Anticoagulation patients should routinely be assessed for drug interactions and warfarin and aspirin should be one of them. Many patients are on both aspiring and warfarin, but do they need to be?
It turns out that a third of patients on warfarin are on aspirin for no good reason. The problem is that patients on aspirin and warfarin have a higher risk of bleeding. Including, major bleeds and hospitalizations compared to those who are on warfarin alone.
A cohort study of adults enrolled at 6 anticoagulation clinics. They enrolled patients at 6 anticoagulation clinics in Michigan from January 2010-2017. And looked at individuals who were receiving warfarin therapy for Afib or for venous thromboembolism, DVT, and/or pulmonary embolus, without any documentation of a recent heart attack or valve replacement, people who don’t have an additional indication to be on aspirin.
They looked at greater than 6,500 patients with an average age of 66 years. It turns out that about a third of them had no clear therapeutic indication to being on aspirin addition to their warfarin. The outcomes when someone is enrolled in an anticoagulation clinic are usually better than the rest of the wide world out there.
At 1 year, patients receiving combination therapy with warfarin and aspirin compared to those who received warfarin alone had higher rates of overall bleeding, 26% vs 20%; higher rates of major bleeding, the warfarin vs aspirin group 5.7% vs 4.6% in the aspirin alone group; a higher rate of emergency department visits, 13% vs 9.8%; a higher rate of hospitalizations for bleeding, 8.1% vs 5.2%.
It’s about a 50% higher rate of hospitalization for bleeding but no improvement in the rate of thrombosis. The take-home point here is a real clear one. We need to look when patients are on warfarin. We need to make sure they’re not also on aspirin if there is no clear indication. Aspirin used to be recommended routinely for primary prevention of stroke and of heart attack. Unless someone has a clear and compelling indication for aspirin, when they’re on warfarin get them off the aspirin.
References: Tillman H, et al. Risk for Major Hemorrhages in Patients Receiving Clopidogrel and Aspirin Compared With Aspirin Alone After Transient Ischemic Attack or Minor Ischemic Stroke: A Secondary Analysis of the POINT Randomized Clinical Trial. JAMA Neurol. 2019 Apr 29 [Epub ahead of print]. doi:10.1001/jamaneurol.2019.0932
Patients who use metformin might experience reduced levels of Vitamin B12. Older patients in particularly can have a decrease in cognitive performance, according to study results published in The Journal of Endocrinology & Metabolism.
Long-term metformin use has been associated with B12 vitamin deficiency. The goal of the study was to investigate the effects of hyperglycemia and metformin use on folate-related B vitamin biomarkers and cognitive performance in older adults. Researchers assessed 4160 community-dwelling older people (average age, 74.1 years) for biomarkers of folate, vitamin B12, vitamin B6, and riboflavin.
Classified as normoglycemic (n = 1856) or hyperglycemic with (n = 318) or without (n = 1986) metformin treatment, each participant was assessed for cognitive ability according to the Repeatable Battery for Assessment of Neuropsychological Status and the Frontal Assessment Battery.
On average, patients with hyperglycemia were older, more overweight, and had worse renal function than patients who were normoglycemic. All groups demonstrated normal mean scores on all cognitive tests.
Compared with patients with normoglycemia and patients with hyperglycemia not treated with metformin, patients with hyperglycemia who received metformin treatment were at greater risk for deficiency in vitamin B12 (combined B12 index ≤-1; odds ratio, 1.45) and B6 levels (plasma pyridoxal 5-phosphate <30 nmol/L; odds ratio, 1.48).
After adjusting for various confounding factors, results from the Repeatable Battery for Assessment of Neuropsychological Status and Frontal Assessment Battery tests demonstrated that metformin use was associated with elevated risk for cognitive dysfunction (1.36 and 1.34, respectively).
Because of the cross-sectional nature of this study, the researchers noted an inability to confirm causal relationships between diabetes/metformin use and B-vitamin deficiency.
From the ADA 2019 guidelines, “A recent randomized trial confirmed previous observations that metformin use is associated with vitamin B12 deficiency and worsening of symptoms of neuropathy (43). This is compatible with a recent report from the Diabetes Prevention Program Outcomes Study (DPPOS) suggesting periodic testing of vitamin B12 (44)”. The recommendation is to test Vitamin B12 periodically, like once a year to make sure patients have not develop Vitamin B12 deficiencies.
