-
Increase with hemolysis?
- KLAMP
- K, LDH, AST, Mg, PO4
-
Sugar to test intestinal vs pancreatic malabsorption?
Xylose (no enzyme required for digestion)
-
Cardiac risk values for HDL
- <40 = positive risk factor
- >60 = negative risk factor
-
Apolipoproteins associated with lipid carrying molecules
- B48: chylomicrons
- B100: VLDL, LDL
- A1: HDL
-
Serum Protein vs UCSF Protein techniques - coomassie brilliant blue, kjeldahl, bromcresol green, HABA, biuret, turbidimetry
- S: kjeldahl, biuret
- UCSF: coomassie brilliant blue, bromcresol green, HABA, turbidimetry
-
SPSP: pH, charge/migration, fractions, increase/decrease, common patterns in disease
- pH 8.6, all proteins negatively charged, migrate to anode (+)
- Albumin to Anode
- Fractions: Albumin, a-1 globulin, a-2-globulins, B-globulins, Y-globulins
Albumin: albumin- ↑ dehydration
- ↓ liver damage, malabsorption, nephrotic syndrome, burns
- a-1-globulins: a-1-antitrypsin, a fetoprotein
- ↑ acute phase, preggo, neural tube defect, liver cancer
- ↓ emphysema, Down's pregnancy
- a-2-globulins: haptoglobin, cerruloplasmin
- ↑ acute phase, nephrotic syndrome, preggo
- ↓ hemolysis, liver disease, tfxn rxn, Wilson's disease
- B-globulins: transferrin, lipoproteins
- ↑ iron def anemia, elevated B lipoproteins
- Y-globulins: immunoglobulins
- ↑ inflammation, cirrhosis, monoclonal gammopathies
- ↓ immunodeficiency
- ***B-Y bridge in cirrhosis
- ***decrease alb increase a2 in nephrotic syn
-
amt of U (IU)
1 umol/min substrate used or product formed
-
5'NT vs ALP?
- ALP increase in liver and bone activity/disease
- 5'NP increased in liver NOT bone activity/disease
- Use both to differentiate liver/bone disease
-
LIVER ENZYME MARKERS (hep vs obstr)
- HepATitis: AST, ALT
- Obstruction: ALP, 5'NT
- Both: GGT, ↑bili
-
measured vitD vs more active vitD. Hormone that stimulates? Why?
- measure: 25-OHD
- active: 1,25-(OH)2D AKA calcitrol
- PTH stimulates this conversion to facilitate increase of serum Ca (increased absorp, bone resorp)
-
Serum iron/Tferrin sat/TIBC/Serum tferrin
storage depletion, iron def anemia, ACD (infl), Thalassemia, Hemochromatosis, Sideroblastic
- Storage Depl: N,N,N,↓
- Iron def: ↓,↓,↑,↓
- ACD: ↓,↓,↓,↑
- Thalassemia: ↑,↑,↓,↑
- Hemochromatosis: ↑,↑,↓,↑
- Sideroblastic: ↑,↑,N,↑
-
Blood Gas/Acid Base rough references
- pCO2: ~100 [80-100]
- pO2: ~45 (~1/2 of pCO2) [35-45]
- HCO3-: ~23 (~1/2 of pO2) [22-26]
- pH: 7.35-7.45
-
↑/↓ for bili (unconj,conj,Ubili,urobil) in prehep, hep, post hep
- pre hep: ↑,N,0,↑
- hep: ↑,↑,0-↑,↑ (everything's up except Ubili)
- post hep: N,↑,↑,↓
-
FFN indicator of?
- FFN is a negative predictor
- neg FFN = no preterm delivery
- pos FFN = not a predictive value
- high specificity
-
Also measure ____ with Theophylline? Procainamide? Primidone?
