ABOARD - This study evaluated a strategy of immediate vs. next-day cardiac catheterization and revascularization in patients with NSTE ACS.
Conclusions - A strategy of immediate PCI does not impact the incidence of death or MI in NSTE ACS
Length of hospital stay was significantly reduced with an immediate PCI strategy

ACTIVE A - This study evaluated treatment with a combination of aspirin and clopidogrel versus aspirin alone in patients with AF who were not candidates for warfarin therapy.
Conclusions -Clopidogrel in addition to aspirin may reduce the risk of stroke in patients with AF who are unsuitable candidates for warfarin therapy
The increased risk of major hemorrhage with aspirin + clopidogrel somewhat attenuates this benefit

ARMYDA-RECAPTURE - This study evaluated the efficacy of an atorvastatin reloading strategy in patients on chronic statin therapy undergoing PCI for stable angina or NSTEMI.
Conclusions -An 80 mg loading dose of atorvastatin followed by a 40 mg preprocedural dose may reduce the incidence of post-procedure MACE in patients on background statin therapy
These data support a strategy of routine atorvastatin reloading prior to PCI in patients on background statin therapy

AURORA - This study evaluated treatment with 10 mg rosuvastatin compared with standard therapy in patients with end-stage renal disease receiving hemodialysis
Conclusions - Low-dose rosuvastatin therapy does not reduce the rate of cardiovascular events in patients with ESRD receiving hemodialysis

EARLY ACS - Patients with NSTE ACS were randomized to upstream eptifibatide and 18- to 24-hour infusion (n = 4,722) versus upstream placebo and provisional eptifibatide immediately prior to PCI (n = 4,684).
Conclusions -Among patients with NSTE ACS treated with aspirin, clopidogrel, and heparin, there was no benefit to upstream eptifibatide compared with provisional use immediately prior to PCI
Upstream use of eptifibatide increased major bleeding

FIX-HF-5 Patients with NYHA III or IV heart failure and narrow QRS were randomized to cardiac contractility modulation plus optimal medical therapy (n = 215) vs. optimal medical therapy alone (n = 213). 
Conclusions -Among patients with advanced heart failure, low ejection fraction, and narrow QRS, cardiac contractility modulation failed to improve the primary efficacy outcome, anaerobic threshold
Cardiac contractility modulation did improve peak VO2 and quality of life

GENIUS-STEMI Patients with STEMI were randomized to the endothelial progenitor cell capture stent (n = 50) vs. a cobalt-chromium BMS (n = 50). Follow-up was 6 months.
Conclusions - Among patients with STEMI, the endothelial progenitor cell capture stent was inferior to a cobalt-chromium bare-metal stent
This experimental stent resulted in increased MACE, TLR, and stent thrombosis...

Glomerulonephritis

Posted by e-Medical PPT

Features of Glomerular Disease
Proteinuria
Haematuria
Renal Failure
Salt and Water Retention results in Hypertension,Oedema and Oliguria
Loin Pain

Proteinuria
Frothing
Marker of renal disease
Risk factor for cardiovascular disease
Dyslipidaemia
Hypertension
Something more?
24 hr protein vs urine protein:creatinine ratio

eGFR and CKD
>50% inaccurate in over 50% patients
Worst hit: females over 60
Quadrupled our referral rate
Mostly inappropriate
Unnecessary worry for patients
Is it really necessary to refer a patient with a stable creatinine of 130 ╬╝mol/l just because you now know their eGFR is 40?

Common Syndromes
Nephrotic Syndrome
Nephritic Syndrome
Rapidly Progressive GN
Loin Pain Haematuria Syndrome

Nephrotic syndrome
Proteinuria (>3g/24 hr)
Hypoalbuminaemia (<30g/l)
Oedema
Hypercholesterolaemia
Thromboses
Infection

Nephritic Syndrome
Haematuria
Hypertension
Oliguria

Rapidly progressive GN
Nephritic or nephrotic onset
ESRF in six months

Loin pain haematuria syndrome
Bilateral or unilateral pain
Macroscopic or microscopic haematuria
Other “functional” disorders common
Young female healthcare professionals

Cirrhosis and its ComplicationsPortal hypertension and variceal bleeding
 Renal : Ascites, Hepatorenal syndrome
 CNS: Encephalopathy
 Cardiovascular: Hyperdynamic circulation
                               Cirrhotic cardiomyopathy
                               Electrophysiological abnormalities
 Pulmonary: Hepatopulmonary syndrome
                       Porto-pulmonary hypertension
                       Hepatic hydrothorax
 Bacterial infection

Risk Factors for Variceal Bleeding
Endoscopic Appearance
      Size of varices, Presence of red signs
      (red wale markings, cherry red spots)
Severity of liver cirrhosis
HVPG > 12 mmHg
Continuous alcohol consumption