Cardioembolism: due to blood stasis primarily in left atrial appendage
AF significantly increases risk of thromboembolic ischemic stroke 5
times compared to patients in sinus rhythm
4 times greater risk of
recurrent stroke
More severe disability
2 times higher mortality
Most serious common complication of AF is arterial thromboembolism, most notably an ischemic stroke. Due to formation of atrial thrombi from blood stasis.
Thromboembolism occurring with AF is associated with greater risk of recurrent stroke, more severe disability, and mortality. Embolization of atrial thrombi can occur with any form of AF. Embolic risk leads to chronic oral anticoagulation.
Oral
anticoagulants have been shown to lower the risk of clinical thromboembolism in
nearly all patients with AF, at all levels of risk and irrespective of its
classification
Estimation
of Thromboembolism
CHA2DS2 VASc
January CT, et al. J Am Coll
Cardiol. 2014;64:21
In
patients with nonvalvular AF, the CHA2DS2-VASc score is recommended for
assessment of stroke risk
To
assess stroke risk
0
= no antithrombotic therapy
1:
no treatment or ASA
Oral
anticoagulation recommended in score 2 or more
Other
Factor Xa inhibitors (edoxaban, betrixaban) not approved at time of guidelines
CHADS
0: ASA may prevent 2 nonfatal strokes per 1000 pt
1: asa + clopidogrel for those unsuitable for/choose not to take AC for reasons other than bleeding (difficult maintaining stable INR, lifestyle limitations regular monitoring, costs)
HAS-BLED
Pisters R, et al. Chest. 2010;138:5
Bleeding risk scores to quantify hemorrhage risk
Other bleeding risk scoring systems: RIETE, HEMORR2HAGES, ATRIA
Helpful in defining patient at elevated bleeding risk, but clinincal utilily is insufficient for use as evidence for recommendations in guideline
Low risk: 0
Moderate: 1-2
A score >/3 indicates potentially “high risk” for bleeding and may require closer observation of a patient for adverse risks, closer monitoring of INRs, or differential dose selections of oral anticoagulants or aspirin
HAS-BLED
> CHADS2 Score
HAS-BLED score ≥3 indicates “high risk” of bleeding
Caution and regular review needed following initiation of AC
Address correctable bleeding risk factors (eg. uncontrolled hypertension,
co-administration of NSAIDs or aspirin, etc).
If HAS-BLED score exceeds CHADS2 score, the risk of major bleeding
may outweigh potential benefit of AC
Use in the Euro Heart Survey on AF population could have prevented
12.1% (4/33) of major bleeds (Pisters R, et al. Chest. 2010;138:1093).
Requires validation in other cohorts of patients with AF
Not yet adopted by the ACC/AHA/HRS AF guidelines AC = oral anticoagulation
Camm
AJ, et al. Eur Heart J. 2010;31(19):2369-2429. Pisters R, et al. Chest. 2010;138:1093-1100.
Lip GY, et al. Am J Med.2010;123(6):484-488.
Why Is
AF Undertreated from an
Anticoagulation
Standpoint?
•Patient
intolerance or poor adherence
•Under-recognition
of AF itself
•Physician
treatment bias:
–Inclination
to correlate burden of AF with stroke risk
–Belief
that aspirin is an acceptable protective
alternative
to oral anticoagulants
–Medical
liability: 27% of patients decline OAC based
on
shared decision-making (i.e., fear of complications)
De Breucker S, et al.
Drugs
Aging.
2010;27(10):807-813. Why
Is AF Undertreated from an
Anticoagulation
Standpoint?
