Saturday 25 January 2014

Compensatory Mechanisms Of Heart Failure

COMPENSATORY MECHANISMS


Several natural compensatory mechanisms are called into action in patients with heart failure that buffer the fall in cardiac output and help preserve sufficient blood pressure to perfuse vital organs. These compensations include (1) the Frank–Starling mechanism, (2) neurohormonal alterations, and (3) the development of ventricular hypertrophy and remodeling (Fig. 9.8).
Figure 9.8 Compensatory mechanisms in heart failure. Both the Frank–Starling mechanism (which is invoked by the rise in ventricular end-diastolic volume) and myocardial hypertrophy (in response to pressure or volume overload) serve to maintain forward stroke volume (dashed lines). However, the chronic rise in EDV by the former and increased ventricular stiffness by the latter passively augment atrial pressure, which may in turn result in clinical manifestations of heart failure (e.g., pulmonary congestion in the case of left-sided heart failure).

Frank–Starling Mechanism

As shown in Figure 9.3, heart failure caused by impaired left ventricular contractile function causes a downward shift of the ventricular performance curve. Consequently, at a given preload, stroke volume is decreased compared with normal. The reduced stroke volume results in incomplete chamber emptying, so that the volume of blood that accumulates in the ventricle during diastole is higher than normal (see Fig. 9.3, point b). This increased stretch on the myofibers, acting via the Frank–Starling mechanism, induces a greater stroke volume on subsequent contraction, which helps to empty the enlarged left ventricle and preserve forward cardiac output (see Fig 9.8).
This beneficial compensatory mechanism has its limits, however. In the case of severe heart failure with marked depression of contractility, the curve may be nearly flat at higher diastolic volumes, reducing the augmentation of cardiac output achieved by the increased chamber filling. Concurrently in such a circumstance, marked elevation of the end-diastolic volume and pressure (which is transmitted retrograde to the left atrium, pulmonary veins, and capillaries) may result in pulmonary congestion and edema (see Fig. 9.3, point c).

Neurohormonal Alterations

Several important neurohormonal compensatory mechanisms are activated in heart failure in response to the decreased cardiac output (Fig. 9.9). Three of the most important involve (1) the adrenergic nervous system, (2) the renin–angiotensin–aldosterone system, and (3) increased production of antidiuretic hormone (ADH). In part, these mechanisms serve to increase systemic vascular resistance, which helps to maintain arterial perfusion to vital organs, even in the setting of a reduced cardiac output. That is, because blood pressure (BP) is equal to the product of cardiac output (CO) and total peripheral resistance (TPR),a rise in TPR induced by these compensatory mechanisms can nearly balance the fall in CO and, in the early stages of heart failure, maintain fairly normal BP. In addition, neurohormonal activation results in salt and water retention, which in turn increases intravascular volume and left ventricular preload, maximizing stroke volume via the Frank–Starling mechanism.
Figure 9.9 Compensatory neurohormonal stimulation develops in response to the reduced forward cardiac output and blood pressure of heart failure.Increased activity of the sympathetic nervous system, renin–angiotensin–aldosterone system, and antidiuretic hormone serve to support the cardiac output and blood pressure (boxes). However, adverse consequences of these activations (dashed lines) include an increase in afterload from excessive vasoconstriction (which may then impede cardiac output) and excess fluid retention, which contributes to peripheral edema and pulmonary congestion.
Although the acute effects of neurohormonal stimulation are compensatory and beneficial, chronic activation of these mechanisms often ultimately proves deleterious to the failing heart and contributes to a progressive downhill course, as described later.