Treatment of Acute Variceal Bleeding
Drug therapy
Endoscopic  treatments
Balloon Tamponade
Transjugular intrahepatic portal-systemic shunt
   (TIPS)
Surgery

Accepted indications
Failed to control acute variceal bleeding after standard medical and endoscopic treatment
Bleeding gastric varices
Bleeding varices prior to liver transplantation
Refractory ascites

Experimental indications
Long-term treatment of portal hypertension
Cirrhotic hydrothorax
Budd-Chiari syndrome
Hepatorenal syndrome

Baveno IV (2005) Consensus Statement of International Portal Hypertension Workshop for Acute Variceal Bleeding
Blood volume restitution should be done cautiously and conservatively.
Antibiotics prophylaxis is an integral part of therapy for patients presenting with variceal bleeding and should be instituted from admission.
Vasoactive drugs should be started as soon as possible, before endoscopy and maintained for 2-5 days.
Ligation is the recommended form of endoscopic therapy for acute EV bleeding although sclerotherapy may be used if ligation
is technically difficult.
Endoscopic treatments are best used in association with pharmacological therapy, which preferably should be started
before endoscopy.
Failure of initial therapy with combined drug and endoscopic therapy are best managed by a second attempt at endoscopic therapy or TIPS.

Prevention of Recurrent Variceal Bleeding
Drug therapy (Non-selective Beta Blockers)
Endoscopic  treatments (Band Ligation)
Transjugular intrahepatic portal-systemic shunt
   (TIPS)
Surgery

Primary Prophylaxis of Variceal Bleeding
Drug therapy (Non-selective Beta Blockers)
Endoscopic  treatments (Band Ligation)

Baveno IV (2005) Consensus Statement of International Portal Hypertension Workshop for Primary Prophylaxis
Beta-blockers reduce the risk of first variceal bleeding.
Prophylactic band ligation is useful in preventing variceal bleeding in patients with medium and large varices.
Band ligation is more effective than beta-blockers in preventing  first variceal bleeding but does not improve survival. However, the long-term benefits of band ligation are uncertain because of the short duration of follow-up.
Band ligation should be offered to patients with medium/large varices and contraindications or intolerance to beta-blockers.

TYPES OF PANCREAS TRANSPLANTATION
SPK : Simultaneous Pancreas - Kidney
PAK: Pancreas After Kidney
PTA: Pancreas Transplantation Alone

INDICATIONS FOR PANCREAS TRANSPLANATION
SPK - Simultaneous Pancreas Kidney tx
Terminal renal insufficiency +  type I diabetes    + complications of diabetes
Pre-terminal renal insufficiency + complications of diabetes
Bilateral nephrectomy in diabetics + complications of diabetes
 Failed kidney transplant in diabetics type I

PAK - Pancreas After Kidney tx
10 % of pancreas tx
previous kidney tx in type I diabetics     + complications of diabetes
2 groups
a. status after kidney tx
b. status after SPK with failed pancreas tx

PTA - Pancreas Transplantation Alone: 3%
1. Hypoglycemic unawareness
2. Incapacitating  clinical & emotional problems with insulin
3. Progressing diabetic complications resistent to intensive               insulin therapy
4. Early diabetic nephropathy associated with complications of diabetes
5. Resistance to SC insulin
6. After total pancreatectomy
7. Insulin allergy

CONTRA-INDICATIONS FOR PANCREAS TX
Absolute contra-indications
    Ischemic heart disease
        inoperable coronary artery disease
        cardiomyopathy with ejection fraction < 35 %
    Peripheral vascular disease
        inoperable aorto-iliac vascular disease
    Malignancy < 3 y
 Relative contra-indications
        HIV infection - hepatitis B+
        peptic ulcer
        complications of diabetes not amenable to improvement
        drug or alcohol abuse
        active infection
        recent retinal bleeding
        obesity - smoking...

RISK FACTORS IN PANCREAS TX
Age > 45 y
Obesity
Hypertension
Blindness (even monocular)
Heart disease: AMI - CABG - PTA
Peripheral vascular disease: CVA - PTA - bypass - TIA
Major amputation
Hyper coagulability
Re-transplantation..

Liver structure and function
Liver is the largest organ
Consist of two lobes; right and left
Functions :
 - Carbohydrate, protein, and fat metabolism
    * glycogenesis, glycogenolysis, gluconeogenesis
    * protein synthesis; albumin, globulin
Albumin   oncotic pressure, carrier for drugs
Globulin  coagulation factors
Fatty acid are taken up by the liver; cholesterol synthesis; bile salt synthesis
Drug metabolism
Enterohepatic circulation

Evaluation of liver function
Aminotransferases (Transaminases)
    - hepatocellular damage
    - alanine aminotransferase (ALT, SGPT) : primarily in the liver
    - aspartate aminotransferase (AST, SGOT); present in many tissues; heart, skeletal muscle, kidney, brain
Alkaline phosphatase
    - bone, intestine, liver, placenta
    - impaired biliary tract function
Gamma-glutamyl transferase (GGT)
    - widely in body tissues
    - increased level: biliary tract disease
Serum protein
    - liver injury may lead to decreased blood levels of albumin, prothrombin, fibrinogen
    - not specific for liver disease
    * Albumin and globulin : long half-life
    * Prothrombin time : shorter half-life