Percutaneous Left Atrial Appendage
Closure
(LAAC)
•Treatment strategy to
reduce the risk of LAA blood clots from entering the bloodstream and potentially
causing stroke in nonvalvular AF patients
•Randomized data only
available for WatchmanTM procedure –Only FDA-approved device
•AmuletTM is being
studied
•Lariat procedure is a
commercially available closure device –FDA approval only for “approximation of
soft tissue” but not LAA closure for stroke prevention Percutaneous Left Atrial
Appendage Closure (LAAC)
Watchman Procedure
Watchman Device
Patient Selection
•Appropriate patients:
–Increased
risk for stroke CHADS >1 or CHA2DS2-VASc
≥2
–Deemed
suitable for warfarin
–Have
appropriate rationale to seek nonpharmacologic
alternative
to warfarin
•Contraindicated:
–Do
not use if thrombus visualized on TEE imaging
–Prior
atrial septal defect (ASD) or patent foramen ovale
(PFO)
repair or closure device
–Contraindications
to use of warfarin, aspirin, or clopidogrel
Additional Considerations
•Risks
include bleeding, perforation, pericardial
effusion,
tamponade, stroke, and death
•Complication
rate of 2-3%
•A
shared medical consensus between 2 physicians
and
the patient is required to qualify for insurance
coverage
PASS Criteria
•Position
–Position
relative to the ostium of the left atrial
appendage
•Anchor
–Are
the fixation anchors engaged?
•Size
–Device
should be compressed 8-20% of original size
•Seal
–Device
should span entire ostium and all lobes should
be
covered
Watchman device placement
Postprocedure Anticoagulation Protocol
Key Points
•Oral
anticoagulation is the preferred therapy to
reduce
stroke risk in patients with AF…
•…but
overall compliance with warfarin and DOACs is
poor
(~50%), especially among those at highest risk
for
stroke
•LAAC
is a second-line therapy for stroke prevention
in
patients with AF and is reasonable alternative for
patients.
ineligible for long-term oral anticoagulation
Supraventricular—originate above bundle of His, char by abnormal P waves w/ normal QRS and QTc intervals
Uncoordinated atrial activation and ineffective atrial contraction
Irregularly, irregular pulse
Atrial Fibrillation (or A. Fib)
Most common cardiac arrhythmia
EKG: irregular R-R intervals, no distinct repeating p
waves, and irregular atrial activity
Worldwide: 33.5 million, ~3-6 million in US
Prevalence increases with age (>65), 3% of men and
2% of women
Contributes to >99,000 deaths per year
20% of patients who have a stroke associated with
AF
receive an AF diagnosis at the time of stroke or
shortly
thereafter
Annual Death Rates from AF (2015)
•AF
was the underlying cause of death in ~24,000
people
and listed on ~150,000 US death certificates
•In
adjusted analyses from the Framingham Heart
Study,
AF was associated with an increased risk of
death
in both males (OR, 1.5; 95% CI, 1.2-1.8) and
females
(OR, 1.9; 95% CI, 1.5-2.2)
–AF
diminishes the survival advantage typically
observed
in females
Classification
Paroxysmal (occasional)
Terminates spontaneously or with intervention within 7 days
Persistent
Continuous—sustained > 7 days
Longstanding persistent
Continuous— > 12 months in duration
Permanent
Acceptance of AF: Permanent: when patient and doctor make joint decision to stop further attempts to restore and/or maintain sinus rhythm
Represents a therapeutic attitude vs. an inherent pathophysiologic attribute of AF
Attitudes
and acceptance of AF may
change
as symptoms, efficacy of therapies,
and
patient/clinician preferences evolve
Nonvalvular
In absence of rheumatic mitral stenosis,
mechanical/bioprosthetic heart valve, or mitral valve repair
Important because it guides therapy
January CT, et al. J Am Coll Cardiol. 2014;64:21
Strokes in AF Lead to More Disability
Lin HJ, et al. Stroke
1996;27(10):1760-1764. Tu HT, et al. Cerebrovasc Dis. 2010;30(4):389-395.
Larger infarcts (52 vs.
15 ml, P=0.05)
Higher mortality (HR=
1.84)
More severe hemorrhagic
transformation (29% vs. 5%, P=0.002)
Risk Factors and Underlying
Comorbidities
to
Address in Chronic AF Management
Major risk factors
Older age
Obesity
(Borderline) hypertension
Other risk factors
•(Pre)
diabetes
•Heart
failure
•Prior
cardiothoracic
surgery
•Smoking
•Prior
stroke
•Obstructive
sleep apnea
•Drug
use Alcohol consumption
•Vascular
disease
•Hyperthyroidism
•Lipid
profile
•Coronary
artery disease
•Physical
inactivity
•Chronic
kidney disease
•COPD
•Valve
disease
•Inflammatory
diseases
Brandes A, et al. Arrhythm Electrophysiol Rev.2018;7(2):118-127.Steinhubl S, et al. JAMA. 2018;320(2):146-155.