Adrenergic Nervous System

The fall in cardiac output in heart failure is sensed by baroreceptors in the carotid sinus and aortic arch. These receptors decrease their rate of firing in proportion to the fall in BP, and the signal is transmitted by the 9th and 10th cranial nerves to the cardiovascular control center in the medulla. As a result, sympathetic outflow to the heart and peripheral circulation is increased, and parasympathetic tone is diminished. There are three immediate consequences (see Fig. 9.9): (1) an increase in heart rate, (2) augmentation of ventricular contractility, and (3) vasoconstriction caused by stimulation of α-receptors on the systemic veins and arteries.
The increased heart rate and ventricular contractility directly augment cardiac output (see Fig. 9.2). Vasoconstriction of the venous and arterial circulations is also initially beneficial. Venous constriction augments blood return to the heart, which increases preload and raises stroke volume through the Frank–Starling mechanism, as long as the ventricle is operating on the ascending portion of its ventricular performance curve. Arteriolar constriction increases the peripheral vascular resistance and therefore helps to maintain blood pressure (BP = CO × TPR). The regional distribution of α-receptors is such that during sympathetic stimulation, blood flow is redistributed to vital organs (e.g., heart and brain) at the expense of the skin, splanchnic viscera, and kidneys.

Renin–Angiotensin–Aldosterone System

This system is also activated early in patients with heart failure (see Fig. 9.9), mediated by increased renin release. The main stimuli for renin secretion from the juxtaglomerular cells of the kidney in heart failure patients include (1) decreased renal artery perfusion pressure secondary to low cardiac output, (2) decreased salt delivery to the macula densa of the kidney owing to alterations in intrarenal hemodynamics, and (3) direct stimulation of juxtaglomerular β2-receptors by the activated adrenergic nervous system.
Renin is an enzyme that cleaves circulating angiotensinogen to form angiotensin I, which is then rapidly cleaved by endothelial cell-bound angiotensin-converting enzyme (ACE) to form angiotensin II (AII), a potent vasoconstrictor (see Chapter 13). Increased AII constricts arterioles and raises total peripheral resistance, thereby serving to maintain systemic blood pressure. In addition, AII acts to increase intravascular volume by two mechanisms: (1) at the hypothalamus, it stimulates thirst and therefore water intake; and (2) at the adrenal cortex, it acts to increase aldosterone secretion. The latter hormone promotes sodium reabsorption from the distal convoluted tubule of the kidney into the circulation (see Chapter 17), serving to augment intravascular volume. The rise in intravascular volume increases left ventricular preload and thereby augments cardiac output via the Frank–Starling mechanism in patients on the ascending portion of the ventricular performance curve (see Fig. 9.3).

Antidiuretic Hormone

Secretion of this hormone (also termedvasopressin) by the posterior pituitary is increased in many patients with heart failure, presumably mediated through arterial baroreceptors, and by increased levels of AII. ADH contributes to increased intravascular volume because it promotes water retention in the distal nephron. The increased intravascular volume serves to augment left ventricular preload and cardiac output. ADH also appears to contribute to systemic vasoconstriction.
Although each of these neurohormonal alterations in heart failure is initiallybeneficial, continued activation ultimately proves harmful. For example, the increased circulating volume and augmented venous return to the heart may worsenengorgement of the lung vasculature, exacerbating congestive pulmonary symptoms. Furthermore, the elevated arteriolar resistance increases the afterload against which the failing left ventricle contracts and may therefore impair stroke volume and reduce cardiac output (see Fig. 9.9). In addition, the increased heart rate augments metabolic demand and can therefore further reduce the performance of the failing heart. Continuous sympathetic activation results in downregulation of cardiac β-adrenergic receptors and upregulation of inhibitory G proteins, contributing to a decrease in the myocardium’s sensitivity to circulating catecholamines and a reduced inotropic response.
Chronically elevated levels of AII and aldosterone have additional detrimental effects. They provoke the production of cytokines (small proteins that mediate cell–cell communication and immune responses), activate macrophages, and stimulate fibroblasts, resulting in fibrosis and adverse remodeling of the failing heart.
Because the undesired consequences of chronic neurohormonal activation eventually outweigh their benefits, much of today’s pharmacologic therapy of heart failure is designed to moderate these “compensatory” mechanisms, as examined later in the chapter.