Jaundice
Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (plasma bilirubin concentrations above 2-2.5 mg/dL)
Unconjugated bilirubin (UCB) = indirect bilirubin
Conjugated bilirubin (CB) = direct bilirubin
Derangements of bilirubin metabolism may occur through any of four mechanisms :
    - overproduction : hemolysis
    - decreased hepatic uptake
    - decreased hepatic conjugation
    - decreased excretion of bilirubin into bile (due to intrahepatic dysfunction or extrahepatic mechanical obstruction)

Hepatocellular failure
Acute liver failure
- Causes :
1. Massive liver cell necrosis due to viral hepatitis (HBV or HCV), some drugs (e.g., halothane, isoniazid, acetaminophen), toxic chemicals (e.g., chloroform, mushroom poisoning)
Acute liver failure
2. Acute fatty change Reye’s syndrome, fatty liver of pregnancy, tetracycline
Chronic liver failure
- Most common causes is cirrhosis, chronic active hepatitis

Hepatocellular failure
Characteristic physiological changes of liver failure include
1. Jaundice
2. Coagulopathy due to malabsorption of vitamin K and reduced synthesis of clotting factors II, VII, IX, and X
3. Changes in neurologic status : hepatic encephalopathy
4. Hypogonadism and gynecomastia due to imabalance of androgen-estrogen levels
5. Palmar erythema
6. Spider angiomatas of the skin
7. Fetor hepaticus
8. Ascites
9. Portal hypertension

Cirrhosis
Irreversible inflammatory disease that disrupts liver structure and function disorganization of hepatic tissues is caused by diffuse fibrosis and nodular regeneration
Liver may be larger or smaller than normal, and usually it is firm or hard when palpatated

Physiology of biliary tract
Gallbladder : a saclike organ : store and concentrate bile between meals
Bile : alkaline, bitter-tasting, yellow green fluid that contains
    * bile salts (conjugated bile acids), conjugate with amino acids (glycine or taurine) in the liver      more water soluble : intestinal emulsification, absorption of fats
     * cholesterol, bilirubin (a pigment), electrolytes, waters....

ESRD: irreversible loss of renal function, accumulation of toxins and loss of internal homeostasis.
Uremia: clinical syndrome resulting from ESRD.
Pathophysiology of Uremia
Excretory Failure: causes >70 chemicals to elevate. Urea= major breakdown of proteins.  Limit protein intake
Biosynthetic Failure: loss of hormones 1,25(OH)3 vit D3 and erythropoietin.
85% of erythropoietin produced by kidney.
Vit. D3 deficiency= secondary hyperparathyroidism, renal bone disease.
Regulatory Failure: over secretion of hormones , disruption of normal feedback mechanisms

Clinical Features of Uremia
Neurologic complications:
Subdural hematoma: 3.5% of ESRD, HTN, head trauma, bleeding dyscrasias, anticoagulants, ultrafiltration.
Uremic Encephalopathy: nonspecific centreal neurologic symptoms, responds to dialysis.
Neurologic complications:
Dialysis Dementia: like uremic encephalopathy but progressive and fatal, seen after 2 years on dialysis
Peripheral neuropathy: >50% of HD patients. “glove and stocking pattern”, improves after transplant
Autonomic dysfunction: common; dizzy, impotence, bowel dysfunction.
Cardiovascular complications:  prevalence is greater in ESRD
d/t pre-existing conditions, uremia, toxins, high lipids, homocystine, hyperparathyroidism, dialysis related conditions..

Hemodialysis
Uses ultrafiltration and clearance to replace nephron.
Solute removal depends on filter pore size and concentration gradient
Heparin 1000-2000 units typically used
Sessions take @ 3-4 hrs.

Vascular Access Complications
Types of Access:
1. A-V fistula
2. Vascular graft: higher complication rates, shorter functional lifes.
3. Tunnel-cuffed catheters; Hickman, Quinton

Complications During Hemodialysis
1. Hypotension:
Most frequent,  10-20% of treatments
Dialysis can remove up to 2 L/hr.
Cardiac compensation limited d/t ↓ diastolic function common in ESRD
Abnormalities in vascular tone; sepsis, anit HTN meds, ↑ nitric oxide
Early hypotension: pre-existing hypovolemia
Peridialysis losses;  starts HD below dry weight;  d/t sepsis, GI bleed, vomiting, diarrhea, decreased salt/water intake
Intradialytic blood loss from tubing/dialyzer leads
Hypotension at end of dialysis: excessive removal, cardiac or pericardial disease.
Intradialytic hypotension:
N/V/anxiety, ortho hypotension, tachycardia, dizzy, syncope.
Tx.; stop HD, Trendelenburg. Salt, broth by mouth, NS 100-200 cc. IV.
If these fail look for other causes than excessive fluid removal

2. Dialysis disequilibrium:
End of dialysis
N/V, HTN...progress to coma, seizure and death
d/t cerebral edema after large solute clearance in HD
Tx.  Stop HD, administer Mannitol IV.