Pathophysiology
AF occurs when structural and/or electrophysiological
abnormalities alter atrial tissue to promote abnormal impulse formation and/or
propagation.
Heart has Purkinje fibers (specialized cardiac
muscle fibers that rapidly transmit impulses from the atrioventricular
node to the ventricles)
Fibers are
split into 2 branches
Normal
Electrical
impulse (action potential) travels down both branches
Meet in the
connecting p/w and cancel each other out
Reentry
When there is a block in one of the branches, the AP only travels down one branch leads to No longer canceled out
Travels retrograde through the block and can then travel down the 1st branch again
leads to indefinite propagation leads to abnormal impulses in AF
These abnormalities are caused by diverse pathophysiological mechanisms
A.Fib Normal vs re-entry
AF begets AF
Atrial structural abnormal
Any
disturbance in atrial structure that increases susceptibility to AF
Most commonly
d/t extracardiac factors that increases left atrium pressure, cause atrial
dilation and alter wall stress
Structural abnormal
à alter impulse
conduction/refractoriness
Mechanisms of AF
Mechanism of A. Fib
Electrophysiological mech
Triggers of AF
Abnormal focal discharges initiate AF
Rapidly firing foci most commonly from left atrium
Conduction abnormal that promote reentry d/t
depolarized resting potentials that promote sodium channel inactivation
Abnormal intracellular calcium handling d/t diastolic
calcium leak from sarcoplasmic reticulum, which can trigger delayed after-depolarization
ANS
Activation of para and/or sympathetic NS can provoke
atrial arrhythmias
Sympathetic: activates beta-1 adrenergic R
Cardiac excitatory effects: increased conduction,
contraction, irritability of foci
Parasympathetic: activates cholinergic R
Cardiac inhibitory effects:
Pathophysiological mechanisms
Atrial tachycardia
remodeling: AF begets AF
Inflammation
and ox stress
Inflammationà increased concentration of C-reactive
protein (marker of inflammation, high-sensitivity C-rp assay can determine risk
for CAD)
RAAS
Angiotensin II, ACE and aldosterone are synthesized
locally in atrial myocardium and are increased during AF
Automaticity: ability of cardiac muscle to
spontaneously depolarize in a reg constant manner
Key Points
•AF
is common
•Prevalence
increases with age
•Proper
diagnosis and classification are key to properly
manage
arrhythmia and minimize stroke risk
Symptoms
Fluttering in the chest
Feeling faint, weakness, syncope
A.Fib increases your risk of thromboembolic stroke
Treatment
Rate Control
Control
ventricular rate with beta blockers or non-DHP calcium channel blockers and AV
nodal ablation
Long-term
management with cardioversion, antiarrhythmics, and radiofrequency catheter
ablation
Attempt made
to restore SR
Anticoagulation
Prevention
of thromboembolism
BB: block sympathetic tone (atenolol, metoprolol,
nadolol, propranolol, carvedilol)
CCB: direct AV nodal effects, block L-type Ca channels
(diltiazem, verapamil)
January CT, et al. J Am Coll Cardiol. 2014;64:21
What Is AF Ablation?
•Cardiac ablation:
Procedure using energy to create lesions (resulting in scarring) in the atria
with the goal of stopping abnormal electrical conduction
•Pulmonary vein (PV) isolation:
Electrical isolation of the PVs, which are well-known triggers for AF and are
the key lesion set for an AF ablation
•Cavo-tricuspid
isthmus ablation: Done in patients with concomitant atrial flutter
•Types of ablation:
–Catheter-based: Minimally invasive
–Surgical: Maze, minimally invasive, usually concomitant with
open-heart surgeries (e.g., CABG)
–Hybrid approach: Catheter-based + minimally invasive surgery
Calkins H, et al.
Heart Rhythm. 2017;14(10);e275-e444.
AADs
•Recurrence
rates
–Amiodarone: 35%
–Sotalol: 63%
–Propafenone: 63%
•Adverse
events
–Amiodarone:
18%
–Sotalol/propafenone:
11%
Singh BN, et
al. N Engl J Med.
2005;352:1861-1872.Pedersen OD, et al. Circulation. 2001;104:292-296.Freemantle
N, et al. Europace. 2011;13:329-345.Piccini JP, et al. J Am Coll Cardiol.
