2/3 of the 16 million diabetic patients in the United States ( 6% of the population) will die of some form of heart or blood vessel diseases
1/3 of these patients will remain undiagnosed.
Although major medical advances have improved overall cardiovascular mortality rates, diabetic patients have ? yet to experience the same degree of risk reductions as their nondiabetic counterparts.

Heart failure
--A clinical syndrome with signs and symptoms of congestion and circulatory failure (regardless of cardiac function).
Final common pathway of most end-stage cardiovascular complications.

--functional pathology of heart muscle
--regardless of symptoms,
--often related to abnormalities in contraction (systolic dysfunction) or relaxation (diastolic dysfunction).

Diabetes is observed in 15% to 25% of HF patients in major clinical trials.
Among all patients hospitalized for heart failure, 25% to 30% patient have DM as a comorbid condition
In large-scale mortality trials, in HF patients with systolic dysfunction, diabetes was an independent risk factor for death.

Framingham Study and  SOLVD
Framingham Study
A direct association between DM and HF was first demonstrated
Risk of developing symptomatic HF
2.4-fold in diabetic men
5-fold in diabetic women,
independent of coexisting hypertension or ischemic heart disease.

Studies of Left Ventricular Dysfunction (SOLVD)
Registry of 6791 patients with heart failure,
1310 diabetic patients were more likely to be hospitalized for HF exacerbation and likely to die.

Cardiomyopathy and Diabetes
A distinctive entity of diabetic CM does exist as a vulnerable alteration to the myocardium
impaired glycemic control
insulin resistance
But direct, concrete evidence is lacking

Similar pathophysiologic processes
Endothelial dysfunction
Oxidative stress
Lead to overt HF that is difficult to treat.
coexisting risk factors
major index events (such as myocardial infarction)...

Surgical Site Infection ( SSI )

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Clinical criteria ( CDC )
A purulent exudate draining from the surgical site
A positive fluid culture obtained from a surgical site that was closed primarily
The surgeon’s diagnosis of infection
A surgical site that requires reopening

SSI is a difficult term to define accurately because it has a wide spectrum of possible clinical features
“It’s hard to define, but I know it when I see it.”
SSI are classified into three categories, depending of which anatomic areas are affected

Definitions of SSI
Superficial incisional SSI: Infection involves only skin and subcutaneous tissue of incision.
Deep incisional SSI: Infection involves deep tissues, such as fascial and muscle layers. This also includes infection involving both superficial and deep incision sites and organ/space SSI draining through incision.
Organ/space SSI: Infection involves any part of the anatomy in organs and spaces other than the incision, which was opened or manipulated during operation.

Risk factors
Decreased host resistance can be due to systemic factors affecting the patient's healing response, local wound characteristics, or operative characteristics.
Systemic factors include age, malnutrition, hypovolemia, poor tissue perfusion, obesity, diabetes, steroids, and other immunosuppressants.
Wound characteristics include nonviable tissue in wound; hematoma; foreign material, including drains and sutures; dead space; poor skin preparation, including shaving; and preexistent sepsis (local or distant).
Operative characteristics include poor surgical technique; lengthy operation (>2 h); intraoperative contamination, including infected theater staff and instruments and inadequate theater ventilation; prolonged preoperative stay in the hospital; and hypothermia

Prophylactic Antibiotics
General agreement exists that prophylactic antibiotics are indicated for clean-contaminated and contaminated wounds
Antibiotics for dirty wounds are part of the treatment because infection is established already.
Clean procedures might be an issue of debate. No doubt exists regarding the use of prophylactic antibiotics in clean procedures in which prosthetic devices are inserted because infection in these cases would be disastrous for the patient.

Systemic preventive antibiotics should be used in the following cases
A high risk of infection is associated with the procedure (eg, colon resection).
Consequences of infection are unusually severe (eg, total joint replacement).
The patient has a high NNIS risk index.

Intraoperative re-dosing
Operation is prolong
If massive blood loss occurs
The patient is obese

Intraabdominal Infection
Usually polymicrobial
There is synergism between aerobic and anaerobic organisms
 Determined by gravity and the physiologic drainage basins of the abdomen
  Subphrenic space, pelvic space, subhepatic space, paracolic gutter, lesser sac, subfascial area

Primary Peritonitis
Microorganisms lodge in the peritoneal cavity without a fundamental intraabd. Process
 Previously occurred in miliary TB, but now commonly occurs in ascites
  Most common organism in ascties is S. pneumoniae

