Cephalosporins
COPD
| Albumin | 3.2 - 5 g/dl | |
| Alkaline phosphatase (Adults: 25-60) | 33 - 131 IU/L | |
| Adults > 61 yo: | 51 - 153 IU/L | |
| Ammonia | 20 - 70 mcg/dl | |
| Bilirubin, direct | 0 - 0.3 mg/dl | |
| Bilirubin, total | 0.1 - 1.2 mg/dl | |
|
Blood Gases |
||
| Arterial | Venous | |
| pH | 7.35 - 7.45 | 7.32 - 7.42 |
| pCO2 | 35 - 45 | 38 - 52 |
| pO2 | 70 - 100 | 28 - 48 |
| HCO3 | 19 - 25 | 19 - 25 |
| O2 Sat % | 90 - 95 | 40 - 70 |
| BUN | 7 - 20 mg/dl | |
|
Complete blood count (CBC) Adults |
||
|
Male |
Female |
|
| Hemoglobin (g/dl) | 13.5 - 16.5 | 12.0 - 15.0 |
| Hematocrit (%) | 41 - 50 | 36 - 44 |
| RBC's ( x 106 /ml) |
4.5 - 5.5 |
4.0 - 4.9 |
| RDW (RBC distribution width) | < 14.5 | |
| MCV | 80 - 100 | |
| MCH | 26 - 34 | |
| MCHC % | 31 - 37 | |
| Platelet count | 100,000 to 450,000 | |
| Creatinine kinase (CK) isoenzymes | ||
| CK-BB | 0% | |
| CK-MB (cardiac) | 0 - 3.9% | |
| CK-MM | 96 - 100% | |
| Creatine phosphokinase (CPK) | 8 - 150 IU/L | |
| Creatinine (mg/dl) | 0.5 - 1.4 | |
|
Electrolytes |
||
| Calcium | 8.8 - 10.3 mg/dL | |
| Calcium, ionized | 2.24 - 2.46 meq/L | |
| Chloride | 95 - 107 mEq/L | |
| Magnesium | 1.6 - 2.4 mEq/L | |
| Phosphate | 2.5 - 4.5 mg/dL | |
| Potassium | 3.5 - 5.2 mEq/L | |
| Sodium | 135 - 147 mEq/L | |
| Ferritin (ng/ml) | 13 - 300 | |
| Folate (ng/dl) | 3.6 - 20 | |
| Glucose, fasting (mg/dl) | 60 - 110 | |
| Glucose (2 hours postprandial) (mg/dl) | Up to 140 | |
| Hemoglobin A1c | 6-8 | |
| Iron (mcg/dl) | 65 - 150 | |
| Lactic acid (meq/L) | 0.7 - 2.1 | |
| LDH (lactic dehydrogenase) | 56 - 194 IU/L | |
|
Lipoproteins and triglycerides |
||
| Cholesterol, total | < 200 mg/dl | |
| HDL cholesterol | 30 - 70 mg/dl | |
| LDL cholesterol | 65 - 180 mg/dl | |
| Triglycerides | 45 - 155 mg/dl (< 160) | |
| Osmolality | 289 - 308 mOsm/kg | |
| SGOT (AST) | < 35 IU/L (20-48) | |
| SGPT (ALT) | <35 IU/L | |
|
Thyroid Function tests |
||
| Free T3 | 2.3-4.2 pg/ml | |
| Serum T3 | 70-200 ng/dl | |
| Free T4 | 0.5-2.1 ng/dl | |
| Serum T4 | 4.0-12.0 mcg/dl | |
| TSH | 0.25-4.30 microunits/ml | |
| Total iron binding capacity (TIBC) | 250 - 420 mcg/dl | |
| Transferrin | > 200 mg/dl | |
| Uric acid (male) | 2.0 - 8.0 mg/dl | |
| (female) | 2.0 - 7.5 mg/dl | |
|
WBC + differential |
||
| WBC (cells/ml) | 4,500 - 10,000 | |
| Segmented neutrophils | 54 - 62% | |
| Band forms | 3 - 5% (above 8% indicates left shift) | |
| Basophils | 0 - 1 (0 - 0.75%) | |
| Eosinophils | 0 - 3 (1 - 3%) | |
| lymphocytes | 24 - 44 (25 - 33%) | |
| Monocytes | 3 - 6 (3 - 7%) | |
Cushing’s syndrome
Syndrome: increase in glucocorticoids (primarily cortisol).
-Disease: happens when the pituitary releases ACTH. ACTH will cause other stuff to be elevated as well such as androgens, and MSH (POMC splits up into ACTH and MSH or melanocyte stimulating hormone)… get other symptoms like hirsuitism and hyperpimentation. Will respond to high dose dexamethasone suppression test.
