Basics of Mechanical Ventilation

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Indications and Rationale for Initiating IPPV
Unprotected and unstable airways (e.g,, coma) 
Intubation and IPPV allows to
-    Secure the airways
-    Reduce the risk of aspiration
-    Maintain adequate alveolar ventilation 

Hypercapnic respiratory acidosis
IPPV and NIPPV 
-    Reduce the work of breathing and thus prevents respiratory muscle fatigue or speeds recovery when fatigue is already present
-    Maintain adequate alveolar ventilation (prevent or limit  respiratory acidosis as needed)

Hypoxic respiratory failure
IPPV and NIPPV help correct hypoxemia as it allows to
-    Deliver a high FiO2   (100% if needed during IPPV)
-    Reduce shunt by maintaining flooded or collapsed alveoli open

Others
Intubation to facilitate procedure (bronchoscopy), bronchial suctioning

Important Pitfalls and Problems Associated with PPV
Potential detrimental effects associated with PPV
Heart and circulation
-    Reduced venous return and afterload
-    Hypotension and reduced cardiac output
Lungs
-    Barotrauma
-    Ventilator-induced lung injury
-    Air trapping
Gas exchange
-    May increase dead space (compression of capillaries)
-    Shunt (e.g., unilateral lung disease - the increase in vascular resistance in the normal lung associated with PPV  tends to redirect blood flow in the abnormal lung)

Important Effects of PPV on Hemodynamics
Decreased preload
Positive alveolar pressure  ↑ lung volume  compression of the heart by the inflated lungs  the intramural pressure of the heart cavities rises (e.g., ↑ RAP)  venous return decreases  preload is reduced  stroke volume decreases  cardiac output and blood pressure may drop. This can be minimized with i.v. fluid, which helps restore adequate venous return and preload.

Patients who are very sensitive to change in preload conditions (e.g., presence of hypovolemia, tamponade,  PE, severe air trapping) are particularly prone to hypotension when PPV is initiated.

Reduced afterload
Lung expansion increases extramural pressure (which helps pump blood out of the thorax) and thereby reduces LV afterload.

When the cardiac performance is mainly determined by changes in afterload than in preload conditions (e.g., hypervolemic patient with systolic heart failure), PPV may be associated with an improved stroke volume. PPV is very helpful in patients with cardiogenic pulmonary edema, as it helps to reduce preload (lung congestion) and afterload. As a result stroke volume tends to increase... 

Dementia with Lewy Bodies

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Dementia with Lewy bodies also known under a variety of other names including Lewy body dementia, diffuse Lewy body disease, cortical Lewy body disease, and senile dementia of Lewy type, is a type of dementia closely allied to both Alzheimers and Parkinson's Diseases. It is characterized anatomically by the presence of Lewy bodies, clumps of alpha-synuclein and ubiquitin protein in neurons, detectable in post-mortem brain biopsies.
Dementia with Lewy bodies overlaps clinically with Alzheimer's disease and Parkinson's disease, but is more associated with the latter.With DLB, the loss of cholinergic (acetylcholine-producing) neurons is thought to account for the degradation of cognitive functioning, as in Alzheimer's disease; while the loss of dopaminergic (dopamine-producing) neurons is thought to account for the degradation of motor control, as in Parkinson's disease.
While the specific symptoms in a person with DLB will vary, core features of DLB are: 1) fluctuating cognition with great variations in attention and alertness from day to day and hour to hour 2) recurrent visual hallucinations (observed in 75% of people with DLB), and 3) motor features of Parkinson's. Suggestive symptoms are rapid eye movement(REM)-sleep behavior disorder and abnormalities detected in PET or SPECT scans.
Parkinson's features could include shuffling gait, reduced arm-swing during walking, blank expression (reduced range of facial expression), stiffness of movements, ratchet-like cogwheeling movements; low speech volume, sialorrhea and difficulty swallowing. Tremors are less common in DLB than in Parkinson's disease.DLB patients also often experience problems with orthostasis, including repeated falls, syncope (fainting), and transient loss of consciousness.One of the most critical and distinctive clinical features is hypersensitivity to neuroleptic and antiemetic medications that affect dopaminergic and cholinergic systems. In the worst cases, a patient treated with these drugs could become catatonic, lose cognitive function and/or develop life-threatening muscle rigidity.
There is no cure for DLB; available treatments offer relatively small symptomatic benefit but remain palliative in nature.