3. Air Embolism:
s/s: dyspnea, chest tightness, unconscious, full cardiac arrest.  Cyanosis, churning sound in heart from bubbles
Clamp venous blood line, place supine
Other Tx’s: percutaneous aspiration from R ventricle, IV steroids, full heparinization, hyperbaric O2 treatment
4. Electrolyte abnormalities
5. Hypoglycemia

Spondylolisthesis

Posted by e-Medical PPT

The term "Spondylolisthesis" refers to a condition where one of the vertebrae (usually L5) becomes misaligned anteriorly (slips forward) in relation to the vertebra below. This forward slippage is caused by a problem or defect within the pars interarticularis. Occasionally, facet joint and/or posterior neural arch defects may also cause this syndrome as well.
The forward slippage does NOT always occur. This non-slipped pars defect is called a "Spondylolysis" and is almost always a precursor to the actual forward slippage.

Developmental anatomy
The first theory proposed a failure of ossification during embryonic development, leading to a pars interarticularis defect at birth
The second theory demonstrated that the pars defect began to appear around age six and became progressively more common till age 16. After age 16, the incidence fell and rarely developed after adolescence
It is currently thought that the defect develops from small stress fractures that fail to heal and form a chronic nonunion.

Classification
Dysplastic spondylolisthesis
Isthmic spondylolisthesis
DEGENERATIVE SPONDYLOLISTHESIS
TRAUMATIC SPONDYLOLISTHESIS
PATHOLOGICAL SPONDYLOLISTHESIS
IATROGENIC SPONDYLOLISTHESIS

Dysplastic spondylolisthesis
Is a true congenital spondylolisthesis that occurs because of malformation of the lumbosacral junction with small, incompetent facet joints.
Very rare, but tends to progress rapidly
Often associated with more severe neurological deficits.

Isthmic spondylolisthesis
SUB-TYPE A:
Is the most commonly found type of spondylolisthesis in people under 50 years of age.
It is believed that "biomechanical stress," such as repetitive mechanical strain from heavy work or sports, causes a fatigue fracture within the pars interarticularis.

SUB-TYPE B:
This type of Isthmic spondylolisthesis is characterized by a elongated pars without separation.
It is believed that the elongation occurs secondary to "repeated, minor trabecular stress fractures of the pars." Each time these possible sub-acute stress fractures occur and heal, the vertebral body is displaced farther and farther forward. Eventually, the pars may fail to heal and result as a full pars defect.

SUB-TYPE C:
These types of spondylolisthesis' are extremely rare and result from an acute pars fracture, often as result of traumatic lumbar hyperextension injury

DEGENERATIVE SPONDYLOLISTHESIS
This is the most common form of spondylolisthesis in patients over 50 years of age and rarely occurs in those under 50
There is no fracture or elongation of the pars interarticularis and the neural arch is intact.  In contrast, patients with isthmic spondyolisthesis almost universally have widening of the central spinal canal at the level of the slip. This narrowing of the canal in degenerative spondylolisthesis has been termed the "napkin ring effect...

Diseases of the Pancreas

Posted by e-Medical PPT

Pancreas anatomyThe pancreas is an elongated, tapered organ located across the back of the abdomen, behind the stomach. The right side of the organ (called the head) is the widest part of the organ and lies in the curve of the duodenum (the first section of the small intestine).
The tapered left side extends slightly upward (called the body of the pancreas) and ends near the spleen (called the tail).
The pancreas is made up of two types of tissue:
exocrine tissue
The exocrine tissue secretes digestive enzymes. These are secreted into a network of ducts that join the main pancreatic duct, which runs the length of the pancreas.
endocrine tissue
The endocrine tissue, which consists of the islets of Langerhans, secretes hormones into the bloodstream.

The pancreas has digestive and hormonal functions:
The enzymes secreted by the exocrine tissue in the pancreas help break down carbohydrates, fats, and proteins in the duodenum.
These enzymes travel down the pancreatic duct into the bile duct in an inactive form.
When they enter the duodenum, they are activated.
The exocrine tissue also secretes bicarbonate to neutralize stomach acid in the duodenum.

The hormones secreted by the endocrine tissue in the pancreas are insulin, glucagon (which regulate the level of glucose in the blood), somatostatin (which prevents the release of the other two hormones), and many others.

