBC is RESISTANT to tartrate (=TRAP, same as hairy cell leuk)
|
|
|
What blood groups have higher NONFASTING alkaline phosphatase?
|
Lewis + group B & O
|
|
|
What form of bilirubin is found in the urine?
What form is responsive to phototherapy? |
Urine only has CONJUGATED
UNconjugated responds to phototherapy |
|
|
autoimmune hepatitis shows polyclonal increase in what globulins?
primary biliary cirrhosis? |
ai: IgG
PBC: IgM |
|
|
Causes of UNconjugated hyperbili?
|
Crigler Najar
Gilbert Bowel obstruction Hemolysis Physiologic jaundice, breast milk jaundice |
|
|
Causes of conjugated hyperbili?
|
Dubin Johnson
Rotor Biliary obstruction Sepsis neonatal hepatitis TPN |
|
|
When to worry about neonatal jaundice:
Threshold for exchange transfusion? |
- 1st 24h of life
- continuing to rise after 1 week - Total bili > 12, conj>2, or increase of >5 in one day exchange transfusion when bili >20 |
|
|
Persistently elevated serum amylase concerning for?
What is the most common cause of a normal amylase in the setting of acute pancreatitis? |
pseudocyst
hypertriglyceridemia (TG inhibit the amylase assay) |
|
|
# isoenzymes of amylase & what are they
|
6
first 3 are salivary on electrophoresis last 3 are pancreatic salivary is inhibited by wheat germ lectin (triticum vulgaris amylase is cleared by the kidneys |
|
|
how do amylase, CEA, CA19-9 vary among pancreatic cysts?
|
pseudocyst has elevated amylase
CEA is elevated in mucinous (mucinous cystadenoma has only CEA elevated, IPMN has all 3 elevated) serous and solid-pseudopapillary have decreased all 3 |
|
|
what is delta-bilirubin?
|
conjugated bili covalently linked to albumin, cannot be readily excreted. thus conjugated bili measurements may persist after treatment
|
|
|
palpable purpura (leukocytoclastic vasculitis)
arthralgia HSG anemia sensorineural deficits glomerulonephritis (most commonly?) |
cryoglobulinemia
MPGN2 |
|
|
Rapid correction of hyponatremia can lead to?
Slow correction? |
CPM
cerebral edema |
|
|
Normal BUN:Cr ratio?
|
10:1
Increased: poor renal perfusion (BUN reabsorbed) Decreased: rare: liver disease, poor intake |
|
|
What 4 hormones share the same alpha subunit?
|
hcg
TSH FSH LH |
|
|
When does hcg peak?
|
end of first trimester
|
|
|
increased hcg & inhibin
decreased AFP & uE |
Trisomy 21
|
|
|
decreased AFP, uE, hcg
|
Trisomy 18
|
|
|
increased AFP only
|
neural tube defect
|
|
|
notable drugs eliminated by zero-order kinetics (most drugs are eliminated by first-order = proportional to drug concentration)
|
EtOH
ASA phenytoin |
|
|
what two toxins will give an osmol gap on the commonly used platform of freezing point depression, but not with the less commonly used vapor pressure osmometry?
|
Ethanol & methanol
|
|
|
Metabolites of methanol? source?
|
formate & formaldehyde
windshield washer fluid |
|
|
Metabolites of ethylene glycol? source?
clues in lab? |
oxalate & glycolate
antifreeze calcium oxalate crystals! |
|
|
What 2 alcohols do not cause acidosis but do produce an OSMOL gap?
|
Ethanol
Isopropanol |
|
|
Treatment of methanol or ethylene glycol OD?
|
Ethanol! competitively inhibits the enzyme alcohol dehydrogenase, which is responsible for producing the toxic metabolites of these drugs
|
|
|
abdominal pain and bilateral wrist drop
|
long-term lead poisoning
|
|
|
How does Fe deficiency perpetuate Pb toxicity (2 ways)?
|
1. Can't make heme molecules so protoporphyrins are increased (precursor)
2. Increased GI uptake of Fe also increased uptake of Pb |
|
|
Elevated free erythrocyte protoporphyrin (FEP) and zinc-protoporphyrin (ZPP) are elevated in what 2 conditions?
|
lead poisoning
iron deficiency |
|
|
What levels of CO are seen in smokers?