Somatoform disorders

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Somatoform symptoms
Symptoms suggest a physical disorder
Symptoms cannot adequately be explained physiologically
Symptoms are often (but not always) described in dramatic ways
Other disorders, such as anxiety disorders, mood disorders, and personality disorders, often co-exist

Somatization Disorder (Briquet’s syndrome)
Many physical complaints
Beginning before age 30
Must include
Four different pains
Two gastrointestinal symptoms
One sexual symptom
One pseudoneurological symptom
Symptoms are unfounded or exaggerated

Conversion Disorder
Physical symptoms suggesting neurological problems
Sensory impairment: Any modality
Paresthesias and paralysis (demonstrate)
Sudden onset, sudden termination, sudden reappearance
Mostly women; men in combat
Often misdiagnosed: Overpathologized
La belle indifference: 1/3 of cases

Pain Disorder
Main symptom is pain
May be exacerbated by psychosocial factors
May be maintained by gain: Eugene
Primary gain
Secondary gain

Hypochondriasis
No physical symptoms are necessary
Preoccupied with the possibility that normal sensations are symptoms of serious disease
Frequent visits to physicians
Persists despite medical reassurance
Over-report bodily sensations

Body Dysmorphic Disorder
Excessive concern with real or imagined defects in appearance, especially facial marks or features.
Frequent visits to plastic surgeons
Culturally-influenced, but not culture-bound
May be a symptom of more pervasive disorders: Obsessive-compulsive or delusional disorder, for example.

Diabetes and renal disease

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Causes of renal disease in diabetes
Diabetic nephropathy
Renal artery stenosis
Myeloma, outflow obstruction, polycystic renal disease, glomerulonephritis, etc
Drugs
 NSAIDS/Cox 2 inhibitors
 Fibrates
 ACEI, ARBs

Diabetic Nephropathy
30% of all end-stage renal disease
Increased co-morbidity and mortality – retinopathy, cardiovascular disease, stroke, peripheral vascular disease
May be prevented/delayed by early screening and treatment

Diabetic nephropathy in type 1 diabetes
Seldom occurs in first 5 years of diabetes
Peak incidence after 15-17 years of diabetes
Following the onset of persistent proteinuria, 25% develop renal failure in 6 years and 75% in 15 years.
Associated with high risk of macrovascular disease

Diabetic nephropathy in type 2 diabetes
May be present at diagnosis
Prevalence of proteinuria 7-10% after 5 years of diabetes and 20-35% after 20-25 years
Most patients die of heart disease or stroke before reaching end-stage renal failure

Estimated (e)GFR (using MDRD equation)
an estimate ofGFR, based on serum creatinine, age, sex and race corrected for body surface area
Normal = 100 ml/min/1.73m2
Wide confidence intervals. Most likely to be inaccurate in malnourished, amputees etc
Not so good near normal (slightly low values should not be overinterpreted)
Underestimates by 20% in Afro-Caribbeans
Creatinine must be stable
Not valid for under 18s, pregnant women

Initial assessment of patient with diabetes and renal impairment
Is this likely to be diabetic nephropathy?
Presence of retinopathy
Microalbuminuria/proteinuria

Is this likely to be renal artery stenosis?
Family history, Drug history, GU history etc
AIP, myeloma screen, PSA
Ultrasound

Renal Artery Stenosis Clinical features and pointers to diagnosis
Peripheral vascular disease, male, smoker
Resistant hypertension
Deteriorating renal function in hypertensive patient, especially on ACE/ARB
Renal impairment with minimal proteinuria
“Flash” pulmonary oedema
>1.5cm difference in renal size on U/sound..

Diabetic foot

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Foot ulceration – 'diabetic foot' – is the commonest reason for people with diabetes to be admitted to hospital in the UK. It is a result of nerve damage (neuropathy) and lack of blood supply (ischaemia). If an ulcer becomes infected and gangrenous this can necessitate amputation.

Ischaemic or Neuropathic Pain
Ischaemic Pain
Persistent pain
Worse on elevation
Relieved by dependency
Pain in calf on exercise (claudication) relieved by rest

Neuropathic Pain
Burning pains
Contact pains due to sheets or other touch
Sharp short shooting pains
Pain relieved by cold
Pain worse during rest

Check for Neuropathy
The method of choice is the 10gm monofilament applied perpendicular to the foot and pressure applied until it bends
Sites to test:
Apex of first, third, and fifth toes and the ball of the foot (MTP joints) of the same toes, dorsum of foot and heel
Vibration sense tested on dorsum of first toe and a site further proximal such as the lateral malleolus using a 128-Hz tuning fork
When testing get the person to close their eyes
Repeat the test three times at each site
One of those three tests should be a non test where the foot is not touched
This is to ascertain whether the person being tested is telling you what they “feel” you want to hear

Check the Foot Pulses
If you palpate either of these pulses it is unlikely there is any significant ischaemia in the foot
If both pulses are not palpable then check the popliteal and femoral pulses
ABPI (Ankle Brachial Pressure Index) can be undertaken but calcification of arteries in Diabetes can lead to falsely high ABPI readings so toe pressures could be undertaken (TBPI)

Neuropathy
Diabetic Peripheral Neuropathy is the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes, after exclusion of other causes e.g. Multiple Sclerosis (Boulton et al 1998)

This can be sub divided into
Motor Neuropathy
Painful Neuropathy
Autonomic Neuropathy
Sensory Neuropathy
Charcot Neuroarthropathy

Diabetic amyotrophy
This is a rare and unusual manifestation which results in poor motor control of the leg muscles usually bilateral leading to muscle weakness and muscle wasting
Usually affects the quadriceps (anterior thigh)
May also affect hamstrings (posterior thigh)
Not always associated with sensory loss..

