Internal Medicine

Cephalosporins

Cephalosporins

1st Generation: Cefazolin, Cephalexin
-Gram+
-PEcK: proteus, E. coli, Klebsiella
 
2nd Generation: cefoxitin, cefaclor, cefuroxime
-Gram+
-HEN PEcKS: Haemophilus, enterobacter, neiseria, Proteus, E. coli, Klebsielia, Serratia
 
3rd Generation: ceftriaxone, ceftaxime, ceftazidine
-Gram+ but covers also more of Gram-
-Good for serous gram-
-covers HEN PEcKS as well
-Ceftriaxone: gonorrhea, Ceftazidine: pseudomonas
 
4th Generation: cefepime, cefpiramide
-increased activity against Pseudomonas, gram+
-can cross BBB
-has gram- activity like 3rd generation and also covers the HEN PEcKS
 
5th Generation: ceftobiprole
-new drug. Good for pseudomonas.
 
 
 
Clindamycin: 
-binds 50s ribosomal unit
-good for anaerobes above diaphragm (bacteroides fragilis, clostridium perfringens)
-community acquired infections: use something like Bactrim or Clinda (as apposed to Vancomycin)
 
Moxifloxacin:
-fluoroquinolone (inhibits DNA gyrase)
-good for gram- rods of Urinary tract and GI tracts (including pseudomonas), Neisseria, and some gram+ organisms.

 

Chronic obstructive pulmonary disease -- chronic bronchitis & emphysema

COPD 

1)      Chronic bronchitis: clinical diagnosis; chronic productive cough (3+ months/yr for at least 2 consecutive years)
2)      Emphysema: pathologic diagnosis; alveolar walls damaged à permanent enlargement of air spaces distal to terminal bronchioles.
 
-tobacco smoke à increases # of activated macropahages and PMNs, inhibits a1-antitripsin, increases oxidative stress à destruction of alveolar walls.
 
-pink puffers (emphysema) vs. blue bloaters (chronic bronchitis)
-see article on reading flow volume loops
 
Treatment: 
1)      stop the smoking
2)      B2 agonists (short acting – albuterol and long acting – salmeterol).
3)      Anticholinergics (inhaled) – ipratropium bromide (slower onset but longer lasting)
------------------------------------above are first line
4)      Corticosteroids (inhaled) – for patients who are not controlled on brochodilators. Are anti-inflammatory.
-------------------------------------
5)      Theophylline?
------------------------------------
6)      Oxygen – can prevent pulmonary hypterension and cor pulmonale. (for severe disease)
7)      Vaccination – against strep pneumo every 5 years.
8)      Surgery: resection & transplantation.
 
Complications:
1)      Acute exacerbations (from infection, noncompliance, cardiac disease)
2)      Secondary polycythemia (Hct>55% in men or >47% in women) from chronic hypoxemia
3)      Pulmonary HTN and cor pulmonale
 
For acute exacerbations: use the above medications but do not use inhaled corticosteroids (have to use Oral and then taper off with oral prednisone once symptoms improve). Antibiotics – azithromycin & levofloxacin. Oxygen. Noninvasive positive-pressure ventilation (such as CPAP & BIPAP)
 
 

 

Clinical Lab Values

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

 

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

 

 

Diagnosing Diabetes

 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.

Diseases of Heart Muscle

Disease of Heart Muscle

Dilated Cardiomyopathy: 
-most common type.
-dysnfunction of left ventricular contractility
-caused by CAD (causing ischemia), MI, infection, alcohol;  tons of other causes.
-get Right and Left sided heart failure
-S3 and S4; tricuspid and mitral insufficiency.
 
Hyptertrophic Cardiomyopathy (HCM)
 
Restrictive Cardiomyopathy
 
Myocarditis

 

EKG values

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

 

Endocrine & Metabolic disturbances in Chronic Renal Failure

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

Heart Sounds

 

Image:Gray1216.svg

Heart Sounds:
 
S1: start of systole; caused by the tricuspid and mitral valves closing.
S2: diastole; aortic and pulmonic valves close
 
S3: inrushing blood from the atria causes oscillation of the blood back and forth in the walls of the ventricles. Occurs in the middle of diastole because initially there is not enough blood in the ventricles to cause the reverberation.
Pathologic causes:
-rapid ventricular filling:
-mitral regurgitation (which means atria will be overfilled in systole and can thus send more blood to ventricles during diastole and thus cause rapid ventricular filling)
-elevated left atrial and left ventricular filling pressures (from a stiff and dilated left ventricle)
            -ventricular septal defect (hole allows rapid filling from other side)
-poor left ventricular function
            -post-MI (dead tissue is stiff and does not relax so filling is quick)
            -dilated cardiomyopathy (thin and stiff walls)
 
S4: atria contracting forcefully to overcome stiff or hypertrophic ventricles. (stiff from post-MI fibrosis, hypetrophy from aortic stenosis, hypertension, overloading).
Occurs immediately before S1. Sometimes heard in healthy children and trained athletes.
If pathologic, will be best heard at apex.

 

Hematology

Findings on Peripheral Blood Smear

 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
 

Hepatic Biliary and Pancreatic ducts

How does the HIV virus infect host cells?