Severe symptoms with lethargy, LOC? |
2-6%
20-50% |
|
|
Time from ingestion for full acetaminophen absorption?
antidote? |
4 hours
N-acetylcysteine (promotes metabolism via conjugation and decreased production of toxic NAPQI) |
|
|
Why do alcoholics have a higher risk of hepatic injury from acetaminophen toxicity?
what zone of the liver shows acetaminophen toxicity? |
Alcohol induces the P450 system in the liver, wchih increases the amount of acetaminophen metabolized to NAPQI
Zone 3 (centrilobular) |
|
|
Bitter almond odor in breath
|
Cyanide toxicity
|
|
|
Clues to cyanide toxicity
mechanism? |
almond breath
cherry red skin severe anion gap metabolic acidosis (LACTATE) inhalation of smoke (insulation) or pesticide increased THIOCYANATE (metabolite) CN binds cytochrome a3 and leads to decreased oxygen-dependent metabolism |
|
|
treatment of CN tox
|
nitrites (form met-hgb) and sodium thiosulfate (forms thiocyanate, harmless compound eliminated by kidneys)
|
|
|
Earliest signs of ASA OD?
|
tinnitus & dizziness
|
|
|
Mortality in aspirin OD is best correlated with the ___-hr plasma salicylate concentration, with values >___mg/dL having a high fatality rate
|
6
130 |
|
|
what are the crazy stages of metabolic / respiratory / acidosis / alkalosis in ASA toxicity?
|
1. Respiratory alkalosis, 3-8h post ingestion, from direct stimulation of respiratory center
2. Compensatory metabolic acidosis, 12-24h, where patients usually present 3. Increased anion gap metabolic acidosis, through metabolic effects such as Krebs cycle inhibition 4. respiratory acidosis from CNS depression |
|
|
Ingested arsenic is largely excreted in the ____ with most of the remainder distributed into ____, _____, and ____.
|
urine
skin, nails, and hair |
|
|
Sx arsenic toxicity
|
vomiting, bloody diarrhea, abdominal pain
cytopenias with basophilic stippling peripheral neuropathy, nephropathy, skin hyperpigmentation and hyperkeratosis |
|
|
2 characteristic syndromes with weird names associated with chronic mercury toxicity
|
1. Acrodynia / Feer syndrome
-autonomic manifestatsions and desquamative erythematous rash palms & soles. - increased urinary catecholamines ~ pheo! 2. Erethism - CNS d/o with personality changes, irritability, fine motor disturbances |
|
|
name 2 toxins that are best screened for with 24-hour urine levels
|
arsenic & elemental mercury
|
|
|
what drug, when taken with digoxin, enhances its toxicity?
|
quinidine
|
|
|
best test of quinidine toxicity
|
EKG (prolonged QT interval, torsades de pointes)
|
|
|
digoxin t 1/2
|
36h
|
|
|
warfarin dosing in a patient with mutations in:
VKORC1 CYP2C9 |
VKORC1: confers warfarin resistance & requires INCREASED dose
CYP2C9: Leads to DECREASED warfarin metabolism, and increased serum levels, so DECREASED dosage is needed |
|
|
Tangier disease
|
AR
Absent Apo-A1, no HDL |
|
|
Metabolites of cocaine
|
Benzoylecgonine
Ecgonine methyl esther these are NONACTIVE metabolites, and metabolism continues after death |
|
|
EtOH + Cocaine = ?
|
Cocaethylene
More lethal than cocaine alone |
|
|
Mechanism of death in cocaine OD
|
Fatal cardiac arrhythmia, from coronary vasospasm or myocardial toxicity
|
|
|
Mechanism of death in heroin
Drug class? |
Acute pulmonary arrest following CNS depression
(Pulmonary edema) Opiate |
|
|
Heroin metabolites
|
6-MAM --> Morphine (liver)
Morphine gives most of the effects |
|
|
Metabolites in death immediately after heroin injection?
|
6MAM >>> morphine
Urine might be negative |
|
|
Metabolites in death some time after heroin injection?
|
Morphine >>> 6MAM
Urine has both |
|
|
Is fentanyl more or less potent than morphine?
|
200x more potent
|
|
|
Fentanyl abuse is more common in what occupations?
|
Medical field
|
|
|
Are deaths from benzodiazepines common?
|
No. Unless combined with EtOH
|
|
|
How does vitreous EtOH level help
|
Reflects blood levels 1-2h prior
Vitreous is 1.2x blood concentration |
|
|
Metabolite of isopropanol?
|
Acetone
|
|
|
Metabolite of methyl alcohol?
|
Formaldehyde, formic acid
|
|
|
How many domains do light chains have?
|
1 variable and 1 constant
|
|
|
How many domains do heavy chains have?
|
1 variable and 3-4 constants
|
|
|
What chromosome is kappa located on?
|
2
|
|
|
What chromsome is lambda located on?