What is Pancreatitis?
Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland
Normally, digestive enzymes do not become active until they reach the small intestine, where they begin digesting food.
But if these enzymes become active inside the pancreas, they start "digesting" the pancreas itself
The gland can sometimes heal without any impairment of function or any morphologic changes.
This process is known as acute pancreatitis.
It can recur intermittently, contributing to the functional and morphologic loss of the gland.
Recurrent attacks are referred to as chronic pancreatitis.

Necrotizing pancreatitis
When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland, the inflammation evolves into hemorrhagic or necrotizing pancreatitis
Pseudocysts and pancreatic abscesses can result from necrotizing pancreatitis because of enzymes being walled off by granulation tissue (ie, pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic tissue (ie, pancreatic abscess formation).
An ultrasound or, preferably, a CT scan can be used detect both....

General Approach ABC’s of Toxicology
A-Antidotes and alter absorption  (in some instances prior to airway-decontamination with organophosphates to protect others, cyanide toxicity where antidotes are lifesaving)
B-Basics; ABC’s
C-Change metabolism (NAC, ethanol)
D-Distribute differently (calcium gluconate, O2)
E-Elimination (diuresis, dialysis, hemoperfusion)

TOXIDROMES
A.Introduction
1.“Physiologic fingerprints” that occur in the form of syndromes or groups of symptoms which are observed to occur together in response to exposure to one of a pharmacologically similar group of agents
2.Useful in determining the class of agents involved in an unknown poisoning
3.Result of receptor interaction or neurotransmitter release leading to stimulation or inhibition of the different divisions of the autonomic nervous system

Sympathetic or sympathomimetic
Presentation: mydriasis, tachycardia, hypertension, hyperthermia, diaphoresis, seizure, central nervous system (CNS) excitation
Similar to withdrawal toxidrome
Similar to anticholinergic toxidrome except:
Diaphoresis and normal bowel sounds with sympathomimetic toxidrome
Dry skin and absent bowel sounds with anticholinergic toxidrome

Cholinergic-Toxidrome (Muscarinic)
Presentation: DUMBBELS
D-Diarrhea U-Urination M-Miosis B-Bronchorrhea B-Bradycardia E-Emesis L-Lacrimation S-Salivation

Anticholinergic Toxidrome
Presentation: “red as a beet (flushing), dry as a bone (dry skin), mad as a hatter (delirium, hallucinations), hot as Hades (hyperthermia), blind as a bat (mydriasis).” Also see hypertension, tachycardia, urinary retention, absent bowel sounds, seizures

Withdrawal Toxidrome
Presentation: diarrhea, piloerection, lacrimation, crampy abdominal pain, hallucinations, mydriasis, tachycardia, hypertension, yawning, seizure (ethanol, benzodiazepine, barbiturate). Similar to sympathetic toxidrome

METHODS OF EMPTYING
Gastric lavage
Large bore orogastric tube (36 - 40 F) Place patient in left lateral decubitus position
Infuse 250 cc aliquots of saline, drain, repeat until clear (at least 2 liters)
Remember airway protection
Complications: aspiration, esophageal rupture, epistaxis, hypothermia

Charcoal-now procedure of choice if appropriate substance. Major risk is aspiration.
May use NG/OG tube or give orally.  If giving orally, assure patient is awake and airway protected.

whole bowel irrigation
Polyethylene glycol electrolyte solution is instilled at a rate of 2 L/hr until the rectal effluent is clear. Often requires nasogastric (NG) placement for administration...

Fever During and After Childbirth

Posted by e-Medical PPT

Providing Prophylactic Antibiotics
Help prevent infection, which can result from certain procedures, including:
Cesarean section
Manual removal of placenta
Correction of uterine inversion
Repair of ruptured uterus
Postpartum hysterectomy
Prolonged rupture of membranes (Group B streptococcus)
If infection is suspected or diagnosed, therapeutic antibiotics are more appropriate
Should be given 30 minutes before procedure, to allow adequate blood levels at time of procedure
Except at cesarean, give antibiotics when cord is clamped after delivery of newborn
One dose is enough (as effective as 3 doses or 24 hours of antibiotics)
If procedure is longer than 6 hours or blood loss is 1500 mL or more, give second dose.

Providing Therapeutic Antibiotics
For general treatment of obstetrical infection or until diagnosis is made, give broad spectrum antibiotics
Treat specific infection with specific antibiotics
If response is poor after 48 hours:
Ensure adequate doses of antibiotics are being given
Re-evaluate woman for other infection or abscess
Treat based on reported microbial sensitivity
End point is when:
Woman is fever-free for 48 hours
Clinical examination shows woman is improving
Woman completes course of antibiotics (in all cases except metritis)

Fever During Pregnancy and Labor: Differential Diagnosis
Cystitis
Acute pyelonephritis
Septic abortion
Amnionitis
Pneumonia
Malaria
Typhoid
Hepatitis

Obstetric and Medical Factors Affecting Postpartum Sepsis
Intervention during labor and delivery
Dangerous infections following prolonged and obstructed labor
Thrombophlebitis, pulmonary embolism, coagulopathy and septic shock may complicate the infection
Remember that clostridium infections may be difficult to detect and occur where contamination with earth or cow dung is possible