Secondary peritonitis
Usually begins with perforation of the GI tract
 From inflammatory or neoplastic process
One major factor in determining severity is the size of the bacterial inoculum
 Perforated appendix has 106 to 107 bacteria per g
 Sigmoid colon has 1010 to 1011 bacteria per g
   Anaerobes exceed aerobes 1,000-fold
Adjuvant factors are also important
 Food, fiber, exfoliated cells, blood, dead tissue
Bacteria that are eliminated are either phagocytized or removed into the lymphatic system

Neonatal Hypotonia
Identification of hypotonia
Holding the infant under the arms
The legs will be extended
Decreased tone of the shoulder girdle allows the infant to slip through the examiner's hands

Identification of hypotonia
Holding the infant in horizontal suspension
The back hangs over the examiner's hand, and the limbs and head hang loosely
Passive extension of the legs at the knees no resistance is met
Pulling the infant from the supine to sitting position the head lags and continues to lag when the sitting position is reached

Central Causes
Cerebral palsy
Hypoxic ischemic encephalopathy
Intracranial hemorrhage
Cerebral malformations
Chromosomal abnormalities (e.g.Trisomy 21, Prader-Willi syndrome)
Congenital infection TORCH
Acquired infections
Peroxisomal disorders
Drug effects (e.g. benzodiazepines)

Spinal cord
Birth trauma (especially Breech delivery)

Anterior Horn Cell
Spinal Muscular Atrophy
Traumatic myelopathy

Neuromuscular junction
Congenital myasthenia gravis
Transient acquired neonatal myasthenia
Infantile botulism

Muscular dystrophies (congenital myotonic dystrophy)
Congenital myopathies (e.g. central core disease)

Peripheral nerves
Hereditary sensory motor neuropathies
Charcot-Marie-Tooth disease

Metabolic myopathies
Acid maltase deficiency
Carnitine deficiency
Cytochrome-c-oxidase deficiency

Liver function Tests

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Liver dysfunction diagnosis
The diagnosis of liver disease depends on a combination of patient history, physical examination, laboratory testing, biopsy and sometimes imaging studies such as ultrasound scans.

Liver function Test
Enzyme tests
    –Alkaline phosphatase
    –Gamma glutamyl transpeptidase
• Tests of synthetic function
    – Prothrombin time
• Tests of hepatic transport capability
    –Serum bilirubin

Total protein
There are 2 major types of protein: albumin and globulin.
Normal range 5.6 -8.4 g/dl
Albumin (ALB) Albumin provides a gauge of nutritional status. It can be reduced due to liver damage and kidney disease. Because albumin is made in the liver, levels tend to drop with cirrhosis.
High albumin levels usually reflect dehydration and use of some drugs
reference values are dependent on many factors, including patient age, gender, sample population, and test method,
Normal range 3.4 -5.4 g%
The microalbumin test measures very small levels of albumin in your urine and may indicate whether you are at risk for developing kidney disease

Globulin This describes the specific level of globulins — which include antibodies. This measure can be raised when liver cells are damaged due to autoimmune liver damage or to long-standing liver disease of many types, particularly when cirrhosis exists, multiple myeloma and chronic infections.

Bilirubin Bilirubin is a by-product of the breakdown of red blood cells. It is the yellowish pigment responsible for jaundice.
Bilirubin levels can be raised due to many different liver diseases, as well as conditions other than liver disease, e.g. gallstones. In cases of long-term liver illness (chronic hepatitis).
In cases of short-term liver illness (acute hepatitis), elevated bilirubin levels indicate the severity of the acute illness.
Normal range 0.2 -1.5 mg/dl

Alanine transaminase (ALT(
also called Serum Glutamic Pyruvic Transaminase  (SGPT) or Alanine aminotransferase (ALAT)
Enzyme produced and present in hepatocytes (liver cells).
ALT rises dramatically in acute liver damage, such as all types of hepatitis (viral, alcoholic, drug-induced etc) or paracetamol (acetaminophen) overdose.
The reference range is 15-45 U/L in most laboratories. Levels of ALT may equate to the degree of cell damage but this is not always the case, particularly with hepatitis C. An accurate estimate of liver cell damage can only be made by liver biopsy.

Aspartate transaminase (AST(
also called Serum Glutamic Oxaloacetic Transaminase (SGOT) or aspartate aminotransferase (ASAT)
Similar to ALT in that it is another enzyme associated with liver parenchymal cells. It is raised in acute liver damage, but is also present in red cells, and cardiac and skeletal muscle and is therefore not specific to the liver.
It does tend to be higher than ALT in cases of alcohol-related liver disease.