|
22
|
|
|
List the 5 ig classesin order of serum concentration
|
IgG, IgA, IgM, IgD, IgE
|
|
|
What is unique about IgG2 andIgG4
|
IgG2 cannot cross the placenta and IgG4 cannot activate complement
|
|
|
What chromosome are the TCR genes located on?
|
7
|
|
|
Which TCR classes are more common in adults
|
Alpha beta
|
|
|
What does Il-5 Stimulate?
|
The terminal differentiation of eosinophils
|
|
|
What is the classic pathway for complement?
|
Activated C1 catalyses C4->C2 - 3,5,6,7,8,9
|
|
|
How is the alternate pathway of the complement cascade activated?
|
Bacterial cell walls, venoms, or endotoxin
|
|
|
What is the overall point of both alternate and classic pathways of complement fixation?
|
To produce C5b, which then complexes and forms the MAC
|
|
|
What are some clues for B cell deficiencies?
|
Recurring bacterial infections, especially upper and lower respiratory tract, and giardia infection
|
|
|
How do T- cell deficiencies generally present?
|
Susceptibility to viral and fungal opportunistic infections
|
|
|
What is an easy way to test for B cell function?
|
Using anti ABO ABs, which should develop by 6 months. Low titer before age 10 isnt specific
|
|
|
What is the screening test for complement?
|
CH50 test - determines what percentage of immunoglobulin coated sheep red cells are lysed by the patient's serum and is thus a gross evaluation of the classical complement pathway
|
|
|
How does the CH50 test change with various complement deficiencies?
|
Qualitative defeciencies of any of the complement components, c1-c9 will lead to a reduced CH50.
|
|
|
How old do are Bruton agammaglobulinemia patients when they present?
|
Usually 6 months
|
|
|
What is the clinical presentation of Bruton agammaglobulinemia?
|
Recurring pyogenic infections, affecting primarily males
|
|
|
What are some lab values associated with Bruton?
|
Markedly reduced serum IgG, reduced mature B cells
|
|
|
What is the transmission pattern of Bruton
|
X linked (atk gene)
|
|
|
What is CVID characterized by?
|
Low serum Ig. Most patients suffer from recurrent URI and intestinal bacterial overgrowth/giardia.
NORMAL amount of B cells |
|
|
What is the most common primary immunodeficiency disorder?
|
Selective IgA deficiency
|
|
|
How does selective IgA deficiency manifest clinically?
|
Patients suffer from recurrent respiratory and gastrointestinal bacterial infections, a high incidence of autoimmunity, and at risk for reaction to IgA containing blood products
|
|
|
What is Job Syndrome?
|
Abnormally high serum IgE, exquisite susceptibility to staph infections, eosinophilia, and eczema (defect in granulocyte chemotaxis)
|
|
|
What do T-cell deficiencies generally present?
|
Usually present earlier than b cell, neonatal period
|
|
|
What is Digeorge syndrome?
|
A velocardiofacial syndrome due to failure of 3rd and 4th pharyngeal pouches to adequately develop
|
|
|
What are some features of Digeorge other than T cell deficiency?
|
hypoplastic thymus, hypoplastic parathyroids, anomalies of the great vessels, typical facies, esophageal atresia
|
|
|
What is the genetic alteration in Digeorge?
|
Del 22q11.2
|
|
|
What is SCID?
|
Syndrome characterized by decreased or absent T cell function, low or undetectable Ig levels, and thymic dysplasia
|
|
|
What are some of the inheritance patterns of SCID?
|
50% X linked recessive due to IL-2 receptor defect
40% are autosomal recessive and due to deficiency in the enzyme adenine deaminase |
|
|
What is Wiskott-Aldrich syndrome?
|
It is an X-linked disease characterized by the triad of eczema, thrombocytopenia, and immunodeficiency. 12% incidence of fatal malignancies
|
|
|
What are the clinical manifestations of Ataxia-Telangiectasia?
|
Cerebellar ataxia, oculocutaneous telangiectasia, recurrent sinopulomonary infections and high incidence of malignancy
|
|
|
What is the genetic mutation and inheritance pattern of Ataxia-Telangiectasia?
|
Autosomal recessive disease caused by mutations in the ATM gene on 11q22.3
|
|
|
What is Duncan-Disease?
|
It is an X-linked lymphoproliferative disease that presents as a fulminant and often fatal immune response to EBV infection.
|
|
|
What organisms are likely to appear when there are defects in phagocytosis?
|
Staph, e coli, strep pneuo, pseudomonas, and candida albicans
|
|
|
What is the pathogenesis of chronic granulomatous disease?
|
Defective intracellular oxidative killing of ingested organisms
|
|
|
What is the deficient enzyme in CGD?