Genitourinary Disorders

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>Urinary Tract Infection
Most common serious bacterial infection in infants and children
Highest frequency in infancy
Uncircumcised males have a ten-fold incidence

Etiology
Anatomic abnormalities
Neurogenic bladder – incomplete emptying of bladder
In the older child: infrequent voiding and incomplete emptying of bladder or constipation
Teenager: sexual intercourse due to friction trauma
Most common in females

Enuresis
Involuntary discharge of urine after the age by which bladder control should have been established, usually considered to be age of 5 years.
Familial history
Males outnumber females 3:2
5 to 10% will remain enuretic throughout their lives
Rule out UTI, ADH insufficiency, or food allergies

Pharmacological intervention:
Desmopressin synthetic vasopressin acts by reducing urine production and increasing water retention and concentration
Tofranil: anticholinrgic effect – FDA approval for treatment of enuresis
Side effect may be dry mouth and constipation
Some CNS: anxiety or confusion
Need to be weaned off

Ambiguous Genitalia
Genital appearance that does not permit gender declaration.

Extrophy of Bladder
Interrupted abdominal development in early fetal life produces an exposed bladder and urethra, pubic bone separation, and associated anal and genital abnormalities.
Occurs is 1 of 30,000 births
Congenital malformation in which the lower portion of abdominal wall and anterior bladder wall fail to fuse during fetal development.
Visible defect that reveals bladder mucosa and ureteral orifices through an open abdominal wall with constant drainage of urine.

Treatment
Surgery within first hours of life to close the skin over the bladder and reconstruct the male urethra and penis.
Urethral stents and suprapubic catheter to divert urine
Further reconstructive surgery can be done between 18 months to 3 years of age

Hypospadias
Most common anomaly of the male phallus
Incomplete formation of the anterior urethral segment
Urethral formation terminates at some point along the ventral fusion line.
Cordee – downward curve of penis.
In Newborn,
Circumcision not recommended.
Foreskin may be needed for reconstructive surgery...

Arrhythmias and Marfan Syndrome

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Cardiovascular Manifestations of the Marfan Syndrome
Major Criteria:
• dilatation of the ascending aorta with or without aortic
regurgitation and involving at least the sinuses of Valsalva; or
• dissection of the ascending aorta

Minor Criteria:
• mitral valve prolapse with or without mitral valve regurgitation
• dilatation of the main pulmonary artery in the absence of valvular
or peripheral pulmonic stenosis or any other obvious cause,
below the age of 40 years
• calcification of the mitral annulus below the age of 40 years; or
• dilatation or dissection of the descending thoracic or abdominal
aorta before the age of 50 years.
For the cardiovascular system to be involved a major criterion or
only 1 of the minor criteria must be present.

Why Might a Person with Marfan SyndromeDevelop an Arrhythmia?
1. Unrelated to Marfan Syndrome
Arrhythmia with a Normal Heart
• caffeine, alcohol, stress, anxiety, lack of sleep, stimulants
• Electrolyte abnormalities (low K+, low Mg++)
Arrhythmia with Underlying Heart Disease
• HTN, CAD, Cardiomyopathy, CHF
• Conduction disease
• Valvular heart disease

2. Related to Marfan Syndrome
Valvular Heart Disease
• Mitral valve prolapse
• Mitral regurgitation
• Aortic insufficiency
Post-operative Arrhythmias
Cardiomyopathy/CHF

Mitral Valve Prolapse and Arrhythmias
1. MVP occurs in 3-5% of general population
2. MVP occurs in >60% of people with the Marfan syndrome
3. Vast majority of people with MVP are asymptomatic

Mitral Valve Prolapse and Arrhythmia
1. Spectrum of arrhythmias have been observed in pts with MVP
PAC’s, PVC’s, WPW, SVT, Ventricular arrhythmias
Can be related to associated cardiac dysfunction: (MR, LAE, LVE)
2. Mechanism of arrhythmia unclear:
Related to mechanical stretch on mitral valve?
Related to underlying cardiomyopathy?
Related to autonomic dysfunction?
3. MVP and Sudden Death
Very rare complication of MVP
Associated with: Severe MR, Severe Valvular deformity, LV
enlargement and dysfunction, Complex ventricular arrhythmia,
Long QT, Abnormal EKG (inferior ST-T), syncope

Marfan Syndrome
• Autosomal Dominant Connective Tissue Disorder
• Fibrillin-1 Abnormality (FBN1)
• Incidence: 1:5000 – 1:10,000
• 25% Cases: Spontaneous Mutation
• 50,000 affected in USA; 200,000 with related connective
tissue disorders
• Multisystem Involvement:
• Cardiovascular, Ocular, Skeletal, Dura

Marfan Syndrome: Clinical Features
Common physical characteristics (outward features)
• Tall, thin stature with disproportionately long arms
• Unusually long lower half of body
• Long, double-jointed fingers, elongated thumb
• Long feet and toes, flat or highly arched feet
• Curvature of the spine (scoliosis)
• Chest wall deformities (pectus excavatum, pectus carinatum)
• Nearsightedness
• Stretch marks (striae atrophicae)

Marfan Syndrome:
Importance of Accurate Diagnosis
• May be diagnosed at birth or not recognized until late in life
• If unrecognized and untreated, the average age of death in Marfan
syndrome is 30 to 40 years.
• Aortic Complications (Aortic Dissection and Aortic Insufficiency)
are responsible for 90% of the Morbidity and Mortality in Marfan
syndrome.
• Careful assessment and long term follow-up are critical to the
outcome of patients with Marfan syndrome.
• Median probability of survival is now into the 70’s.