Natriuretic Peptides

In contrast to the ultimately adverse consequences of the neurohormonal alterations described in the previous section, the natriuretic peptides are natural “beneficial” hormones secreted in heart failure in response to increased intracardiac pressures. The best studied of these are atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). ANP is stored in atrial cells and is released in response to atrial distention. BNP is not detected in normal hearts but is produced when ventricular myocardium is subjected to hemodynamic stress (e.g., in heart failure or during myocardial infarction). Recent studies have shown a close relationship between serum BNP levels and the clinical severity of heart failure.
Actions of the natriuretic peptides are mediated by specific natriuretic receptors and are largely opposite to those of the other hormone systems activated in heart failure. They result in excretion of sodium and water, vasodilatation, inhibition of renin secretion, and antagonism of the effects of AII on aldosterone and vasopressin levels. Although these effects are beneficial to patients with heart failure, they are usually not sufficient to fully counteract the vasoconstriction and volume-retaining effects of the other activated hormonal systems.

Other Peptides

Among other peptides that are generated in heart failure is endothelin-1, a potent vasoconstrictor, derived from endothelial cells lining the vasculature (see Chapter 6). In patients with heart failure, the plasma concentration of endothelin-1 correlates with disease severity and adverse outcomes. Drugs designed to inhibit endothelin receptors (and therefore blunt adverse vasoconstriction) improve LV function in heart failure patients, but long-term clinical benefits have not been demonstrated.

Ventricular Hypertrophy and Remodeling

Ventricular hypertrophy and remodeling are important compensatory processes that develop over time in response to hemodynamic burdens. Wall stress (as defined earlier) is often increased in developing heart failure because of either LV dilatation (increased chamber radius) or the need to generate high systolic pressures to overcome excessive afterload (e.g., in aortic stenosis or hypertension). A sustained increase in wall stress (along with neurohormonal and cytokine alterations) stimulates the development of myocardial hypertrophy and deposition of extracellular matrix. This increased mass of muscle fibers serves as a compensatory mechanism that helps to maintain contractile force andcounteracts the elevated ventricular wall stress (recall that wall thickness is in the denominator of the Laplace wall stress formula). However, because of the increased stiffness of the hypertrophied wall, these benefits come at the expense of higher-than-normal diastolic ventricular pressures, which are transmitted to the left atrium and pulmonary vasculature (see Fig. 9.8).
The pattern of compensatory hypertrophy and remodeling that develops depends on whether the ventricle is subjected to chronic volume or pressure overload. Chronic chamber dilatation owing to volume overload (e.g., chronic mitral or aortic regurgitation) results in the synthesis of new sarcomeres in series with the old, causing the myocytes to elongate. The radius of the ventricular chamber therefore enlarges, doing so in proportion to the increase in wall thickness, and is termedeccentric hypertrophy. Chronic pressureoverload (e.g., caused by hypertension or aortic stenosis) results in the synthesis of new sarcomeres in parallel with the old (i.e., the myocytes thicken), termed concentric hypertrophy. In this situation, the wall thickness increases without proportional chamber dilatation, and wall stress may therefore be reduced substantially.
Such hypertrophy and remodeling help to reduce wall stress and maintain contractile force, but ultimately, ventricular function may decline, allowing the chamber to dilate out of proportion to wall thickness. When this occurs, the excessive hemodynamic burden on the contractile units produces a downward spiral of deterioration with progressive heart failure symptomatology.

Friday 24 January 2014

Medical Mnemonics

MEDICAL MNEMONICS
Mnemosyne was the Greek goddess of memory,  Her namesake, mnemonics, 
simply means "memory aid".

IF YOU FIND REFERENCES TO FEMALE/MALE ANATOMY OFFENSIVE, THIS LIST IS DEFINITELY NOT FOR YOU!!

ANATOMY 



Head & Neck
CRANIAL NERVES: I-Optic, II-Olfactory, III-Oculomotor, IV-Trochlear, V-Trigeminal, VI-Abducens, VII-Facial, VIII-Acoustic (Vestibulocochlear), IX-Glossophrayngeal, X-Vagus, XI-Spinal Accessory, XII-Hypoglossal
On Old Olympus Towering Tops, A Finn And German Viewed Some Hops (older and cleaner)
Oh Oh Oh To Touch And Feel A Girls Vagina And Hymen (newer and, well ...)  