|
NADPH oxidase
|
|
|
What is the screening test for CGD?
|
Nitroblue tetrazolium test (normal cell converts yellow to blule)
|
|
|
How does Chediak-Higashi present?
|
It presents as neutropenia, recurrent infection, thrombocytopenia, and oculocutaneous albinism
It late stages may have lympoma like proliferations within the viscera |
|
|
What is May-Hegglin anomaly?
|
Autosomal dominant condition manifesting as dohle-like bodies in granulocytes and monocytes, large platelets and thrombocytopenia.
|
|
|
Deficiency of C2 and C3 leads to what types of infections?
|
Recurrent infections with gram-positive encapsulated organisms
|
|
|
What do the y and x intercepts on a lineweaver-burke plot represent?
|
Y = 1/vmax
X = -1/Km |
|
|
How does a lineweaver-burke plot change with a noncompetitive enzyme?
|
The y intercept is changed, and the x intercept is unchanged
|
|
|
How does a lineweaver-burke plot change with a competitive enzyme?
|
The Y intercept is unchanged, while the slope, which equals Km is decreased
|
|
|
What is an IU?
|
1 IU = the amount of enzyme that catalyzes the conversion of 1 micromole of substrate per minute
|
|
|
What is a Katal?
|
1 katal = the amount of enzyme that catalyzes the conversion of 1 mole of substrate per second
|
|
|
How many katals in an IU
|
1 IU = 16.7 nanokatals
|
|
|
Where are AST and ALT located in the cell?
|
AST mostly mitochondrial, ALT is cytoplasmic
|
|
|
How does renal failure affect AST and ALT?
|
It lowers the values
|
|
|
Where are LD1 and LD2 traditionally found?
|
Red cells, heart, kidney (fast moving isoenzymes)
|
|
|
Where is LD4 and LD5 found?
|
Liver and skeletal muscle
|
|
|
Where is LD3 found?
|
lung, spleen, lymphocytes, and pancreas
|
|
|
What are the comparative concentrations of LD isoenzymes in normal serum?
|
LD2>LD1>LD3>LD4>LD5
|
|
|
What three possibilites exist with an LD1>LD2?
|
Acute MI, hemolysis, and renal infarction
|
|
|
Elevated LD1 and LD5 points to what?
|
AMI with liver congestion or chronic alcoholism that has been complicated by liver damage and megaloblastic anemia
|
|
|
Where is alk phos produced?
|
Bone, bile ducts, intestine, placenta
|
|
|
How many isoenzymes of ALK phos are there?
|
4
|
|
|
How does heat inactivate the different alk phos isoenzymes?
|
Bone burns (90%) inactivation, 0% inactivation of placental alk phos
|
|
|
What is the most sensitive marker of hepatic masses?
|
Biliary alk phos
|
|
|
What cell in the bone produces alk phos?
|
Osteoblasts
|
|
|
What conditions display elevated 5' nucleotidase?
|
Cholestatic conditions
|
|
|
What are the characteristics of physiologic jaundice?
|
Noted from 2-3 days of neonatal life and rarely rises at a rate greater than 5mg/dl/day, usually peaks by day 4-5
|
|
|
AST > 3000 suggests what etiology?
|
Toxin in 90% of cases
|
|
|
How many serum amylases are there?
|
6, 3 salivary and 3 pancreatic
|
|
|
Where is CK-BB found and what is the migration pattern?
|
It is found primarily in the brain, most widely distributed, and is the fastest migrating on electrophoresis (CK1)
|
|
|
Where is CK-MM found and what is the migration pattern?
|
CM-MM (CK3) is found in skeletal and cardiac muscle. MM is the slowest migrating faction
|
|
|
Where is CK-MB found and what is the migration pattern?
|
CK-MB (CK2) is found in cardiac and skeletal muscle (30% in cardiac muscle). MB migrates between MM and BB on eletrophoresis.
|
|
|
What is Macro-CK?
|
it is a CK-Ig complex that migrates between MM and MB
|
|
|
What is mitochondrial CK?
|
It migrates close to MM. It is seen in patients with advanced, often disseminated malignancies and is assocatiated with a poor prognosis
|
|
|
Where is BNP stored?
|
Ventricular myocytes
|
|
|
List the order of densities of the lipoproteins?
|
Chylomicrons
|
|
|
What enzyme converts VLDL to IDL?
|
Lipoprotein lipase (LPL)
|
|
|
What receptors mediate endocytosis of the LDL particle?
|
Apolipoprotein B-100 and LDL receptor
|
|
|
What is the function of HDL?