Molecular Basis of the Marfan Syndrome
• Genetic linkage analysis excluded the collagens as candidate molecules.
• Fibrillin, a 350 kDa glycoprotein component of connective tissue is described
and localized in tissues commonly involved in the Marfan syndrome. (Sakai,
1986)
• Immunohistochemical studies (utilizing antifibrillin antibodies) of cultured
skin fibroblasts suggested decreased fibrillin secretion in the Marfan syndrome.
(Hollister, 1990)
• Family linkage studies map Marfan syndrome to chromosome 15q15-q23 in 5
Finnish families. (Kainulainen 1990, Dietz 1991)
• A probe from the partially cloned fibrillin gene was mapped to the same
region on chromosome 15 (15q15-21) by in situ hybridization.
• DNA polymorphism in the fibrillin gene was tightly linked to the Marfan
syndrome phenotype by family linkage studies (LOD = 7.56). (Lee, 1991)
• Using clones of the fibrillin gene, de novo point mutations were documented
in sporadic cases of Marfan syndrome. (Dietz and Maslen, 1991)
• To date, >100 mutations in fibrillin-1 (FBN-1) have been described in Marfan
syndrome.

Fluid and Electrolyte Physiology

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Hyponatremia
Defined as serum [Na+] less than 136 mEq/L
Water shifts into cells causing cerebral edema
125 mEq/L – nausea and malaise
120 mEq/L – headache, lethargy, obtundation
115 mEq/L – seizure and coma

1.  Assess plasma osmolality
2.  Assess volume status of patient
Hypervolemic, Euvolemic, Hypovolemic
3.  Assess Urine Sodium Concentration
Needed for definitive diagnosis, not needed for treatment purposes
4.  Calculate Na+ Deficit
0.6 x weight (kg) x (130 – plasma [Na+])
5.  Correct at no more than 0.5mEq/L per hour or 12 mEq/L per 24 hours

Hypernatremia
Defined as serum [Na+] greater than 146 mEq/L
Lethargy, weakness, and irritability that progress to seizure, coma, and death
Usually occurs in adults with altered mental status or no access to water

1.  Assess volume status
2.  Measure urine [Na+]
3.  Calculate water deficit
0.6 x weight (kg) x ([Na+]/140 -1)
4.  Correct with free water no faster than 0.5 mEq/L/hour or 12 mEq/L/day

Hyperkalemia
Defined as a serum [K+] greater than 4.6 mEq/L
Changes in cellular transmembrane potentials can lead to lethal cardiac arrhythmias
Most often associated with renal impairment coupled with exogenous K+ administration or drugs that increase K+
Transcellular shifts – acidosis, succinylcholine, insulin deficiency, massive tissue destruction
Massive blood transfusions
Pseudohyperkalemia - Thrombocytosis, hemolysis, leukocytosis
Urine K+ excretion rate can be used to determine exact cause of hyperkalemia

Drugs causing hyperkalemia – K+ sparing diruetics, ACEI, NSAIDs, Heparin, Cyclosporin, Tacrolimus, Bactrim
EKG Changes
5.5 – 6.5 mEq/L – peaked T-waves
6.5 – 7.5 mEq/L – loss of P-waves
> 8.0 mEq/L – widened QRS

Hypokalemia
Defined as serum [K+] less than 3.6 mEq/L
Occurs in up to 20% of hospitalized patients
2.5 mEq/L – muscular weakness, myalgia
<2.5 mEq/L – cramps, parasthesias, ileus, tetany, rhabdomyolisis, PVCs, A-V block, V-tach, V-fib

Modified Mammography

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Mammography is the process of using X-rays to visualise the human breast and is used as a diagnostic and a screening tool. The goal of mammography is the early detection of breast cancer, typically through detection of characteristic masses and/or microcalcifications. Mammography is believed to reduce mortality from breast cancer. In many countries routine mammography of older women is encouraged as a screening method to diagnose early breast cancer.The U.S. Preventive Services Task Force recommended that women begin having mammograms at age 50, instead of the previous 40-years-of-age starting point. This shift in government guidelines was met with swift negative reaction by several cancer and women’s organizations. Nonetheless, the USPSTF still recommends screening mammography, with or without clinical breast examination, every 2 years for women aged 50 to 74.
Like all x-rays, mammograms use doses of ionizing radiation to create images. Radiologists then analyze the image for any abnormal findings.
At this time, mammography along with physical breast examination is the modality of choice for screening for early breast cancer.In screening mammography, both head-to-foot (craniocaudal, CC) view and angled side-view (mediolateral oblique, MLO) images of the breast are taken. Diagnostic mammography may include these and other views, including geometrically magnified and spot-compressed views of the particular area of concern. Ultrasound, ductography, positron emission mammography (PEM), and magnetic resonance imaging are adjuncts to mammography. Ultrasound is typically used for further evaluation of masses found on mammography or palpable masses not seen on mammograms. Ductograms are still used in some institutions for evaluation of bloody nipple discharge when the mammogram is non-diagnostic. MRI can be useful for further evaluation of questionable findings as well as for screening pre-surgical evaluation in patients with known breast cancer to detect any additional lesions that might change the surgical approach, for instance from breast-conserving lumpectomy to mastectomy.
Breast self-examination (BSE) was once promoted as a means of finding cancer at a more curable stage, however, it has been shown to be ineffective, and is no longer routinely recommended by health authorities for general use.Awareness of breast health and familiarity with one's own body is typically promoted instead of self-exams.
Mammography has a false-negative rate of at least 10 percent. This is partly due to dense tissues obscuring the cancer and the fact that the appearance of cancer on mammograms has a large overlap with the appearance of normal tissues.