Which cranial nerve is Sensory, Motor, or Both- Some Say Marry Money, But My Brother Says Big Breasts Matter More  

BRANCHES OF FACIAL NERVE: Temporal, Zygomatic, Buccal, Mandibular, Cervical
Ten Zebras Beat My Cock
Two Zulus buggered my cat –(for the sicker, amongst you!)  

You have I nose. You have II eyes. (I - Olfactory; II -- Optic)  

Standing Room Only -Exit of branches of trigeminal nerve from the skull S
V1 -Superior orbital fissure, V2 -foramen Rotundum, V3 -foramen Ovale


For the order of nerves that pass through the superior orbital fissure:
               "Lazy French Tarts Lie Naked in Anticipation."
                (Lacrimal, Frontal, Trochlear, Lateral, Nosociliary, Internal,
                Abducens)


2  Muscle of mastication- Lateral Lowers- lateral pterygoid is the one that opens the jaw
4  Muscles of Mastication MTPP( which couldbe read as "Empty Peepee") -masseter, temporal, lateral and medial pterygoids --

Arteries as they come off the external carotid:
Superior thyroid, Ascending pharyngeal, Lingual, Facial, Occipital, Post Auricular, Superficial temporal, Maxillary
Some Anatomists Like Fucking, Others Prefer S & M
Some Angry Lady Figured out PMS
  


Innervation of Extraocularmotor Muscles:LR6 SO4 3
LR6--Lateral rectus--> VI abductens
SO4--Superior Oblique--> IV Trochlear
3--The remaining 4 eyeball movers = III Oculomotor

ABC'S of the aortic arch!
Aortic arch gives off the Bracheiocephalic trunk,
the left Common Carotid, and the left
Subclavian artery


BRACHIAL PLEXUS: Roots, Trunks, Divisions, Cords, Branches
Robert Taylor Drinks Cold Beer.  

CERVICAL SPINAL NERVES:
c345 keeps the phrenic alive (innervation of phrenic nerve) c345 keep the diaphragm alive (innervation of diaphragm)
c5-6-7 raise your arms to heaven (nerve roots of long thoracic nerve innervate serratus anterior)  


Cranial Bones 
     Annoying, aren't they? 
     The cranial bones are the PEST OF 6... 
  
     Parietal, Ethmoid,Sphenoid,Temporal,Occipital,Frontal- 6 ? (6-the number of bones!)
     ( another one)  Old People From Texas Eat Spiders.



LOCATION OF THORACIC DUCT: The duck is between two gooses (duck = thoracic duct) 2 gooses = azyGOUS and esophaGOUS 



Cartilages of the Larynx - There are 4 cartilages in the larynx whose initial letters are TEAC (also the brandname of a home stereo). 
  Thyroid, Epiglottis, Arytenoid, Cricoid



Abdomen-Pelvis 
 
INNERVATION OF PENIS:
Parasympathetic puts it up; sympathetic spurts it out
Point , Shoot, Score! (erection, emmision ,ejaculation) Parasympathetic, Sympathetic , Somatomotor
"S2, 3, 4 keep the penis off the floor" Innervation of the penis by branches of the pudental nerve, derived from spinal cord levels S2-4


Structures perforating the esophagus
"At T8 you see, perforates the IVC" (inferior Vena Cava)
the "EsoVagus" pierce T10 (esophagus, vagus nerve)
T12 - red, white and blue (aorta,thoracic duct,azygous vein)


Femoral Sheath (lateral to medial) order of things in thigh -NAVEL
Nerve, Artery, Vein, Empty, Space, Lymphatics


Radial n. innervates the BEST!!!!
Brachioradialis
Extensors
Supinator
Triceps


Course of Ureters
Water runs under the bridge (uterine a. and ductus deferens)


Carotid Sheath-- VAN
Internal Jugular Vein
Common carotid Artery
Vagus Nerve


Dermatomes
C3 is a high turtleneck shirt
T4 is at the nipple
L1 is at the inguinal ligament (or L1 is IL -Inguinal ligament)
Randy Travis Drinks Cold Beer--Brachial plexus
Robert Taylor Drinks Cold Beer
Roots, Trunks, Divisions, Cords, Branches