|
To scavenge cholesterol from the periphery and return it to the liver.
|
|
|
What is the Friedwald equation?
|
LDL cholesterol = total cholesterol - HDL cholsterol - TG/5
|
|
|
What is the friedwald equation not considered valid?
|
If TG>400, if chylomicrons are present, or in type III dyslipidemia
|
|
|
What is the major alipoprotein of LDL and VLDLD?
|
Apo B
|
|
|
What is the major alipoprotein of HDL?
|
Apo A1
|
|
|
Which Frederickson phenotypes have elevated Tg only?
|
I, IV, V
|
|
|
Which Frederickson phenotypes show elevated LDL
|
IIA
|
|
|
Which Frederickson phenotypes show elevated Tg and LDL
|
IIB, III
|
|
|
What are 2 type I lipid disorders?
|
Familial LPL deficiency, Familial apo C-II deficiency
|
|
|
Familial hypercholesterolemia is considered what phenotype?
|
IIa
|
|
|
Apolipoprotein E deficiency is considered what phenotype?
|
IIB
|
|
|
Familial dysbetalipoproteinemia is considered what phenotype?
|
III
|
|
|
Familial hypertriglyeridemia is considered what phenotype?
|
IV, or V
|
|
|
Familial combined hyperlipidemia is considered what phenotype?
|
II or IV
|
|
|
What are some clinical features of type I lipid disorders?
|
Eruptive xanthomas, pancreatitis
|
|
|
What are some clinical features of type IIa lipid disorders?
|
Tendinous xanthomas, premature atherosclerosis
|
|
|
According to the ATPIII what are the ranges for cholesterol, (desirable, borderline, high)
|
Desirable <200
Borderline 200-239 High >240 |
|
|
According to the ATPIII what are the ranges for LDL?
(Optimal, Near optimal, borderline, high, veryhigh) |
Optimal <100
Near optimal 100-129 Borderline 130-159 High 160 - 189 Very High >190 |
|
|
According to the ATPIII what are the ranges for HDL?
|
Low <40
High >60 |
|
|
In type I dyslipidemia, what is the major component of triglycerides?
|
Chylomicrons
|
|
|
In type IV dyslipidemia, what is the major component of triglycerides?
|
VLDL
|
|
|
In type V dyslipidemia, what is the major component of triglycerides?
|
VLDL and Chylomicrons (think type 1 + 4 = 5)
|
|
|
What hormones stimulates prolactin?
|
TRH, Dopamine antagonists
|
|
|
What hormones inhibit prolactin
|
dopamine
|
|
|
What are some causes of increased prolactin?
|
Adenoma, pituitary stalk compression, H2 blocker, phenothiazines, TRH
|
|
|
A prolactin level of >200 indicates what?
|
A tumor
|
|
|
An elevated prolactin but less than 100 ng/ml suggests what?
|
A cause other than a tumor
|
|
|
What stimulates the release of growth hormone? Inhibits?
|
Stimulated by GHRH, inhibited by somatostatin. Also stimulated by sleep, acute stress, fasting, hypoglycemia
|
|
|
How do we evaluate growth hormone production?
|
Look at growth hormone levels and IGF-1 levels
|
|
|
Underproduction of GH causes?
|
Rare cause of dwarfism
|
|
|
Overproduction of GH?
|
Gigantism or acromegaly
|
|
|
What does LH regulate?
|
The gametes, oogenesis, and sex hormone production (estrogen and testosterone)
|
|
|
What does FSH regulate?
|
Primarily for gamete development. Acts on the supporting cells. Granulosa cells and sertoli cells, inhibin (major feedback)
|
|
|
What stimulates gonadotropins?
|
Cyclic GnRH, norepinephrine, light
|
|
|
What do theca cells produce?
|
Androstenedione -> estradiol or testosterone
|
|
|
How are estradiol and testosterone found in circulation?
|
Bound to SHBG or albumin
|
|
|
How does obesity affect SHBG levels?
|
inhibits production
|
|
|
What part of HCG is tested with the assay
|
the beta subunit
|
|
|
What are the 2 major physiologic causes of amenorrhea?
|
Menopause, increased FSH, pregnancy, increased HCG
|
|
|
What are causes of hirsutism?
|
PCOS high LH FSH ratio
Cushing syndrome CAH - high steroid precursors |
|
|
How is extracellular calcium forms transported?
|
Free 50%, protein bound 40%, complexed 10% (PO4, HCO3)
|
|
|
How does PTH act?
|
Acts on the bone to mobilize calcium from the osteocytes
Also acts on the kidneys to cause loss of the complexing ions increasing free calcium |
|
|
How is calcitriol produced?