Urinary Incontinence 2

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Urinary incontinence is the inability to control urination which results in unintended urinary flow or leakage
Normal Bladder Function and Continence
Detrusor muscle:
under simultaneous sympathetic and parasympathetic control
Filling phase:
sympathetic tone predominates
allows relaxation of detrusor and tightening of internal sphincter

Voluntary voiding:
sensation of bladder fullness mediated by proprioceptive fibers in detrusor
reflex arc between detrusor and brainstem initiates bladder contraction via increase in parasympathetic and decrease in sympathetic stimulation
reflex under cortical inhibition
voiding occurs with release of inhibition and voluntary relaxation of external sphincter
urethrovesicular angle changes to allow full drainage of bladder

Classification of Urinary Incontinence
6 major subtypes of urinary incontinence:
Urge (“overactive bladder”)
Other (deformity/lack of continuity)

Stress incontinence
urethral hypermobility due to pelvic floor laxity
difficult or multiple vaginal deliveries
other perineal injury (e.g. radiation)
intrinsic urethral sphincter deficiency
autonomic neuropathy
inadequate estrogen levels
partial denervation

Urge incontinence (overactive bladder, detrusor instability)
Inappropriate contraction of detrusor muscle during bladder filling
related to aging (unclear mechanism)
decreased cortical inhibition (CVA, Parkinson’s disease, Alzheimer’s disease, brain tumor)
bladder irritation (UTI, bladder CA, stones)

Reflex incontinence (FYI)
variant of overactive bladder caused by SCI, MS, neurosyphilis, or cord compression
loss of central control leads to detrusor spasticity and functional outlet obstruction
frequent voiding without warning
moderate volumes
equal frequency day and night
decreased perineal sensation and sphincter control
sacral reflexes intact..

Tube Thoracostomy Module

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Tube Thoracostomy Module
1. Drainage of hemothorax, or large pleural effusion of any cause
2. Drainage of large pneumothorax (greater than 25%)
3. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center
4. Flail chest segment requiring ventilator support, severe pulmonary contusion with effusion

1. Infection over insertion site
2. Uncontrolled bleeding diathesis

Preprocedure patient education
1. Obtain informed consent
2. Inform the patient of the possibility of major complications and their treatment
3. Explain the major steps of the procedure, and necessity for repeated chest radiographs

1. Examine the patient and assess need for placement of a thoracostomy tube. Obtain pre-procedure chest X-ray
2. Select site for insertion: mid-axillary line, between 4th and 5th ribs…this is usually on a line lateral to the nipple
3. Don mask, gown and gloves;
4.Prep and drape area of insertion. Have patient place ipsilateral arm over head to “open up” ribs
5. Widely anesthetize area of insertion with the 2% lidocaine. Infiltrate skin, muscle tissues, and right down to pleura

Chest tube insertion
After infiltrating insertion site with local anesthetic, make a 3-4 cm incision through skin and subcutaneous tissues between the 4th and 5th ribs, parallel to the rib margins
-Continue incision through the intercostal muscles, and right down to the pleura
-Insert Kelly clamp through the pleura and open the jaws widely, again parallel to the direction of the ribs (this “creates” a pneumothorax, and allows the lung to fall away from the chest wall somewhat
Insert finger through your incision and into the thoracic cavity. Make sure you are feeling lung (or empty space) and not liver or spleen
-Grasp end of chest tube with the Kelly forcep (convex angle towards ribs), and insert chest tube through the hole you have made in the pleura. After tube has entered thoracic cavity, remove Kelly, and manually advance the tube in
-Clamp outer tube end with Kelly
-Suture and tape tube in place
-Attach tube to suction unit
-Obtain post procedure chest Xray for placement; Tube may need to be advanced or withdrawn slightly..

Pathophysiology of Hepatic Failure

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Hepatic insufficiency
Process characterized by restriction, suppression or failure of hepatic function which is manifested by homeostatic imbalance in the functions provided by the liver cells.
Manifestation of the failure is present when the hepatic cells are required to provide more  „metabolic work“. In basal conditions The failure could not be necessarily manifested.