Bones of the wrist -Scaphoid, Lunate, Triquetrum, Pisiform, Trapezium,
Trapezoid, Capitate, Hamate
 
1. Slowly Lower Tilly's Pants To The Curly Hairs
2. Swifty Lower Tilly's Pants to try coitus here. (the risque version)
3.Scared Lovers Try Positions That They Can't Handle. (Classic version)
 
 
 


Pelvic Diaphragm
PICOLO(A) -Posterior to anterior
PIriformis
COccygeus
Levator Ani


Pelvic Splanchic-Parasympathetic
Sacral Splanchic-Sympathetic


Armies travel over bridges, the Navy travels under.
(Bridge is the ligament...reference to suprascapular artery and nerve.)


Pad, dab. Dorsal ABduct...Palmar ADduct...interosseous muscles of hand/foot.


Layers of the epidermis-Germinativum or Basale, Spinosum, Granulosum, Lucidum, Corneum
Grandpa Shagging Grandma's Love Child. 

Limbic System- the 5 F’s- Feeding, Fighting, Feeling, Flight and Fucking



The 5 sphincters found in the Alimentary Canal are APE OIL:
Anal, Pyloric, Lower Esophogeal, Oddi, and Ileocecum.


  Sally Thompson Loves Sex And Pot pie. The branches of the Axillary Artery are: Superior Thoracic, Thoracoacromial, Lateral Thoracic, Subscapular, Anterior Circumflex Humeral, Posterior Circumflex Humeral, and Profunda Brachii.



TIRE- four abdominal muscles -- transversus, internal oblique, rectus abdominus, and external oblique



GFR -Layers of the adrenal:-- Glomerular, Fascicular, Reticular 


 
BIOCHEMISTRY


In the Phasted State Phosphorylate
Phosphorylation cascade active when blood glucose low.


Exons expressed, Introns in the trash--DNA expression into mature mRNA


Pyrimidines are CUT from purines.
Pyrimidines are Cytosine, Uracil, Thiamine and are one ring structures.
Purines are double ring structures.


Amino Acids:The ten essential amino acids:
                "These Ten Valuable Amino Acids Have Long Preserved Life In
                Man."
                (Threonine, Tryptophan, Valine, Arginine, Histidine, Lysine,
                Phenylalanine, Leucine, Isoleucine, Methionine)

INsulin gets sugar INto cells- (Excess sugar is removed via urine.The  Romans noticed bees attracted to the urine of diabetics and coined the term "diabetes" to describe the overflow of sugar.)


GOAT FLAP- Eight hormones: Growth hormone, Oxytocin, Adenocorticotropin, Thyroid stimulating hormone, Follicle stimulating hormone, Leutinizing hormone (interstitial cell stimulating hormone in males), Anti-diruetic(Vasopressin), and Prolactin
(shhhh.... also Melatonin!)
 
 


PHARMACOLOGY


Morphine excites men, but sedates cats.


One heart two lungs--beta receptor activity
Beta-1 primarily on heart; airway is beta-2 receptors


CLINICAL


Meckel’s diverticulum- rule of 2’s
2 inches long,
2 feet from the ileocecal valve,
2% of the population
commonlly presents in the first 2 years of life
may contain 2 types of epithelial tissue  

Pheochromocytoma-rule of 10s:
10% malignant
10% Bilateral
10% extraadrenal
10% calcified
10% children
10% familial
* discussed 10 times more often than actually seen  

Aphasia
"BROKen aphasia" (Broca’s aphasia-broken speech)
"Wordys aphasia" (Wernicke’s aphasia- wordy, but making no sense)  

GET SMASH'D--Causes of Acute pancreatitis
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune(PAN), Scorpion bites, Hyperlipidemia, Drugs(azathioprine, diuretics)


(Multiple endocrine neoplasia) Each of the MENs is a
disease of three or two letters plus a feature.
"MEN I" is a disease of the 3 Ps (pituitary, parathyroid and pancreas)
plus adrenal cortex.
"MEN II " is a disease of the two Cs (carcinoma of the thyroid and
catacholamines [pheochromocytoma]) plus parathyroid for MEN IIa or
mucocutaneous neuromas for MEN IIb (aka MEN III).