|
By the kidney, stimulates by PTH
|
|
|
What does calcitriol do?
|
It acts on the bone to increased mobilized CA. Acts on the intestinal tract and increases absorption, and then inhibits PTH production and it's own production.
|
|
|
What level do you check for VIt D deficiency?
|
25-hydroxy vitamin D
|
|
|
Where is calcitonin produced?
|
parafollicular C cells i thyroid, lung
|
|
|
What is the function of calcitonin?
|
Inhibits bone resorption
|
|
|
How does gadolinium affect calcium?
|
Will lead to falsely low calcium results
|
|
|
What is the halflife of PTH?
|
3-5 minutes
|
|
|
What are the three etiologies responsible for 99% of hypercalcemia cases?
|
Hemoconcentration, Primary hyperparathyroidism, Maignancy
|
|
|
How many hydroxyl groups in 25 OHD?
|
2 hydroxyl groups
|
|
|
Causes of hypocalcemia?
|
Low albumin, renal failure
Uncommon - hypmagnesemia, malapsorption, vit D deficiency, Hypoparathyroidism, sepsis, shock, pancreatitis |
|
|
What are the labs seen in secondary hyperparathyroidism?
|
PTH much higher than primary hyperpara
More severe bone disease Due to chronic hypocalcemia Often associated with high phoshate when due to renal failure |
|
|
What is seen in FHH? (Familial hypocalciuric hypercalcemia)
|
Abnormal receptors which dont respond to calcium, leading to more pth and hypercalcemia
Decreased urine excretion of calcium |
|
|
What are the side effects of too rapid a correction of hyponatremia? Too slow?
|
Too rapid - central pontine myelinosis
Too slow - Cerebral edema |
|
|
What are some causes of pseudohyponatremia?
|
hyperglycemia, hyperlipidemia, hyperproteinemia
|
|
|
What are some causes of hypovolemic hyponatremia with increased Urine sodium?
|
Diuretics, renal medullary disease, addison disease, RTA type I
|
|
|
What are some causes of hypovolemic hyponatremia with decreased urine sodium?
|
GI losses, third spacing
|
|
|
What are some causes of euvolemic hyponatremia?
|
SIADH, psychogenic polydipsia, drugs with ADH like effect (ecstacy)
|
|
|
What are some causes of hypervolemic hyponatremia?
|
CHF, cirrhosis, nephrotic syndrome
|
|
|
Most common cause of hypernatremia?
|
Dehydration
|
|
|
What are some causes of hypokalemia with decreased urine potassium?
|
Vomiting, NG tube, diarrhea, villous adenoma
|
|
|
What are some causes of hypokalemia with increased urine potassium?
|
Diruetics, hypomagnesemia, antibioteics, aldosterone excess, RTA 1 and 2, cushing, CAH, too much renin
|
|
|
What is the differential diagnosis of hyperkalemia?
|
Acidosis, renal failure, potassium sparing diuretics, adrenal insufficiency, rhabdomyolysis
|
|
|
What two types of renal tubular acidosis are not associated with hyperkalemia
|
Type 1 and 2
|
|
|
Explain the effects on primary hyperparathyroidism on calcium, phosphate, chloride, camp
|
Increased calcium, decreased phosphate, increased chloride, increase nephrogenous camp
|
|
|
What are 2 hereditary conditions linked with primary hyperparathyroidism?
|
Men1 and Men2a
|
|
|
What is the cause of secondary hyperparathyroidism?
|
Peripheral resistance to the action of PTH (hypocalcemia)
|
|
|
What is tertiary hyperparathyroidism?
|
Hyperparathyroidism that persists in patients post renal transplant (Autonomous parathyroids)
|
|
|
What are some clinical presentation signs of hypercalcemia?
|
nephrolithiasis, lethargy, hypo-reflexia, slowed mentation, nausea, vomiting, constipation, peaked T waves on ECG
|
|
|
Which terminal of the PTH peptide is more specific to the intact hormone?
|
the N-terminus
|
|
|
How much serum calcium is bound to protein?
|
50%
|
|
|
What is the effect of acidosis on free calcium?
|
Increases calcium by competing for the binding sites on albumin (opposite for alkalosis)
|
|
|
How do you acquire the sample for an ionized calcium measurement?
|
drawn from an artery, not exposed to air, not drawn into EDTA or citrate, no fist clenching, kept cool and delivered rapidly
|
|
|
What is the correction for calcium in a patient with low protein
|
0.8 mg/dl CA per 1 g/dl protein lost
|
|
|
What are some clinical signs/symptoms of hypocalcemia?