Health Service Factors Affecting Postpartum Sepsis
Majority of deaths occur between first and second week of puerperium and are linked to medical and midwifery/nursing staff factors:
 Inadequate:
monitoring of temperature
bacteriological investigations
treatment with antibiotics or operative intervention
 Lack of:
asepsis and antisepsis
blood for transfusion
appropriate drugs

Ovarian Cysts

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General principles for management of ovarian cysts:Establish the type of cyst.
Avoiding surgery for functional cyst.
Exclude malignancy ( U/S, Doppler  and  tumor marker like Ca-125) .
Age of patient must be considered (Surgery may be  recommended in post menopausal women or in prepubertal).
Gynecologists should be aware of the role of Interventional ultrasound!!!!?

Ovarian Cysts
Non Neoplastic
  Physiological
   Follicular.   
   Theca Lutein
  Pathological        
   Endometriotic.   
   Inflammatory   
   PCOS

Neoplastic
    Epithelial Tumours
    Sex cord Tumours
    Germ cell Tumours

Ovarian Cyst Aspiration
Maybe an alternative for laparotomy or laparoscopy.
Is a matter of controversy .
 High recurrence rate.
 Unreliable cytology .
 Risk of dissemination of Neoplastic cells.

Interventional Ultrasound for Ovarian Cyst Aspiration ?
1)Functional ovarian cysts
2)Pre menopausal ov cysts
3)Ovarian cyst during second  trimester  of pregnancy .
4)Retention cysts after GnRH analogue during long protocol of A.R.T  cycle.
5)Some Endometriotic cyst
6)Ovarian cysts in fetuses         

Postmenopausal Ovarian cyst
There is no physiological Ovarian cyst cyst in postmenopausal  women
Aspiration is not recommended for the management of ovarian cysts in postmenopausal women.

Liver Disease with Pregnancy

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Liver disease is a rare complication of pregnancy, but when it occurs it may do so in a dramatic and tragic fashion for both mother and infant. Diseases such as acute fatty liver of pregnancy (AFLP) may begin innocuously with mild symptoms and liver enzyme abnormalities but, if left untreated, can progress to jaundice, liver failure, and death.
Some of the normal physiologic changes of pregnancy can mimic abnormalities associated with liver disease.
Telangiectasia, particularly on the chest, back, and face, and palmer erythema occur in up to 60 percent of normal pregnant women but disappear after delivery.

Summary of physiological changes in the liver during pregnancy   
Increased:
Blood volume and cardiac ouput rise by 35%–50%
Alkaline phosphatase levels rise threefold or fourfold due to
placental production
Clotting factor changes create a hypercoagulable state
Decreased:
Gallbladder contractility
Hemoglobin
Uric acid levels
Albumin, total protein, and antithrombin III concentrations
No change:
Liver aminotransferase levels (aspartate aminotransferase,
alanine aminotransferase, gamma-glutamyl transferase)
Bilirubin level
Prothrombin time

Spectrum of liver diseases in pregnancy
Preexistent liver diseases
Portal hypertension, cirrhosis, primary biliary cirrhosis
Autoimmune hepatitis
Wilson disease
Chronic infection with hepatitis B or hepatitis C virus
Alcoholic liver disease

Liver diseases coincidental with but not induced by pregnancy
Acute viral hepatitis and other viral infections
Alcohol-related diseases
Gallstone disease
Budd-Chiari syndrome

Liver diseases induced by pregnancy
First trimester
Hyperemesis gravidarum
Second and third trimesters
Intrahepatic cholestasis of pregnancy
Preeclampsia, eclampsia, and the HELLP syndrome
(hemolysis, elevated liver enzymes, low platelet counts)
Acute fatty liver of pregnancy

Intrahepatic Cholestasis of Pregnancy
The syndrome has been variously called recurrent jaundice of pregnancy, cholestatic jaundice of pregnancy, jaundice of late pregnancy, and hepatosis of pregnancy. ICP, however, is the preferred term, because jaundice is inconstant in any type of cholestatic disorder.
Clinical Description
Pruritus is the dominant and  initial symptom and appears in the third trimester in more than 70% of cases. Most of the remaining patients date their onset of symptoms to the second trimester.
The symptom may become very severe and usually involves the trunk and the extremities, including the palms and the soles of the feet. As a result of the pru­ritus, insomnia, fatigue, and even mental disturbances have been reported
Many patients report the appearance of dark urine without frank jaundice shortly after the onset of pruritus. Only a minority of patients develop obvious jaundice, and this is usually mild.
It is notable that abdominal pain, biliary colic, fever, anorexia, nausea, vomiting, and arthralgias are absent.
The improvement in both pruritus and jaundice begins to occur quite promptly after delivery, most often within 24 hours. However, jaundice may continue for several days after delivery, and some of the abnormal chemistry profiles persist for as long as several months.
Subsequent pregnancies are frequently accompanied by recurrences of the syndrome.