2009;54:1089-1095.The AFFIRM First Antiarrhythmic Drug Substudy Investigators.J
Am Coll Cardiol. 2003;42:20-29.Lafuente-Lafuente C, et al.Cochrane Database
Syst Rev. 2007;(4):CD005049.
Key
Points
•Rate
control is an option for patients with few
symptoms
and in whom maintaining SR will be risky,
challenging,
or unsuccessful
–Can
be achieved with medications or AV junction
ablation
and pacing
•Rhythm
control is an option for symptomatic patients,
or
those who develop a cardiomyopathy–Better
option for younger patients with less advanced
heart
disease
A recent article in the Lanceton the efficacy and safety of statin therapy in older adults. It was a meta-analysis of individual participant data from 28 randomized trials. The article brings into question the practice of using statins for primary prevention in older adults, those aged 70-75 years.
The authors remarkably analyzed individual participant data from 22 trials of over 130,000 individuals. They also included detailed summary data from one trial of over 12,000 individuals, as well as trials of statin therapy, high-dose vs low-dose, which was another 40,000 individuals. So, almost 200,000 individuals were enrolled in randomized, blinded control studies.
Approximately 8% of those individuals, over 14,000 people, were older than 75 years of age at the time of randomization. The median duration of follow-up was about 5 years.
Overall, statin therapy worked very well at reducing future major vascular events. There was also a 21% reduction in major vascular events for every 40 mg/dL decrease in LDL cholesterol.
However, the benefit was seen in people who had a history of vascular events. But, when looking at people older than 70-75 years of age, who had no history of previous vascular events, the authors noted the use of statin therapy showed no evidence of benefit on cardiac endpoints. In other words, statin therapy for primary prevention in those >70-75 years of age did not appear to be beneficial in this meta-analysis.
Take-away message
Well, greater than 30% of individuals over 70 years of age are currently on statins. This analysis suggests that we should really use a shared decision-making model when discussing the use of statin therapy in individuals >70-75 years of age who don’t have a history of previous vascular events.
For secondary prevention, statins work. Patients who have had an MI or a stroke, regardless of age, should be on a statin. But, for healthy patients without a history of vascular events, the pooled cohort equation and traditional thinking of “if someone has a >7.5% 10-year risk of cardiac disease, they should be on a statin,” does not necessarily apply to this older age group.
Is this a practice changer?
This meta-analysis clearly shows that statin therapy as primary prevention in individuals >70-75 years of age may not be beneficial, and we should use a shared decision-making model when considering the addition of statin.
This next generation insulin, resulted in a
more rapid appearance of insulin in the blood after injection and a better
coverage of the mealtime excursion in glucose that is associated with Type 1
Diabetes, resulting in fewer peaks and troughs in insulin levels 3–4 hours from
injection of the insulin at mealtime.
After the development of continuous glucose
monitoring (CGM) systems, we discovered that these fast-acting mealtime insulins
were still too slow and that peaks and troughs in glucose levels still occur
after meals. We discovered that these insulins should ideally be injected not
immediately before meals but 10–20 minutes before the meal.
However, this is not convenient for patients before
breakfast when trying to get ready and even before some of the other meals. Many
patients inject during their meal or even after the meal if there is
uncertainty about what patients will eat (for example children and elderly
patients). Hence Industry has been working on extra-fast insulins.
These have altered the excipients in which the
insulin aspart is solubilized. They have added L-arginine and vitamin B, two
natural agents that are approved by the European Medicines Agency and the US
Food and Drug Administration. These facilitate the rapid movement of insulin
through the capillaries into the blood. The pharmacokinetic profiles show 5-minute shift to the left. Fiasp is also 2.5-minute absorption into the blood stream. This will have a great
impact on the quality of life of our patients as it will allow them to inject
insulin at a time closer to the meal and will better cover glucose excursions.
Studies have compared injections of Fiasp immediately before a meal with insulin aspart and found that Fiasp gives smaller glucose excursions as well as a small but statistically significant difference (around 0.1%) in glycated hemoglobin (HbA1c) after 6 months and 1 year. We have also demonstrated that injection of Fiasp within 20 minutes after starting a meal gives the same effect as if it was injected before the meal. This is useful if people forget their injections or if it is not possible to predict what a patient will eat.