Managing neurogenic voiding dysfunction

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Normal Voiding Function
Unique function of bladder and rectum;Autonomic and somatic control.
Distention and capacitance role for storage and emptying
Reflexic and conscious emptying.
Learned behaviors to coordinate voiding cycle and response to stimuli
Requires physical integrity of supporting structures

Innervation of the
Lower Urinary Tract
Cerebral function;anterior frontal gyrus
Pontine micturition center; coordination
Sacral reflex arcs through S3 and S4
Parasympathetic and sympathetic influences
Afferent feedback
Importance of pelvic floor

Spectrum of dysfunction in TM
Great variation in dysfunction - Mild to severe
Urinary retention – Frequency/urgency –Incontinence (spontaneous, exertional)
Degree of bladder dysfunction does not always mirror other deficits
Degree of bladder dysfunction does not always mirror recovery
Don’t forget bowel function

Evaluation
Urodynamic testing
The bladder is a poor witness
Can define accomodation of the bladder(compliance)
Sensation, residual volume, capacity
Spontaneous activity
Coordination and competence of sphincter
Voiding pressure and flow efficiency

Therapy for Neuropathic voiding
dysfunction: Hyperreflexia
Behavioral modification
Pelvic floor retraining/reeducation
Medication; oral, transdermal, intravesical
Biofeedback, E-stim, magnetic stim, PT
Sacral nerve stimulation
Denervation; surgical, chemical (botox)
Surgery; augmentation cystoplasty, urinary diversion


Neurogenic Voiding Dysfunction

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Complications of Neurogenic voiding dysfunction
Severe lower urinary tract symptoms: dysuria, incontinence, retention
Urinary tract infection: APN, cystitis, prostatitis, epididymitis
Renal function impairment: hydronephrosis, vesicoureteral reflux, renal scarring, ESRD

Objectives of urological care for neurogenic voiding dysfunction
Preservation of renal function
Adequate bladder emptying
Prevention of UTI
Establishment of continence
Freedom of catheter
Spontaneous voiding

Urodynamic Classification NVD
Cerebral lesion – detrusor areflexia; detrusor hyperreflexia with coordinated external sphincter
Suprasacral cord lesion– autonomic dysreflexia (lesion above T6); detrusor hyperreflexia with external sphincter dyssynergia
Sacral cord lesion – detrusor areflexia with non-relaxing urethra; atonic urethra
Peripheral neuropathy – detrusor areflexia with discoordinated urethral sphincter

In Stroke
Initial retention, bladder neck is closed
Detrusor hyperreflexia & incontinence
Continence reappears by 6 Mo in 80%
Irritative LUTS: DH
Dysuria and obstructive LUTS: DHIC,BPO, poor relaxation of external sphincter (frontoparietal & internal capsule lesion)
Subcortical lesion: areflexia, retention (47%)
Areflexia in 85% hemorrhage, 10% ischemia

Stroke and Bladder outlet obstruction
Detrusor hyperreflexia in 82% after stroke, obstruction was noted in 63%
Pseudodyssynergia may be a urodynamic finding for obstructive symptoms
Incidence of BOO is equally distributed in patients with irritative and obstructive LUTS
Prostatectomy should not be done in 1 year after stroke..

Preload
Preload: load imposed on a muscle before the onset of contraction
Muscle stretches to new length
Stretch in cardiac muscle determined by end diastolic volume
At bedside, use EDP as surrogate for ventricular preload
i.e. assume EDV = EDP

How can we measure EDP? - Pulmonary Capillary Wedge Pressure

How does wedge pressure work?

A balloon catheter is advanced into PA
Balloon at the tip is inflated
Creates static column of blood between catheter tip and left atrium
Thus, pressure at tip = pressure in LA

Ventricular function is mostly determined by the diastolic volume
Relationship between EDV/EDP and stroke volume illustrated by ventricular function curves

Contractility
The ability of the cardiac muscle to contract (i.e. the contractile state)
Reflected in ventricular function curves

Afterload
Afterload: Load imposed on a muscle at the onset of contraction

Wall tension in ventricles during systole

Determined by several forces
Pleural Pressure
Vascular compliance
Vascular resistance

Pleural Pressure
Pleural pressures are transmitted across the outer surface of the heartNegative pressure increases wall tension. Increases afterload
Positive pressure Decreases wall tension. Decreases afterload.