Acute pneumonia caused by Pyogenic bacteria--PMN infiltrate
Acute pneumonia caused by Miscellaneous microbes --Mononuclear infiltrate


Takayasu's diz = pulseless diz, therefore when you have
Takayasu's, I can't Tak'a yu pulse.


Argyll-Robertson Pupil--syphilitic pupil (AKA "Prostitute's pupil" - Accommodates, but doesn't react )
Accommodation reflex present, Pupillary reflex absent


CAGE--alcohol use screening
1. Have you ever felt it necessary to CUT DOWN on your drinking?
2. Has anyone ever told you they were ANNOYED by your drinking?
3. Have you ever felt GUILTY about your drinking?
4. Have you ever felt the need to have a drink in the morning for an EYE OPENER?


P-Q-R-S-T--eliciting and HPI and exploring symptoms
P--palliative or provocative factors for the pain
Q--quality of pain(burning, stabbing, aching, etc.)
R--region of body affected
S--severity of pain(usually 1-10 scale)
T--timing of pain(eg.-after meals, in the morning, etc.)


The five W's--post-operative fever
Wind--pneumonia, atelectasis
Water--urinary tract infection
Wound--wound infections
Wonderdrugs--especially anesthesia
Walking--walking can help reduce deep vein thromboses and pulmonary embolus


ACID or "Anna Cycled Immediately Downhill"
classification of hypersensitivity reactions
Type I - Anaphylaxis
Type II - Cytotoxic-mediated
Type III - Immune-complex
Type IV - Delayed hypersensitivity


WBC Count:
"Never Let Momma Eat Beans(60, 30, 6, 3, 1)
Neutrophils 60%
Lymphocytes 30%
Monocytes 6%
Eosinophils 3%
Basophils 1%


A-P-G-A-R:
A - appearance (color)
P - pulse (heart rate)
G - grimmace (reflex, irritability)
A - activity (muscle tone)
R - respiratory effort 

Predisposing Conditions for Pulmonary Embolism: TOM SCHREPFER
T--trauma
O--obesity
M--malignancy
S--surgery
C--cardiac disease
H--hospitalization
R--rest (bed-bound)
E--estrogen, pregnancy, post-partum
P--past hx
F--fracture
E--elderly
R--road trip  

The 4 P's of arterial Occlusion: pain pallor pulselessness paresthesias
 

The 4 T's of Anterior Mediastinal Mass:Thyroid tumor,Thymoma,Teratoma, Terrible Lymphoma

Wednesday 22 January 2014

Under Eye Bags & Dark Circles

Medical Causes of Under Eye Bags & Dark Circles


dark circles fade
A person's face tells the whole story of what's going on in their body, good or bad. For the most part, dark circles under the eyes are only a cosmetic bother, with no negative health effects. But on some rare occasions, dark circles can be a minor symptom of something worse.
If eye bags are more than just a random occurrence for you, it could be a sign of a more serious health problem.

Causes of Periorbital Dark Circles

  • Eczema and Hay Fever - Under eye darkness and eye itchiness is a common symptom of allergic reaction such as hay fever. Eczema causes inflammation and rashes, in addition to dark circles under the eyes.
  • Periorbital Hyperpigmentation - This genetic condition is usually a result of allergies or familial heredity, typically for those of Mediterranean descent. The skin under and around the eyes is usually darker than other areas.
  • Anemia - Because anemics suffer from a deficiency of iron and other vital nutrients, there is not enough oxygen flowing through the underlying skin beneath the eyes, making bluish dark circles more apparent.
  • Liver disease - itchy skin, red swollen eyes, and dark circles under the eyes, as well as the excess visibility of blood vessels in the face, are common symptoms of a diseased liver.
  • Pregnancy or Menstruation - Menstruation and pregnancy deplete iron levels in the body, making skin paler. Pale skin beneath the eyes turns purple or bluish in color due to the visibility of veins beneath the semi-translucent skin.
Aside from these medical conditions, dark circles are caused by bruising genes and other hereditary factors, such as the thickness of the skin under your eyes. These blemishes are unsightly, but otherwise harmless, and are fairly easy to treat with dark circles products.