|
Neurologic excitability, muscle spasms, hyperreflexia, paresthesia, QT interval lengthening, dysrhythmia
|
|
|
What is the differential diagnosis of hypocalcemia?
|
Vit D deficiency, CRF, drugs, hypoparathyroidism, MTC, hypoproteinemia (often with normal ionized calcium), massive transfusion
|
|
|
What is the henderson-hasselbach equation?
|
pH=pK + log(base/acid)
|
|
|
What is the normal pK in individuals?
|
6.1
|
|
|
How do you calculate the anion gap?
|
Na - (Cl+Hco3)
|
|
|
What is the normal anion gap
|
<12
|
|
|
What is the anion gap calculation for hypoalbuminemia?
|
Na-(Cl+HCO3) + 2.5(4-albumin)
|
|
|
How do you calculate the osmolal gap?
|
Gap = osm measured - (2[NA] + [GLU]/18 +BUN/2.8)
|
|
|
What is the normal osmolal gap?
|
<10
|
|
|
Causes of metabolic acidosis with increased anion gap?
|
MUDPILES
Methanol, Uremia, Diabetes (ketoacids), paraldehyde, lactic acidosis, ethylene glycol, salicylate |
|
|
Causes of metabolic acidosis with increased osmolal gap?
|
Methanol, propylene glycol, diethylene glycol, paraldehyde
|
|
|
Causes of increased osmolal gap without metabolic acidosis?
|
isopropyl alcohol, glycerol, sorbitol, acetone, mannitol
|
|
|
How is urea measured?
|
By the measurement of urea nitrogen
|
|
|
Why does BUN slightly underestimate GFR?
|
Because urea is partially reabsorbed by the nephron
|
|
|
What is azotemia?
|
An increase in BUN
|
|
|
How do you calculate GFR based on creatinine clearance?
|
Cl(cr) = U(cr) x V(ur)/P(cr)
|
|
|
Under what circumstances can the MDRD equation be used?
|
Caucausian and AA with GFR <60 between the ages of 18 and 70
|
|
|
What variables make up the MDRD equation?
|
serum creatinine, patent age,sex, race
|
|
|
What is the normal BUN/Creatinine ratio?
|
10:1
|
|
|
An elevated BUN/creatinine ratio suggests what?
|
Prerenal or post renal azotemia
|
|
|
A decreased BUN/creatinine ratio suggests what?
|
Rare. suggests dietary protein insufficiency or severe liver disease.
|
|
|
What is cystatin C?
|
A cysteine protease inhibitor produced by nearly all cells in the body that has been demonstrated to be better than creatinine for estimating the GFR.
|
|
|
What is the range of normal proteinurea?
|
Does not exceed 150 mg/day
|
|
|
What is the definition of significant proteinurea
|
>300 mg/day on 24 hour urine collection
|
|
|
What two assays can be used to detect tubular dysfunction?
|
B2 microglobulin and lysozyme.
|
|
|
How do you define chronic kidney disease?
|
GFR < 60 ml per minute per 1.73 m2 of body surface rea or albuminuria for 3 or more consecutive months
|
|
|
BUN/Cr ratio in pre-renal vs renal ARF?
|
>20:1, <20:1 renal
|
|
|
Urine specific gravity in prerenal versus renal ARF
|
Prerenal - high >1.020
Renal - low <1.010 |
|
|
Urine osmolarity in prerenal vs renal ARF
|
prerenal - high - >500mmol/kg
renal - low < 300-500 |
|
|
FENa in prerenal vs renal ARF
|
prerenal - <35%
Renal >35% |
|
|
Anticholinergic Toxidrome and Agents
|
Hyperthermia, dry skin, flushing, AMS, psychosis, mydriasis, constipation
Agents: Atropine, Antihistamines, Tricyclics, Scopolamine |
|
|
Cholinergic Toxidrome and Agents
|
Salivation, lacrimation, urination, diarrhea, cramps, emesis, diaphoresis, miosis, and wheezing
Agents: Organophosphates, pilocarpine, carbamate |
|
|
Adrenergic Toxidrome and Agents
|
Hypertension, tachycardia, mydriasis, anxiety, hyperthermia
Agents: Amphetamines, cocaine, PCP, pseudoephedrine ephedrine |
|
|
Sedative Toxidrome and Agents
|
AMS, slurred speech, hypopnea/apnea
Agents: Barbituates, alcohols, opiates |
|
|
Hallucinogenic toxidrome AGENTS
|
LSD, PCP, Amphetamines, cocaine
|
|
|
Agents that increase the osmolal gap?