Mood (Affective) Disorders

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Mood disorders are very common, their life prevalence is up to 20 %, and they have a high level of morbidity and mortality as well as an immense impact on disabilities worldwide.
The fundamental disturbance is a change in mood or affect, usually to depression (with or without associated anxiety) or to elation. The mood change is usually accompanied by a change in the overall level of activity.
Most of these disorders tend to be recurrent, and the onset of individual episodes is often related to stressful events or situations.
The mood disorders may be subdivided into unipolar and bipolar types:
those that are characterized by depression only
those that are characterized by manic episode either alone or in combination with depression

Classification of Mood Disorders
International Classification of Diseases (ICD-10) came into use in WHO Member States as from 1994

F30   Manic episode
F31   Bipolar affective disorder
F32   Depressive episode
F33   Recurrent depressive disorder
F34   Persistent mood (affective) disorders
F38   Other mood (affective) disorders
F39   Unspecified mood (affective) disorder

Depressive episode:
depressed mood
loss of interest and enjoyment
reduced energy leading to increased fatigability and diminished activity
marked tiredness after only slight effort
reduced concentration and attention
reduced self-esteem and self-confidence
ideas of guilt and unworthiness
bleak and pessimistic views of the future
ideas or acts of self-harm or suicide,
disturbed sleep and diminished appetite

Clinical presentation shows marked individual variations
in some cases, anxiety, distress, and motor agitation may be more prominent at times than the depression
the mood change may also be masked (masked depression) by added features such as irritability, excessive consumption of alcohol, histrionic behaviour, and exacerbation of pre-existing phobic or obsessional symptoms, or by hypochondriacal preoccupations.

Depressive episode should last at least 2 weeks (typically several months), but shorter periods may be reasonable if symptoms are unusually severe and of rapid onset.
The lifetime prevalence: 17%; risk of recurrence >50%.

The lowered mood varies little from day to day, is unresponsive to circumstances and may be accompanied by so-called „somatic“ symptoms:
loss of interest or pleasure in activities that are normally enjoyable (anhedonia)
lack of emotional reactivity to normally pleasurable surroundings and events
waking in the morning 2 hours or more before the usual time
depression worse in the morning
objective evidence of definite psychomotor retardation or agitation
loss of appetite
weight loss
loss of libido

Manic Episode
Hypomania is characterized by
persistent mild elevation of mood for at least several days
increased energy and activity
usually marked feelings of well-being and both physical and mental efficiency
Increased sociability, talkativeness, overfamiliarity, increased sexual energy, and a decreased need for sleep are often present but not to the extent that they lead to severe disruption of work or result in social rejection. There are no hallucinations or delusions

Bipolar Affective Disorder
Bipolar affective disorder is characterized by repeated, at least two episodes in which the patient’s mood and activity levels are significantly disturbed (manic or depressive syndromes, patients who suffer only from repeated episodes of mania are comparatively rare).
The first episode may occur at any age from childhood to old age.
The frequency of episodes and the pattern of remissions and relapses are both very variable.
The lifetime prevalence is between 0,5 an 1 %. Suicidality – about 19%. Comorbidity with alcohol and drug abuse
The rapid-cycling specifier identifies those patients who have had at least four episodes of a major depressive, manic, or mixed episode during the past 12 months.

Bone scintigraphy(Bone Scan)

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A bone scan or bone scintigraphy is a nuclear scanning test to find certain abnormalities in bone which are triggering the bone's attempts to heal. It is primarily used to help diagnose a number of conditions relating to bones, including: cancer of the bone or cancers that have metastasized to the bone, locating some sources of bone inflammation (e.g. bone pain such as lower back pain due to a fracture), the diagnosis of fractures that may not be visible in traditional X-ray images, and the detection of damage to bones due to certain infections and other problems.

Nuclear medicine bone scans are one of a number of methods of bone imaging, all of which are used to visually detect bone abnormalities. Such imaging studies include magnetic resonance imaging (MRI), X-ray computed tomography (CT) and in the case of 'bone scans' nuclear medicine. However, a nuclear bone scan is a functional test, which means it measures an aspect of bone metabolism.

Nuclear bone scans are not to be confused with the completely different test often termed a "bone density scan," DEXA or DXA, which is a low exposure X-ray test measuring bone density to look for osteoporosis and other diseases where bones lose mass, without any bone re-building activity. The nuclear medicine scan technique is sensitive to areas of unusual bone re-building activity because the radiopharmaceutical is taken up by osteoblast cells which build bone. The technique therefore is sensitive to fractures and bone reaction to infections and bone tumors, including tumor metastases to bones, because all these pathologies trigger bone osteoblast activity. The bone scan is not sensitive to osteoporosis or multiple myeloma in bones, and therefore other techniques must be used to assess bone abnormalities from these diseases.