Hip Disorders

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Slipped capital femoral epiphysis (SCFE)Traumatic hip dislocation
Osteoarthritis

"Slipped upper femoral epiphysis" is a medical term referring to slippage of the overlying epiphysis of proximal femur posteriorly and inferiorly due to weakness of the growth plate. Most often, it develops during periods of accelerated growth, shortly after the onset of puberty.
A Klein line is a line drawn along the superior border of the femoral neck that would normally pass through a portion of the femoral head. If not, slipped capital femoral epiphysis is diagnosed.
The patient's left hip (arrow) shows that a slight shift of the head of the femur occurred through the growth plate.

Risk Factors
Most common in the adolescent period (boys aged 10-16 y, girls aged 12-14 y).
Males have 2.4 times the risk as females.
Obesity is a risk factor because it places more shear forces around the proximal growth plate in the hip at risk.
Bilateral slippage is common (but the left hip is affected more commonly than the right).

Etiology
Overweight
Endocrine disorders (e.g adiposogenital dystrophy, primary or secondary hypothyroidism).
Deficiency or increase of androgens.
Acute trauma.
Slipping of the upper femoral epiphysis occurs predominantly in obese children with underdeveloped sexual characteristics and less commonly, in tall, thin children.

Pathology
The slip occurs in the hypertrophic zone of the growth plate.
70% slow and progressive (This is gradual, with slowly     increasing symptoms over a period of weeks or even months. In chronic slipping, there may be no history of trauma and the symptoms are often quite mild).
30% acute due to trauma (Least common, this usually follows severe trauma such as a fall from a height ).
If the slip is sever anterior retinacular vessels are torn → avascular necrosis.
Physeal slip → premature fusion of the epiphysis within 2 years.

Clinical Features
1.  Pain : in the groin and around the knee.
2.  Limp (intermittent).
3.  Shortening of the affected limb (1-2 cm).
4.  The limb is in external rotation.
5.  Flexion, abduction, medial rotation are limited.
6.  External rotation, adduction are increased.

Diagnosis
The diagnosis is a combination of clinical suspicion plus radiological investigation. 20-50% of SCFE are missed or misdiagnosed on their first presentation to a medical facility. This is because the common symptom is knee pain. This is referred pain from the hip. The knee is investigated and found to be normal
Ultra sound :
AP X-ray : (melting ice cream cone)
 1. Widening of the growth plate.
 2. Trethowan’s sign : Line up superior margin of neck should intersect epiphysis (usually 20% of the femoral head lateral to this line)
 3. Capeners sign : In pelvic AP view in the normal hip, the posterior acetabular margin cuts across the medial corner of the upper femoral metaphysis. With slipping, the entire metaphysis is lateral to the posterior acetabular margin
Lateral X-ray :
 Slip
 Posterior horn of the neck is lower than anterior horn....

Scoliosis and Kyposis

Posted by e-Medical PPT

SCOLIOSIS
A condition that involves complex lateral and rotational curvature of the spine.
Dextroscoliosis is a scoliosis with the convexity on the right side.
Levoscoliosis is a scoliosis with the convexity on the left side.

Classification
Postural Scoliosis
 The deformity is secondary or compensatory to some condition outside the spine; when the patient sits (thereby cancelling leg asymmetry), the curve disappears.
Conditions that lead to postural scoliosis :
Short leg
Pelvic tilt due to contracture of the hip
Local muscle spasm @ prolapsed lumbar disc

Structural Scoliosis
 It is always accompanied by bony abnormality or vertebral rotation. The deformity is fixed and does not disappear with change in posture.
 Secondary curves nearly always develop to counterbalance the primary  later,  they may become fixed too.

Idiopathic scoliosis 80%
Infantile <3yrs
Juvenile 4-9 yrs
Adolescent >10yrs (Most common)

Scoliosis due to known causes 20%
Osteopathic: due to Congenital vertebral anomalies. Rare but dangerously progressive
Neuropathic: due to asymmetrical muscle weakness (e.g. in cerebral palsy and Poliomyelitis)
Myopathic: seen in the rare muscular dystrophies
Neurofibromatosis: associated with severe deformity

Cobb’s Angle
     Measurement used for evaluation of curves in scoliosis on an AP radiographic projection of the spine. When assessing a curve, the apical vertebra is first identified, the end or transitional vertebra are then identified through the curve above and below.

The apical vertebra is most likely displaced and rotated vertebra with the least tilted end plate.
The end/transitional vertebra is most superior and inferior vertebra which are least displaced and rotated and have the maximally tilted end plate. A line is drawn along the superior end plate of the superior end vertebra and a second line drawn along the inferior end plate of the inferior end vertebra.