Acute failure - per acute / fulminant course of hepatitis, toxic injury
Chronic failure – cirrhosis

Exogenous failure  - induced or provoked by external noxas, like alcohol, GUT bleeding, drugs, increased protein in take

Endogenous failure – as a natural consequence of internal hepatic disease /consequence of hepatitis,  biliar cirrhosis... /

Hepatorenal syndrome
functional acute renal failure which is present in patients suffering from severe hepatic diseases followed by ascites and by changes in systemic circulation

increased stimulation of RAA  -  impairment of renal regional circulation
decrease of glomerular filtration
extreme retention of Na and fluids in the body
decreased water elimination

Clinical course of renal failure copy the clinical course of hepatic failure, if liver is being „better“ the kidneys are better too, a vice versa

Portal hypertension
Long lasting increase of blood pressure in v. portae , more than 5-15 mmHg
Pre hepatic portal hypertension
Causes:obliteration of v. porte, v. lienalis (infection, trauma,
  thrombosis, tumor invasion)
Hepatic portal hypertension
Causes:cirrhosis of the liver (alcohol, biliar cirrhosis, hemo-
  chromatosis, Wilson's disease)
- myeloproliferat. diseases (liver and spleen)
- m. Hodgkin, leukemia (infiltration of  peri portal fields)
- sarcoidosis – pathogenesis unknown
- alcohol induced hepatopathy without cirrhosis
- metastasis of tumors
- cystic diseased of the liver

Post hepatic portal hypertension
block of hepatic veins or VCI (Budd - Chiari sy.)
extra hepatic causes (constrictive pericarditis, severe heart failure)..

Autoimmune Hepatitis

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Also Known as Active chronic hepatitis or chronic active hepatitis,Chronic aggressive hepatitis,Lupoid hepatitis,Plasma cell hepatitis and Autoimmune chronic active hepatitis

Chronic hepatitis of unknown etiology
Can progress to cirrhosis
Characteristics include:
 presence of autoimmune antibody
 evidence of hepatitis
 elevation of serum globulins

Accounts for 5.6% of liver transplants in the US
Affects women more than men (3.6:1)
If untreated approximately 40% die within 6 months
40% develop cirrhosis

ANA or Anti-Smooth Muscle antibody positive
Titer usually > 1:100
10% will have an antibody to Soluble Liver antigens (SLA)
Other Antibodies: anti-DNA, ANCA, Anti-mitochondrial, Anti-Actin (AAA), cytoskeletal antibody, nuclear envelope proteins lamin A and C, plasma membrane sulfatides
Bimodal Age distribution (ages 10-20 and 45-70)
Female:male (3.6:1)
Associated with extrahepatic manifestations:
Autoimmune thyroiditis, graves disease, chronic UC
Less commonly with RA, pernicious anemia,  systemic sclerosis, ITP, SLE
40% present with acute onset of symptoms similar to toxic hepatitis or acute viral hepatitis

Presence of anti-Liver/Kidney Microsome Antibodies or anti-Liver Cytosol antibody (ALC-1)

Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis

5% of patients with chronic hepatitis C will have an ANA titer of >1:100
A homogeneous pattern of staining is more common in ANA positive autoimmune hepatitis compared to that of  ANA positive chronic hepatitis C...

Sexually transmitted infections (STI), also previously referred to as sexually transmitted diseases are illnesses that has a significant probability of transmission between humans by means of human sexual behavior.Some STIs can also be transmitted via the use of IV drug needles after its use by an infected person, as well as through childbirth or breastfeeding.

Cause of STI
    Chancroid (Haemophilus ducreyi)
    Chlamydia (Chlamydia trachomatis)
    Granuloma inguinale or (Klebsiella granulomatis)
    Gonorrhea (Neisseria gonorrhoeae)
    Syphilis (Treponema pallidum)
    Viral hepatitis (Hepatitis B virus)
    (Note: Hepatitis A and Hepatitis E are transmitted via the fecal-oral route; Hepatitis C is rarely sexually transmittable,and the route of transmission of Hepatitis D (only if infected with B) is uncertain, but may include sexual transmission.
    Herpes simplex (Herpes simplex virus 1, 2) skin and mucosal, transmissible with or without visible blisters
    HIV (Human Immunodeficiency Virus)—venereal fluids, semen, breast milk, blood
    HPV (Human Papillomavirus)—skin and mucosal contact. 'High risk' types of HPV cause almost all cervical cancers, as well as some anal, penile, and vulvar cancer. Some other types of HPV cause genital warts.
    Molluscum contagiosum (molluscum contagiosum virus MCV)—close contact..