As more and more of my patients switch to e-cigarettes or vaping when trying to quit smoking. What do you tell patients about vaping? In 2016 the number of middle schoolers who reported they used electronic cigarettes was 63% and 11.3 of high schoolers used e-cigarette reported by CDC.
One of my diabetes patients came in reporting that he had
stopped smoking and had switched to vaping now. So is vaping better than
smoking cigarette? There are now about 500 different brands of e-cigarettes.
The academy of pediatrician reports that it is not vapor but is aerosol because
there is particulate matter.
Brief history
2003-2007 the first commercially produced e-cigarettes were
produced overseas in Asia and between 2006 and 2007 smokeless e-cigarettes were
introduced in the US.
Most of the data reported were done with the first and second
generations of e-cigarettes which did not have set amounts of nicotine. In the
US we are now using the fourth generation of e-cigarettes. New e-cigarettes
were more powerful, more liquid and are now more popular.
What is in the pods?
Ingredients can vary but most contain some toxicants and
carcinogens and the pods come in a range of nicotine. Traditional cigarettes
contain 10-30 mg of actual absorbable nicotine 0.05-3 mg. Compared to pods that
range from 0 to 36 mg/ml. Most of the e-cigarette pods contain:
propylene glycol
glycerol (sugar)-fruit flavoring
diacetyl- bronchiolitis obliterans (popcorn
lung)
aldehydes
metals
tobacco alkaloids, nitrosamines
hydrocarbons
flavors- over 7000 flavors
Toxicants and carcinogens are in less amount than in
cigarettes. This are easily accessible in stores and online. One popular vapor product:
sales up 641% over one year and had 515% increased in market share and went
from 2.2 to 16.2 million in revenue.
58.8% were current smokers who also use
e-cigarettes (dual users)
11.4% had never been regular smokers
In 2016 there were 3.2 % of US adults. In 2018 e-cigarettes
are the most common tobacco product used in US youth. 40% of current ENDS users
are age 18-24 years have never been cigarette smokers.
Teens who have used e-cigarettes are more likely than those
who have not used e-cigarettes to go on to smoke real cigarettes.
FDA declared Teen Vaping an epidemic and now bans tobacco
and e-cigarettes to people under age 18.
Does vaping help quit smoking regular cigarettes?
The FDA has not approved e-cigarettes the conclusion was
that they are not associated e-cigarettes as smoking cessation products because
in the studies done with 1st generation cigarettes were not
associated with successful cessation.
The CDC in 2018 stated is not safe for kids, adolescents,
pregnant women and any one who is not currently smoking. The American Cancer
Society stated that current generation of e-cigarettes are less harmful than
smoking tobacco, however long-term harms are unknown.
Known Risks
E-cigarettes can expose others to second hand smoke and
third hand aerosol pollutants. Residual aerosol that acts as dust on surfaces
that can be re-emitted.
Burns and injury- some have been known to explode
Toxicants and carcinogens
Risks to children of poisoning- children opening and
drinking pod contents
Addictive- could be as addictive as cigarettes.
What advice would you give your patient?
First congratulate patients for stop smoking cigarettes.
Then would advise patients to start to decrease amount of nicotine and amount
of use and try to stop using e-cigarettes.
Yf
Recently my doctor told me that I have a fatty liver. After going for an ultrasound to see if I have goldstones, my doctor told me I have a fatty liver and should reduce my fat intake and reduce my weight. What is a fatty liver and why we should worry about it?
Nonalcoholic fatty liver disease (NFLD) As the name implies, the main characteristic of nonalcoholic fatty liver disease is too much fat stored in liver cells.
Nonalcoholic fatty liver disease is common around the world, especially in Western nations. In the United States, it is the most common form of chronic liver disease, affecting an estimated 80 to 100 million people. Globally 1 in 4 people have NFLD and in the USA is not like 1 in 3.
Why should we worry about it?
Nonalcoholic steatohepatitis, a potentially serious form of the disease, is marked by liver inflammation, which may progress to scarring and irreversible damage. This damage is similar to the damage caused by heavy alcohol use. At its most severe, nonalcoholic steatohepatitis can progress to cirrhosis and liver failure.
In the USA, NFLD cost is a 32 million dollars, close second to Stroke spending which is a 34 million dollar disease. This cost come from both inpatient and outpatient treatment, emergency room visits, organ transplantation, procedures, medications and mortality.