Causes of Puffiness & Eye Bags

Puffy eyes (aka periorbital puffiness) also has various different medical causes. Eye bags form due to excess fluid buildup or swelling of the tissues around and underneath your eyes. Some causes of eye bags include:
  • Crying - Aside from making your eyes feel tired and sore, the saltiness of tears causes fluid retention around the eyes, making them look dark and puffy.
  • Mononucleosis - In the early stages of a mono infection, eyes can become swollen and irritated
  • Oversleeping or Sleep Deprivation - Too much sleep or too little can completely derail your physical health and appearance. Tired, dark and swollen eyes are a common symptom of poor sleeping habits.
  • Hypothyroidism - This thyroid hormone deficiency causes paleness, dry, itchy skin, and puffiness around the eyes. This happens as a result of fluid retention in the periorbital tissue, which is caused excess hyaluronic acid and chondroitin sulfate mucopolysaccharides.
  • Chagas disease - This infection is caused by a parasite, which causes the eyes to swell up dramatically (also known as Romaña's sign). Although painless, young people are more likely to suffer from periorbital edema caused by Chagas.
  • Nephrotic Syndrome - This disorder is the result of kidney damage, and causes edema all over the body, usually starting with your face and eyes. Edema is an abnormal (and scary-looking) occurrence of extreme fluid retention beneath the skin. Massively swollen and puffy eyes are one of the first symptoms of nephrotic syndrome.
  • Periorbital cellulitis - This infection causes severe inflammation in the infected eyelid and surrounding skin. Blurred vision, redness, teary eyes, and dark circles are all common symptoms.
  • Trichinosis - This parasitic disease is caused by eating raw, undercooked pork. Symptoms around the eyes include mild puffiness, periorbital edema, swelling and pain. The blood vessels beneath the eyes become swelled to the point of destruction (also known as vasculitis).

How to Treat Dark Circles

If you suspect that you may be suffering from one of the above medical conditions, you should definitely consult a doctor to determine the best treatment for you.
However, if your dark circles are the result of fatigue or stress and not a medical problem, these blemishes can be treated safely by a wide array of home remedies and natural eye creams.

Monday 20 January 2014

NEMONIC for causes of CLUBBING>>>

the mnemonic is C.L.U.B.B.I.N.G, while the L has an extension of A.B.C.D.E.F

Cyanotic heart disease
Lung disease

Abscess
Bronchiectasis
Cystic Fibrosis
Dont say COPD
Empyema
Fibrosis

Ulcerative Collitis + Inflammatory Bowel Disease(Crohn's Disease)
Biliarty cirrhosis
Birth Defects
Infective Endocarditis
Neoplasm(eg. Lung cancer or mesothelioma)
Gastrointestinal malabsorption syndrome(Coeliac disease)

Friday 17 January 2014

Secondary Hypertension

Secondary Hypertension 

 "Alcoholic Obese Pregnant Drug abuser showing Endocrine abnormality diagnosed with Coarctation of aorta"

Thursday 16 January 2014

Respiratory System Examination

Respiratory Examination

This is essentially an examination of the patient’s lungs; however it is a complex examination which also includes examination of other parts of the body including the hands, face and neck.
The respiratory examination aims to pick up on any respiratory (breathing) pathology that may be causing a patient’s symptoms e.g. shortness of breath, cough, wheeze etc.  Common conditions include chest infections, asthma and chronic obstructive pulmonary disease (COPD).  This examination is performed on every patient that is admitted to hospital and regularly in clinics and general practice.
Like most major examination stations this follows the usual procedure of inspect, palpate, percuss, auscultate (look, feel, tap, listen).  It is an essential skill to master and is often examined in OSCEs.

Subject steps

  1. Whilst using the stethoscope, ask the patient to again say “99″ whilst listening in all areas – this is a more reliable test than the one described earlier.
  2. Thank your patient and allow them to dress.  Wash your hands and report your findings to your examiner.
- See more at: http://www.osceskills.com/e-learning/subjects/respiratory-examination/#sthash.F9UV535w.dpuf