- Theophylline: caffeine
- Pocainamide: NAPA
- Primidone: Pheobarbital
-
Osmolality calculation
2*Na + Glucose/18 +BUN/2.8
-
Creat clearance calc
- Ucreat/Pcreat*Uvol (mL)/Utime (min)
- *1.73/area to factor in SA
-
Normal BUN:creat
10:1-20:1
-
Graves disease
- autoimmune (TRAb,TSI)
- thyroid-stim Abs cause ↑T3/T4 ↓TSH
- "Go getter Graves" everything ↑ except TSH
- Primary hyperthyroidism, increased metab, bulging eyeballs, etc
-
Myxedema
- Thyroid deficiency (primary hypothyroidism)
- "Morbid Myxedema" everything ↓ except TSH
-
Hashimoto's
- autoimmune (TPO Ab, TgAb)
- anti-thyroid antibodies cause thyroid damage ↑TSH ↓T3/T4
- Primary hypothyroidism, weight gain, etc
-
Cushing's
- Cushy Carl = Everything ↑ (Cortisol, glucose, Na, urinary steroids, aldosterone)
- Obesity, hypertension, moon face, poor healing
- Cushing's Disease (secondary Cushings)= ACTH-releasing tumors AKA secondary
- Primary Cushings = cotrisol-releasing carcinoma
- *no diurnal variation in this syndrome
-
Addison's
- Anemic Addison = Everything ↓ **ACTH can be ↑ (coristol, Na, Hb, Alodsterone, urinary steroids)
- Primary adrenal insufficiency (destruction of adrenal cortex)
- ACTH stimulation test NEGATIVE
-
catecholamines?
- "Adrenal Medusa guards the Lions D.E.N. in the catecombs"
- Dopamine, Epinephrine, Norepinephrine
-
Hypothalamus -> pituitary -> (target organ) axis -> resulting substance (5)
- TRH -> TSH -> (Thyroid) -> T3/T4
- CRH -> ACTH -> (Adrenals) -> cortisol, aldosterone, catecholamines
- GnRH -> LH/FSH -> (ovaries/testes) -> sex steroids
- GHRH/GHIH -> GH -> (bones/cartilage) -> insulin-like growth factors
- PIF/PRL -> PRL -> (mammary glands)
-
aldosterone function
Increase blood volume (increase Na reabs, decrease K reabs)
-
Hormones increased at NIGHT?
- GH (serotonin stims)
- Prolactin
-
Conn's
- Primary hyperaldosteronism (aldosterone-releasingadrenal adenomas)
- Increased BP, Na
- Decreased renin, K
-
Urea formation?
- Major product of protein breakdown!!!
- AA breakdown -> NH4+ -> urea (via urea cycle)
- prevents NH4 toxicity
- *note - freely filtered, but passively resabs (~50%)
-
Calcium breakdown in blood
- 1% in blood, of that...
- 45% bound to protein
- 10% complexed with anions
- 45% free/ionized *ACTIVE FORM
-
Metabolic syndrome
- 3/5
- Waist >40in
- Trig >150
- HDL <40
- BP >130/85
- Fgluc >100
-
Common bili "diseases" and their effect
- Glibert's: decreased glucoronyl transferase activity
- increased ubili
- benign
- common
- Crigler-Najjar: severely decreased or no glucoronyl activity
- very increased ubili
- decreased cbili, urobil, fecal urobil
- kernicterus, jaundace
- very rare
- Dublin-Johnson/Rotors: increased cbili, ubili
-
Typical pathway of bili.
- unconjugated (circ, spleen) --glucoronyl transferase (liver)--> conjugated (bile duct, intestines)
- conjugated (bile duct, instestines) --bacteria (intestines)--> urobilinogens (intestines)
- urobilinogens (intestines) --20% reabsorp (intestines)--> urine
- urobilinogens (intestines) --oxidation (intestines)--> urobilin (brown feces)
-
RAAS very basic
- Angiotensinogen --(renin)--> angiotensin I --(ACE in lungs)--> angiotensin II -> vasoconstriction, aldosterone release
- acts in increase BP, Na
-
[HCO3-]:[H2CO3] normal
20:1
-
hypoventilation vs hyperventilation
- Hypo: increased pCO2 (decreased pH)
- Hyper: decreased pCO2 (increased ph)
-
Methemoglobin change?
Ferric in place of Ferrous ion
-
TDM - steady state, first order kinetics
- steady state after 5 1/2 half lives
- 1st order k: clearance proportional to [drug], halflife = 0.693/K
- *note- ethanol, theophylline, salicylates, phenytoin NOT 1st order
-
Hormones that increase bone breakdown and decrease bone breakdown
- increase: PTH, T4 (thyroxine), cortisol
- decrease (increase formation): estrogen, testosterone, calcitrol (vit D), calcitonin, insulin
-
hsCRP values
- 0.5: low risk
- 1.5: average risk
- 3.5: high risk
- 10: inappropriate test
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