KYPHOSIS
Definition
 The term kyphosis is used to describe both;
 The normal (the gentle rounding of the dorsal spine) and
The abnormal (excessive dorsal curvature).
In the latter sense it signifies a well-recognized deformity which may be progressive

Postural kyphosis
It is common (‘round back’ or ‘drooping shoulders’) and may be associated with other postural defects such as flat-feet

Structural kyphosis
Is fixed and associated with changes in the shape of the vertebrae. It may occur in osteoporosis of the spine (the commonly round back of elderly people), in ankylosing spondylitis and in scheuermann’s disease (adolescent kyphosis)

Q-Fever(Coxiella burnetii)

Posted by e-Medical PPT

Q fever is a zoonotic disease caused by Coxiella burnetii
Obligate intracellular, gram negative bacterium
Distributed globally
Found in many species of animals

Transmission
Most common route is inhalation of aerosols
Contaminated dust, manure, birthing products
Tick bites (rare)
Human to human also very rare

Symptoms
Acute Q fever
Self-limiting, flu-like disease
Fever, nausea, headaches, vomiting, chest/abdominal pain
Pneumonia and granulomatous hepatitis

Chronic Q fever (> 6 months)
Endocarditis & meningoencephalitis
Pre-existing disease

Diagnosis
Hard to diagnose because:
Asymptomatic in most cases
Looks like other disease (Flu or cold)
Serology continues to be best method
PCR, ELISA and other methods
Bio safety level 3 (BSL-3) facility
Very infectious (one organism causes infection)
Listed by the CDC as a potential bioterrorism agent.
Isolated in cell cultures or embryonated eggs

Control/Prevention
Pasteurization and sterilization of milk and other dairy products
Disinfect utensils, machines used in farm areas for birthing
Regular testing of animals and those who work closely with them
Protective Personal Equipment

Fever in ICU Patients

Posted by e-Medical PPT

Fever is a common problem in the ICUCould be due to infectious and non-infectious causes
Objective is to review a rational approach to the management of fever in ICU patients

How to measure temperature in the critically ill patient?
Peripheral temperature measurements
  • Measured in the outer 1.6 mm of skin or mucus membranes
  • Considered unreliable as influenced by environmental temperatures, mouth breathing etc.
  • Examples – oral temperature, axillary, skin temperature
Core temperature measurements
  • Not influenced by external factors
  • More accurately reflects temperature in the internal organs
  • Examples – pulmonary, rectal, esophageal, urinary, tympanic
Optimal site
Pulmonary – but invasive, need equipment

Alternatives
Tympanic – easy but can be off by even 2O
Urinary – good alternative
Rectal – uncomfortable
Oesophageal

Approach to fever in the ICU
Acute undifferentiated fever
Fever with thrombocytopenia
  • Malaria (notably falciparum)
  • Dengue
  • Leptospirosis
  • Rickettsial infections
  • Viral fevers
Fever with hepato-renal dysfunction
  • Malaria (falciparum)
  • Leptospirosis
  • Scrub typhus   
  • Fulminant hepatic failure with hepatorenal
Fever with pulmonary renal syndrome
  • Malaria (falciparum)
  • Leptospirosis
  • Scrub typhus   
  • Hantavirus infection
  • Severe legionella / pneumococcal pneumonia
Fever with altered sensorium
  • Malaria – cerebral malaria
  • Encephalitis
  • Meningitis
  • Typhoid fever
  • Septic encephalopathy
  • Brain abscess..


    Idiopathic Thrombocytopenic Purpura

    Posted by e-Medical PPT

    The etiology is still unknown and the pathogenesis is complex and possibly depends on disturbed antigen presentation, T cell activation and signaling, disregulated B cell stimulation and antibodies, unbalanced activation / suppression of complement.
    Affected children are young (peak age ~ 5 yrs) and previously healthy, and they typically present with the sudden onset of petechiae or purpura a few days or weeks after an infectious illness.
    Boys and girls are equally affected.
    In more than 70% of children, the illness resolves within six months, irrespective of whether they receive therapy.By contrast, ITP in adults is generally chronic.
    The bone marrow in patients with ITP contains normal or increased numbers of megakaryocytes.

    The diagnosis of ITP remains one of exclusion.
    Secondary forms of the disease occur in association with SLE, the antiphospholipid syndrome, immunodeficiency states (IgA   deficiency and common variable hypogammaglobulinemia), Lymphoproliferative disorders (CLL, Large granular lymphocytic leukemia, and lymphoma), infection with HIV and hepatitis c virus, and therapy with drugs such as heparin and quinidine.         
    The guidelines of the American  Society of Hematology state that a bone marrow examination is not required in adults younger than 60 yrs of age if the presentation is typical but is appropriate.
    Marrow examination is necessary in the presence of atypical features (e.g., those with additional cytopenias, protracted fever, bone or joint pain, unexplained macrocytosis ), or in patients who do not have a brisk or robust response to therapy.

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