Principles of Nuclear Medicine

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Nuclear medicine is a branch or specialty of medicine and medical imaging that uses radionuclides and relies on the process of radioactive decay in the diagnosis and treatment of disease.
In nuclear medicine procedures, elemental radionuclides are combined with other elements to form chemical compounds, or else combined with existing pharmaceutical compounds, to form radiopharmaceuticals. These radiopharmaceuticals, once administered to the patient, can localize to specific organs or cellular receptors.Then, external detectors (gamma cameras) capture and form images from the radiation emitted by the radiopharmaceuticals. This process is unlike a diagnostic X-ray where external radiation is passed through the body to form an image. This property of radiopharmaceuticals allows nuclear medicine the ability to image the extent of a disease-process in the body, based on the cellular function and physiology, rather than relying on physical changes in the tissue anatomy. In some diseases nuclear medicine studies can identify medical problems at an earlier stage than other diagnostic tests.
Nuclear medicine tests differ from most other imaging modalities in that diagnostic tests primarily show the physiological function of the system being investigated as opposed to traditional anatomical imaging such as CT or MRI. Nuclear medicine imaging studies are generally more organ or tissue specific (e.g.: lungs scan, heart scan, bone scan, brain scan, etc.) than those in conventional radiology imaging, which focus on a particular section of the body (e.g.: chest X-ray, abdomen/pelvis CT scan, head CT scan, etc.). In addition, there are nuclear medicine studies that allow imaging of the whole body based on certain cellular receptors or functions. Examples are whole body PET scan or PET/CT scans, gallium scans, indium white blood cell scans, MIBG and octreotide scans.

Joint stiffness
The symptom of pain on moving a joint, and loss of range of motion
All above conditions are made worse by
Prolonged immobilization
Position of joint, why?
Cause if they were held in which ligaments are at their shortest, no exercise will succeed in stretching these tissue and restoring the lost movement completely.

Treatment
Elevation.
Functional bracing (orthopaedic brace) used to immobilize a joint or body segment, restrict movement in a given direction.
Exercise.
Splinted.
In stiff joints, prolonged and patient physiotherapy can work wonder.
Surgery.

Heterotopic ossification
is the process by which bone tissue forms outside of the skeleton
Clinical features
Pain
Local swellings

X-ray will appear normal at first but Bone scan shows increased activity
 next 2-3 weeks
  pain gradually subside
  limited joint movements.
  X-ray - fluffy calcification in soft tissue
By 8 weeks  - Palpable bony mass that clearly defined in x-ray

Muscle contracture
the muscle and its tendons shorten, resulting in reduced flexibility.
Following arterial injury or compartment syndrome, the patient may develop ischaemic contracture or
  (volkman’s ischaemic contracture)
Nerve injury by ischaemia sometimes recover.

Tendon rapture
After fracture.
 treatment is direct suture.
Tendon transfer of extensor indicis proprius to distal stump of the ruptured thumb tendon.
No treatment usually in late rupture of the long head of biceps after fractured head of femur.

Nerve entrapment
nerve becomes trapped or pinched due to some physiological abnormalities.
Numbness (parasthesia)
Loss of power
Muscle wasting in distribution of the affected nerve.
Claw hand in ulnar nerve entrapment

Complex regional pain syndrome
(CRPS) is a chronic progressive disease characterized by severe pain, swelling and changes in the skin
International Association for the Study of Pain has divided CRPS into two types based on the presence of nerve lesion following the injury.
Type I, also known as reflex sympathetic dystrophy (RSD), Sudeck's atrophy, reflex neurovascular dystrophy (RND) or algoneurodystrophy, does not have demonstrable nerve lesions.
Type II, also known as causalgia, has evidence of obvious nerve damage.
The cause of this syndrome is currently unknown.

Acquired Immunity

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Defensive mechanisms include :
1) Innate immunity (Natural or Non specific)
2) Acquired immunity (Adaptive or Specific)
Cell-mediated immunity
Humoral immunity
Aquired (specific) immunity
* The acquired immune response is more specialized
than innate immune response
* The acquired immune response involves a combination
of two mechanisms :
1) Humoral immune response
2) cell mediated immune response
* They interact with one another to destroy foreign body
(microorganisms, infected cells, tumor cells)

Two mechanisms
1) Humoral immune response:
- Antibodies are produced by B-lymphocytes
- These have the ability to recognize and bind
specifically to antigen that induced their formation

2) The cell mediated immune response (CMI)
- It is mediated by certain types of T-lymphocytes
- T-lymphocytes recognize foreign material by
means of surface receptors
- T-lymphocytes attack and destroy foreign material
directly or through release of soluble mediators
i.e. cytokines

Characters Of Acquired Immune Response
1) Highly specific for the invading organism

2) Discrimination between “self and “non self” molecules
The response only occurs to “non self” molecules

3) Diversity:
- It can respond to millions of different antigens
- Lymphoctes population consists of many different clones (one cell and its progny)
- Each clone express an antigen receptor and responds only to one antigenic epitope

Mechanism Of Acquired Immune Response
Acquired immune response is initiated by:
* Recognition of the antigen by specific lymphocytes
* Activation of these specific lymphocytes
* Proliferation and differentiation into effector cells;
-The effector cells eliminate the antigen
-Return of homeostasis and development of memory cells
* Memory cells evoke a more rapid and long response on re-exposure to same antigen