Acute Renal Failure

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To function properly, the kidney requires: (1) normal blood flow; functioning glomeruli and tubules to separate and process an ultafiltrate containing waste products from the blood; and (3) drainage and elimination of formed urine from the body. The sudden interruption of any of these processes will lead to Acute Renal Failure (ARF). Disorders causing ARF are classified on the basis their primary site of interference with these processes. Conditions which interfere with blood delivery to the kidney are called Prerenal, and are most commonly functional (and potentially reversible) in nature (e.g., ECF volume contraction, congestive heart failure) but on occasion may be structural (e.g., renal artery stenosis). Diseases which cause intrinsic injury to the kidney proper (glomeruli, tubules, interstitium, small blood vessels) are grouped under Renal causes of ARF (e.g., acute glomerulonephritis, acute tubular necrosis, acute interstitial nephritis or small vessel vasculitis). Acute Tubular Necrosis is a distinctive clinicopathological syndrome in which the tubules are the primary site of injury. The terms ARF and ATN should not be used interchangeably. Finally, conditions which interfere with normal drainage and elimination of formed urine are classified as Postrenal (e.g., prostatic outlet obstruction, bilateral ureteral obstruction). Pre-renal ARF (also commonly referred to as “pre-renal azotemia”) and acute tubular necrosis (ATN) are the most common causes of acute renal failure in hospitalized patients.

Some combination of hypovolemia, hypotension and diminished renal perfusion is the most common cause of ARF in hospitalized patients. Identification of pre-renal (functional) ARF is important because it is generally reversible. Pre-renal ARF may evolve from blood loss, sodium depletion (due to diarrhea, excessive diuresis or congenital or acquired salt-wasting disorders), redistribution of plasma volume to a so-called “third space” (e.g., ascites in patients with hemorrhagic pancreatitis or hepatic cirrhosis), or reductions in effective arterial blood volume with consequent renal hypoperfusion (as in congestive heart failure, hepatic cirrhosis or nephrotic syndrome). In other situations, especially when for one reason or another renal perfusion is tenuous or already compromised, drugs which affect afferent and/or efferent arteriolar resistance (e.g., NSAIDs, ACE inhibitors) can precipitate pre-renal azotemia....


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1° Syphilis: indurated, nontender ulcerative lesion accompanied by nontender, nonsuppurative regional LAN
2° Syphilis = spirochetemia: fever, malaise, diffuse LAN; patchy alopecia; HA; hyperpgimented maculopapular rash on palms/soles
Latent Syphilis: recognized only by reactivity on serologic testing; no clinical findings; variable course
3° Syphilis: neurosyphiliis, CV, gummatous; pathophysiology is mainly endarteritis

3° Syphilis
neurosyphilis: to be discussed below
CV syphilis:
endarteritis of vasavasorum  progressive necrosis and loss of elastic tissue  dilatation  aneurysm;
esp of aortic arch and proximal thoracic aorta; rarely dissect;
cause symptoms by encroachment/erode chest wall, SVC, recurrent laryngeal nerve, trachea and bronchi
Gummatous syphilis: indolent, destructive granulomatous lesions of soft tissue/bone scarring and disfigurement [BENIGN??]

So How to Dx?
Exams of the lesions/chancre
 ulcer itself not adequate
 Dark field microscopy of exudate
  Corkscrew morphology
  Time and Tx sensitive
 Direct flourescent Ab [DFA-TB] applied to exudate
Serology: 2 stages
Non Treponemal Serolgoic Tests: VDRL, RPR, etc.
 Quantitative results 2/2 dilution
 Need fourfold decrease for clinical significance
Treponemal Specific Tests: not quantitative
 FTA-ABS (fluorescent treponemal antibody absorption)
 TP-PA (T. pallidum particle agglutination

Clinical Syndromes of Neurosyphilis
Asymptomatic: continuation of disease within CNS and absence of ANY CNS symptom
Meningovascular: endarteritis with infarction; same as any other CVA; anywhere within CNS; takes 5-12 years at minimum
Parenchymal: direct invasion of CNS parenchyma; pathology: fibrosis and atrophy
  General paresis
  Tabes dorsalis

Symptomatic Meningitis
Typically w/in first year of infection
HA, confusion, N/V, stiff neck
Cranial neuropathies, esp II, VII, VIII
Less likely is myelitis

Meningovascular Syphilis
Average presentation in 7 years, but can occur months after primary infection
Infectious endarteritis of CNS vasculature
Prodrome: HA, dizzy, personality changes preceding stroke (2/2 meningitis?)
Can affect any vessel, but MCA and branches most common
Think of it in CVA with young person, STI exposures

Tabes Dorsalis
A disease of posterior columns and dorsal roots
Lancinating pains: sudden, brief, severe stabs of pain affecting limbs/back/face lasting minutes/days
Gastric crises: recurrent attacks of severe epigastric pain, nausea, vomiting
Pupillary irregularities: ½ Argyll-Robertson
Absent LE reflexes, impaired vibratory/position sense

The Argyll Robertson Pupil
Small, nonresponsive to light, contracts normally to accommodation and convergence, dilates imperfectly to mydriatics, does not dilate to painful stimuli..

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