|
Ethanol, Ethylene glycol, methanol, isopropyl alcohol, propylene glycol, glycerol, acetone, mannitol, radiocontrast media, hypermagnesemia
|
|
|
Source and metabolite of Ethylene glycol?
|
Source: Antifreeze
Metabolite : Oxylate & glycolate |
|
|
Source and metabolite of isopropyl alcohol?
|
Source: Rubbing alcohol
Metabolite: acetone |
|
|
Source and metabolite of methanol?
|
Source: Windshield washer fluid
Metabolite: Formate and formaldehyde |
|
|
FEP and ZPP are raised in what 2 conditions?
|
Iron deficiency and lead poisoning
|
|
|
In what two ways does iron deficiency anemia enhance lead toxicity?
|
1. The final step in heme biosynthesis is further inhibited by low iron
2. the upregulated intestinal absorptio of iron also leads to increased absorption of lead |
|
|
Abdominal pain and bilateral wrist drop?
|
Lead toxicity
|
|
|
What is the cutoff to determine elevation of blood lead levels?
|
>10 g/dl
|
|
|
Levels of CO in
Non smoker and smoker |
Non smoker 0.4 to 2%
Smoker 2-6% |
|
|
What level of CO leads to coma and death?
|
>50%
|
|
|
What instrument can measure CO?
|
Co-oximeter
|
|
|
What is a toxic dose of tylenol in healthy individuals?
|
150 mg/kg
|
|
|
What is the mainstay of treatment for tylenol overdose?
|
N-acetylcysteine
|
|
|
Mechanism of cyanide?
|
Inhibition of cytochrome a3 and uncoupling of the electron transport system
|
|
|
Metabolite of cyanide?
|
thiocyanate
|
|
|
Treatment of cyanide poison?
|
sodium nitrate and amyl nitrite
|
|
|
Order of effect on pH of aspirin?
|
1. respiratory alkalosis (3-8 hours)
2. Metabolic acidosis (12-24 hrs) 3. Loss of buffering leads to increased anion gap metabolic acidosis |
|
|
At what level of aspirin poisoning is there a high fatality rate?
|
>130 mg/dl
|
|
|
Mechanism of TCAs
|
Block dopamine and epi reuptake
|
|
|
What is the major lipid in chylomicrons and VLDL?
|
Triglycerides
|
|
|
How is total cholesterol measured?
|
Enzymatically (color change) with spectrophotometer
|
|
|
What is the friedwald equation?
|
LDL Cholesterol = total cholesterol - HDL - TG/5
|
|
|
How does CEA vary with grade?
|
Inversely with grade. Higher with low grade
|
|
|
What is Tumor associated trypsin inhibitor?
|
a marker that has been used for mucinous ovarian carcinoma, urothelial ca and RCC
|
|
|
What is considered with the most accurate test for screening for pheo?
|
Free plasma metanephrine
|
|
|
What s the final metabolic product of dopa? epinephrine?
|
HVA
VMA |
|
|
What does the high dose DST test for?
|
It answers is the patients cushing syndrome (hypercortisolism) due to a pituitary adenoma
Non suppression points to either ectopic ACTH production by a tumor or primary adrenal hypercortisolism |
|
|
What is the metyrapone test used for?
|
To determine whether the pituitary is to blame when a patient is deficient in cortisol (Addisonian)
|
|
|
How does the metyrapone test work?
|
It blocks conversion of 11 deoxycortisol to cortisol. THis leads to increased ACTH production by the pituitary which in a healthy patient can overcome the block. Those who cannot have impaired pituitary function.
|
|
|
21 hydroxylase ( salt wasting, virilization, and hypertension)
|
Salt wasting +, Virilization +, Hypertension -
|
|
|
11-hydroxylase deficiency (salt wasting, virilization, hypertension)
|
Salt wasting -, virilization + and hypertension +
|
|
|
Pituitary acidophils secrete?
|
prolactin and growth hormone
|
|
|
Pituitary basophils secrete?
|
FSH, LH, ACTH, TSH (B-FLAT)
|
|
|
Postmortem Glucose trend?
|
Increases in serum, decreases in vitreous
|
|
|
BUN/Cr change after death?
|
Stable
|
|
|
Hyaline casts represent?
|
Nonspecific, dehydration, exercise
|
|
|
Red cell casts represent?
|
Glomerulonpehritis
|
|
|
White cell casts represent?
|
pyelonephritis, tubulointerstitial nephritis
|
|
|
Granular casts represent?
|
nonspecific
|
|
|
Waxy casts represent?
|
Some kind of renal disease
|
|
|
Broad casts represent?
|
ESRD
|
|
|
Fatty casts represent?
|
Nephrotic syndrome
|