Mechanism of Humoral immunity
Antibodies induce resistance through:
1) Antitoxin neutralize bacterial toxins (diphtheria,tetanus)
Antitoxin are developed actively as a result of:
a- Previous infection
b- Artificial immunization
c- Transferred passively as antiserum
* Neutralization of toxin with antitoxin prevents a combination with tissue cells

2) Antibodies attach to the surface of bacteria and
a- act as opsonins and enhance phagocytosisd
b- prevent the adherence of microorganisms to
their target cells, e.g. IgA in the gut
c- Activate the complement and lead to bacterial lysis
d- Clump bacteria (agglutination) leading to
phagocytosis

Behcet Disease

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Behçet's disease is a rare immune-mediated systemic vasculitis that often presents with mucous membrane ulceration and ocular involvements. As a systemic disease, it can also involve visceral organs such as the gastrointestinal tract, pulmonary, musculoskeletal, and neurological systems. This syndrome can be fatal, due to ruptured vascular aneurysms, or severe neurological complications.

Signs and Symptoms
Skin and mucosa
Nearly all patients present with some form of painful oral mucocutaneous ulcerations in the form of aphthous ulcers or non-scarring oral lesions.The oral lesions are similar to those found in inflammatory bowel disease and can be relapsing.Painful genital ulcerations usually develop around the anus, vulva or scrotum and cause scarring in 75% of the patients.

Ocular system
Eyes
Inflammatory eye disease can develop early in the disease course and lead to permanent vision loss in 20% of cases. Ocular involvement can be in the form of posterior uveitis, anterior uveitis, or retinal vasculitis. Anterior uveitis presents with painful eyes, conjuctival redness, hypopyon, and decreased visual acuity, while posterior uveitis presents with painless decreased visual acuity and visual field floaters.

Optic nerve involvement in Behçet's disease is rare, typically presenting as progressive optic atrophy and visual loss.

Signs and symptoms of acute optic neuropathy include painless loss of vision which may affect either one or both eyes, reduced visual acuity, reduced color vision, relative afferent pupillary defect, central scotoma, swollen optic disc, macular edema, or retrobulbar pain.
Gastrointestinal tract (bowels)
GI manifestations include abdominal pain, nausea, and diarrhea with or without blood, and they often involve the ileocecal valve.
Lung involvement is typically in the form of hemoptysis, pleuritis, cough, or fever, and in severe cases can be life threatening if the outlet pulmonary artery develops an aneurysm which ruptures causing severe vascular collapse and death from bleeding in the lungs.
Arthralgia is seen in up to half of patients, and is usually a non-erosive poly or oligoarthritis primarily of the large joints of the lower extremities.
Neurological involvements range from aseptic meningitis to vascular thrombosis such as dural sinus thrombosis and organic brain syndrome manifesting with confusion, seizures, and memory loss.They often appear late in the progression of the disease but are associated with a poor prognosis.

Management of traumatized patient

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Immediate treatment of airway obstruction in facial injured patient
Clearing of blood clot and mucous of the mouth and nares and head position that lead to escape of secretions (sit-up or side position)
Removal of foreign bodies as a broken denture or avulsed teeth which can be inhaled and ensuring the patency of the mouth and oropharynex
Controlling the tongue position in case of symphesial bilateral fracture of mandible and when voluntary control of intrinsic musculature is lost
Maintaining airway using artificial airway in unconscious patient with maxillary fracture or by nasophryngeal tube with periodic aspiration
Lubrication of patient’s lips and continuous supervision

Additional methods in preservation of the airway in patient with severe facial injuries
Endotracheal intubation
    Needed with multiple injuries, extensive soft tissue destruction and for serious injury that require artificial ventilation

Tracheostomy
    Surgical establishment of an opening into the trachea
    Indications: 1. when prolonged artificial ventilation is necessary
                                2. to facilitate anesthesia for surgical repair in  certain cases
                                3. to ensure a safe postoperative recovery after extensive surgery
                                4. following obstruction of the airway from laryngeal edema
                                5. in case of serious hemorrhage in the airway

Circothyroidectomy
    An old technique associated with the risk of subglottic stenosis development particularly in children. The use of percutaneous dilational treachestomy (PDT) in MFS is advocated by Ward Booth et al (1989) but it can be replaced with PDT.

Control of hemorrhage and Soft tissue laceration
    Repair, ligation, reduction of fracture and Postnasal pack

Cervical spine injury
Can be deadly if it involved the odontoid process of the axis bone of the axis vertebra
If the injury above the clavicle bone, clavicle collar should minimize the risk of any deterioration

Emergency treatment in case of chest injury
Occluding of open chest wounds
Endotreacheal intubation for unstable flail chest
Intermittent positive pressure ventilation
Needle decompression of the pericardium
Decompression of gastric dilation and aspiration of stomach content

Circulatory collapse leads to low blood pressure, increasing pulse rate and diminished capillary filling at the periphery
Patient resuscitation - Restoration of cardio-respiratory function
Shock management - Replacement of lost fluid...

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