-Ectopic ACTH ( small cell carcinoma of the lung – bronchial carcinoma & thymoma). Will not respond to dexamethosone.
-Adrenal tumor: get low ACTH but high Cortisol.
Hypothalamus—PVN (paraventricular nucleus) à CRH à Pituitary à ACTHà Adrenal glands à Cortisol
Diagnosis of Diabetes is done using one of the following criteria:
1) glucose lvl of 125mg/dL or higher after an 8 hour fast. Have to see this on two separate occasions.
2) Random glucose of >200 mg/dL
3) HgA1C >6.5 %. Have to see this on two separate occasions. Although you can still use the 8 hour fast, using the HgA1C is now becoming preferred.
4) Glucose tolerance test >200mg/dL within 2 hours of giving 75g oral glucose.
Disease of Heart Muscle
1 small box = 1 mm = 40ms = .1mV amplitude
1 large box = 5 mm = 200ms = .5mV amplitude
Normal PR = 120-200 ms (3 to 5 small boxes)
.... prolonged in incrased K or Mg, first degree heart block (AV node block)
.... shortened in pre-excitation via accessory pathway (Wolff-Parkinson-White sydnrome)
Normal QRS = 60-100ms (3 small squares or less)
...widened in increased K or Mg,
Q wave should be less than 1/3 the height of the R wave. If its higher.... think Myocardial Infarction.
T waves
-peaked --> hyperkaelemia
-negative... normal in lead aVR. (also possible in aVL, aVF, III) Lead V1 may have a positive, negative, or biphasic T wave.
..otherwise, can indicate Coronary ischemia, LVH.
U waves -- come right after T waves
-in hypokalemia, hypercalcemia, thyrotoxicosis
Chronic renal failure--> decreased clearance of phosphate --> hyperphosphatemia --> decreased production of activated vitamin D (1,25 dihydroxy) --> hypocalcemia --> hyperparathyroidism --> hypercalcemia, renal osteodystrophy
hyperphosphatemia --> vascular calcifications --> calciphylaxis (necrotic skin lesions)
Men: decreased testosterone
Women: amenorrhea, infertility, hyperprolactinemia
Pruritis
Appearance of Red Blood cells on a peripheral smear can give clues regarding the pathology in a patient:
Hypersegmented neutrophils: folate/ B12 deficiency
Sickled cells: sickle cell disease
Hypochromic and microcytic RBCs: iron deficiency
Polychromasia of reticulocytosis: hemolysis
Rouleaux formation: multiple myelmoa
Parasites in RBCs: malaria, babesiosis
Iron inclusions in RBCs in bone marrow: sideroblastic anemia
Teardrop-shaped RBCs: myelofibrosis
Schistocytes, helmet cells, fragmented RBCs: intravascular hemolysis
Spherocytes, elliptocytes: hereditary spherocytosis, elliptocytosis
Acanthocytes, spur cells: abetalipoproteinemia
Target cells: thalassemia, liver disease
Echniocytes: burr cells, acanthocytes: uremia
Basophilic stippling: lead poisoning
Heinz bodies: glucose-6-phosphate deficiency
Bite cells: glucose-6-phosphate deficiency
Howell-Joly bodies: asplenia

How does AIDS virus infect?
Proviral DNA is integrated into the Host genome (Latent stage)... it can remain like this for a while producing low-level virion production. However, it can be reactivated (possibly by infection of EBV or CMV).
Spread: blood, semen, vaginal secretions, breast milk, saliva
We normally experience symptoms of hyponatremia when sodium levels fall below 120 mEq/L. However, an exception to that is during states of increased intracranial pressure (as in a head injury).
The Monro-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is a fixed volume. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.[5]
So, if somebody gets hit in the head with a bat and start bleeding (thus having an increased ICP) and then on top of that has hyponatremia...which causes the brain to swell (brain cell uptake water)... the ICP will rise even more... so the patient will experience symptoms of hyponatremia earlier than somebody without increased ICP to begin with.
Increased ICP is a clinical feature of hyponatremia (so somebody without any increase in ICP will eventually have an increased ICP given that the Na goes down enough to cause the brain to swell). Increased ICP and cerebral edema are the cause of the neurological features in hyponatremia: headache, delirium, brisk DTRs, weakness, seizures, coma. Increased ICP will also cause hypertension.
Lung Neoplasms
DKA (Diabetic ketoacidosis)
-make sure not hypokalemic, give k 1-2 hr after starting insulin
-hydration -- start immediately
-insulin -- .1u/kg infusion, then .1/kg/hr till you get to 250 mg/dL glucose.. then add 5% glucose D5 1/2 NS.