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

 

ID Gram+ and Gram- Organisms

 

Gram +
 
I.                    Rods:
a.       Bacillus
b.      Listeria
c.       Actinomyces
d.      Nocardia
e.       Clostridium
f.        Corynebacterium
II.                 Cocci
a.       catalase+ --> staph
                                                               i.      -coagulase+ --> s. aureus (b hemolytic)
                                                             ii.      -coagulase-
1.      novobiocin sensitive à s. epidermidis
2.      novobiocin resistant à s. saprophyticus
b.      catalase- --> strep
                                                               i.      -a hemolytic (green color)
1.      optichin sensitive, quelung+, bile soluble --> strep pneumo
2.      optichin resistant, quelung-, bile insol -->viridians strep (s. mutans)
                                                             ii.      -b hemolytic (clear color)
1.      bacitracin sensitive --> group a --> s. pyogenes
2.      bacitracin resistant --> group b --> s. aglactiae
                                                            iii.      -y hemolytic (no hemolysis)
1.      enterococcus (E. faecalis)
2.      peptostreptococcus (an anaerobe)
 
 
Gram –
 
I.                    Cocci
a.       Maltose fermenter: Neiserria meningitides
b.      Maltose nonfermenter: Neiserria gonorrhea
II.                 Coccoid rods
a.       Haemophilus influenzae
b.      Pasteurella
c.       Brucella
d.      Bordetella pertussis
e.       Bacteroides
III.               Rods
a.       Lactose Fermenters
                                                               i.      Fast fermenters
1.      Klebsiella
2.      E. coli
3.      Enterobacter
                                                             ii.      Slow fermenters
1.      Citrobacter
2.      Serratia
b.      Lactose Nonfermenters
                                                               i.      Oxidase Positive
1.      pseudomonas
                                                             ii.      Oxidase negative
1.      Proteus
2.      Salmonella
3.      Shigella

 

Increased intracranial pressure and hyponatremia

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

Lung Neoplasms

 
I.                    Lung cancer
a.       Small cell lung cancer –25%; centrally located; can cause SVC syndrome, SIADH, ectopic ACTH,
                                                               i.      Chemotherapy is the usually treatment since they are unresectable when diagnosed.
b.      Non-small cell lung caner—75%;
                                                               i.      Types:
1.      Large cells: peripheral
2.      Adenocarcinoma: peripheral; lowest association with smoking.
3.      Squamous cell carcinoma: central
                                                             ii.      Surgery best option. Radiation along with surgery. Chemo uncertain benefit.
II.                 Mediastinal Masses
a.       Anterior: thyroid, teratogenic, thymoma, lymphoma
b.      Middle: lung cancer, lymphoma, aneurysms, cysts, Morgagni hernia (an opening in the right side of the diaphragm. One of 2 congenital hernias)
c.       Posterior: neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek’s hernia (the other congenital hernia… on left side).

 

Managing DKA and HHNS

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

Meningitis

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.

 

 

 

Pleural Diseases

Disease of the Pleura

I.                    Pleural Effusion
a.       Transudative: from either elevated capillary pressure (CHF) or decreased oncotic pressure (hypoalbuminemia);
                                                               i.      Causes: CHF, cirrhosis, PE, nephrotic syndrome, hypoalbuminemia, peritoneal dialysis, atelectasis.
b.      Exudative: increased permeability (from damage caused by infection, malignancy, embolism);;
                                                               i.      Causes: viral infection, bacterial pneumonia, PE, TB, malignancy (lung, breast, lymphoma).
                                                             ii.      Dx:
1.      effusion
a.       protein pleural/ protein serum >.5
b.      LDH pleural/ LDH serum >.6
c.       LDH > 2/3 the upper limit of normal serum LDH
2.      xray: 
a.       blunting of costophrenic angles, at least 250 mL of fluid necessary. 
b.      Lateral decubitus xray is best
3.      thoracentesis
a.       Don’t do thoracentesis if you see effusion <10mm thick (can cause a pneumothorax)
b.      If thoracentesis is done, Order 4 Cs on the fluid drained: Cytology, Cell count, Culture, Chemistry (glucose, protein included).
                                                            iii.      Treatment:
1.      transudative: diuretics, sodium restriction. If massive, can do thoracentesis
2.      exudative: treat underlying disease
3.      parapneumonic (in presence of pneumonia)
a.       antibiotics
b.      if complicated or empyema:
                                                                                                                                       i.      chest tube
                                                                                                                                     ii.      thrombolytic agents (streptokinase + urokinase)
                                                                                                                                    iii.      surgical lysis of adhesions may be necessary
II.                 Empyema: pus within the pleural space
a.       Complication of pneumonia
b.      Extension of other foci (mediastinitis or abscess) into the pleural space
c.       Treatment: thoracentesis, antibiotics, rib resection/open drainage.
III.               Pneumothorax: air in pleural space
a.       Spontaenous – without any trauma
                                                               i.      Primary (simple)
1.      occurs in happy individuals
2.      rupture of subpleural blebs (air-filled sacs on the lung) at the apices of lungs… causing parts of lung to collapse… usually asymptomatic and no treatment necessary… since these patient have good pulmonary reserve.
3.      recurrence is up to 50% in 2 years.
                                                             ii.      Secondary (complicated)… to underlying disease (COPD, asthma, ILD, neoplasms, CF, TB.
1.      more dangerous – these patients have less pulmonary reserve.
b.      Traumatic: thoracentesis, central lines, transthoracic needle aspiration. So you need to get a CXR after these procedures.
c.       Treatment: nothing if small, one-way vale chest tube (small chest tube), oxygen, chest tubes,
IV.              Tension Pneumothorax: air enters the pleural space but is unable to escape à causes ipsilateral lung to collapse and shifts the mediastinum away from the pneumothorax.
a.       Causes: mechanical ventilation, CPR, trauma

 

Reading Flow volume loops

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.

Skin conditions

Allergic reactions to fulvic acid

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.

 

Scabies

Scabies Bite Photos

Scabies bite pictures

Small bowel obstruction vs. Large bowel obstruction

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)

Vasculitis diagnosis symptoms

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,