HHNS (hyperosmolar hypeglycemic nonketotic syndrome)
-1 L NS fluids in first hour, then 1 L NS over next 2 hours
-1/2 NS once patient is stable
-give D5 1/2 NS (add 5% glucose) once the glucose level is down to 250 mg/dL.
...> you dont want to lower glucose too fast as it can cause cerebral edema
-give Insuline 5-10 U bolus. then 2-4U/hr
Acute Bacterial Meningitis
causes::
Neonates -- Group B strep > E. Coli > Listeria monocytogenes
Children>3m -- Neisseria meningitidis > Strep Pneumo > Listeria
Adults (18-50) -- S. Pneumo > Neisseria > Haemophilus Influenza
Elderly (>50) -- S. Pneumo > Neisseria > Listeria
tx: ceftriaxone or cefotaxime+vancomycin+ampicillin
Immunocompromised -- Listeria > gram-neg bacilli > S. pneumo
tx: ceftazidime+ampicillin+vancomycin
CSF::
Aseptic -- mostly lymphocytes and monocytes, WBC <1,000, normal glucose.
Bacterial -- mostly PMNs. high WBC (>1,000), Low glucose.
Clinical:
symptoms: headache, fever, stiff neck, n/v, photophobia, Altered mental status.
signs: stiff nech, Rashes (neisseria-> purpura), vesicular lesions (HSV, Varicella), increase in ICP (causes papilledema, seizures), CN palsies,
Kernig's sign-- cant extend knees when lying down with hips flexed 90 degrees
Brudzinski's sign-- passive flexion of the neck causes flexion of the legs and thighs.
Disease of the Pleura
Reading Flow volume loops
... can be somewhat confusing. the axis are all screwed up in my opinion... thats what i determined after looking at this for the past 10 minutes.
Anyhow, you wanna look at things like TLC (total lung capacity), FEV1 (amount of air the person can blow out in the first second), and FEF50%.
FEF50% -- forced expiratory flow (the average speed of air coming out of the lung during middle portion of expiration)... which is low in both obstruction and restriction (but especially in an obstruction).
TLC is increased in obstructive.

A- normal
B-obstructive
C-restrictive
D-obstruction of upper airway.
Allergic reactions to fulvic acid
Fulvic acid is derived from the microbial degredation of plant an animal tissues. There is very little evidence of health benefits, allergies, side-effects related to its ingestion.
Comparison of small bowel obstruction (SBO) and LBO features :
Small bowel------------------------Large bowel
Bowel diameter (cm)
>3 and <--------------------------- >5
Position of loops
Central-----------------------------Peripheral
Number of loops
Many-------------------------------Few
Bowel markings
Valvaulae---------------------------Haustra
(all the way across)-----------------(partially across)
Diagnosis and symptoms of vasculitis.
There are 3 main categories of vasculitis. In all types, the blood vessels get inflammed and the organ supplied by that blood vessel can get necrosed (so you can even have tongue necrosis in something like Temporal arteritis if the blood vessels). Symptoms are based on the endorgans affected. Diagnosis usually requires measuring lvls of ESR, certain antibodies (p-ANCA, c-ANCA) and most importantly biopsy of effected tissue.
Large Vessel:
-Temporal arteritis (aka Giant Cell arteritis, older females, associated with polymalgia rheumatica, involves most commonly the temporal artery, biopsy is 90% sensitive, elevated ESR)
-Takayasu's (young Asian women, involves aortic arch and its branches, diagnose with arteriogram)
Medium Vessel:
-Kawasaki's (in kids)
-Churg-strauss (involves many organ systems, p-ANCA association, poor prognosis, biopsy of lung or skin tissue to confirm diagnosis)
-Wegner's granulomatosis (involves mainly the kidneys and upper/lower respiratory tracts, nodules/infiltrates on chest radiographs, c-ANCA association, very high ESR, open lung biopsy to confirm diagnosis)
-Polyarteritis nodosa or PAN (No pulmonary involvement, involves GI and nervosus system vessels, biopsy of involved tissue or mssenteric angiography)
-microscopic polyangiitis
Small Vessel:
-Henoch-Schonlein purpura
-Hypersensitivity vaculitis (caused by drug reaction, infection or other stimuli, Skin involvment: palpable pupura, macules, or vesicles, have to do biopsy to diagnose)
-Bechet's syndrome (oral and genital ulcers, have to do biopsy to diagnose)
-Buerger's disease (aka Thromboangiitis Obliterans, associated with smoking, affects arms and legs,