Treatment
Treat the obesity, recommend weight loss. Weight loss along with increase exercise and healthy low fat diet.
In obese and morbidly obese patients would recommend weight loss medications if not able to loose weight. Can also consider gastric bypass or sleeve in patients who are morbidly obese or obese with at least one risk factor such as diabetes or hypertension.
Weight loss tips: which is better low fat or low calorie diet. While low fat diet maybe a better option either one when done correctly can lead to weight loss.
While exercise doesn’t lead to weight loss, it can increase metabolic rate and increase caloric deficiency. Being a couch potato will lead to increase risk of obesity and metabolic syndrome. Most metabolic syndrome patients will have a non-alcoholic fatty liver.
Adding fiber to the diet can help lead to weight loss. The pilot study in which patients did not change their usual diet and did not exercise. Patients had to consumed 35 gm of fiber per day and modified their protein to be lean and was limited to 0.8gm/kg/day. These patients lost an average of 4.4 lbs. in 12 weeks.
Another reason to love fiber:
In a recent Randomized Controlled Trial (RTC) study conducted in diabetes patients show that 10.5 gm of psyllium per day lead to:
Decrease in weight of 7 lbs. of the psyllium group vs the control group after 8 weeks.
A decrease in A1C from 8.5 to 7.5.
The good news is that with treatment a fatty liver can be reverse before you advance to cirrhosis.
Fatty Liver can also be the result of several conditions and diseases
Diabetes (Type 2) Being overweight or obese High cholesterol or triglycerides Metabolic syndrome Polycystic ovary syndrome Sleep apnea Underactive thyroid (hypothyroidism) Underactive pituitary gland (hypopituitarism)
Non-alcoholic Fatty Liver Disease is mostly associated with insulin resistance and there for is most common in patients with diabetes and obese patients.
Milk Thistle
Milk Thistle has been used in Europe to treat liver problems and hepatitis. Clinical trials have had mixed results, two rigorous studies found no benefit.
What foods to avoid:
Alcohol
sugar
soda
trans fats
starchy carbohydrates
Avoid OTC medications, foods with a lot of preservatives and chemicals.
Try to eat more non-starchy vegetables, fruits, whole grains, lean protein, and healthy fats. Keep in mind small portions are better than large meals.
Pancreatitis is inflammation of the pancreas. It happens when pancreatic enzyme secretions build up and begin to digest the organ itself. The pancreas is a long gland located behind the stomach. The Pancreas secretes digestive juices into the small intestine. The pancreas has two main functions: an exocrine function that helps in digestion and an endocrine function that regulates blood sugar.
Acute pancreatitis develops suddenly, most often as a result of gallstones or alcohol ingestion. Reaction to certain medications, trauma, and infectious causes can also lead to acute pancreatitis. Acute pancreatitis can be life-threatening, but most patients recover completely.
Chronic pancreatitis ongoing process in which the pancreas continues to sustain damage and lose function over time. The majority of cases of chronic pancreatitis result from alcohol abuse, but some cases are hereditary or due to diseases such as cystic fibrosis.
Symptoms of Acute Pancreatitis
• Severe, steady pain in the upper-middle part of the abdomen, often radiating into the back
• Jaundice
• Low-grade fever
• Nausea or vomiting
• Lowered blood pressure
• Clammy skin
• Unusual abdominal hardness or mass that can be felt
• Abdominal bloating and tenderness
Symptoms of Chronic Pancreatitis
Symptoms may develop over a period of time. It can develop acute episodes. In chronic pancreatitis, there is a decrease in the secretion of enzymes needed for digestion and absorption of dietary fats. Fat digestion is impaired, resulting in fatty stools. Recurrent abdominal pain may be accompanied by nausea and weight loss.
Symptoms of chronic pancreatitis include:
• Abdominal and/or back pain
• Weight loss
• Nausea and vomiting
• The onset of diabetes mellitus
• Pale colored, oily stools
Treatment
Treatment for acute pancreatitis may include nutritional support with feeding tubes or intravenous (IV) nutrition, antibiotics, and pain medications. Treatment for chronic pancreatitis may involve IV fluids; pain medication; a low-fat, nutritious diet; and enzyme supplements. Surgery may be necessary for both acute or chronic pancreatitis.
Enzyme Supplementation:
Enzyme supplements begin predigesting food while it is in the stomach. This helps reduce the stimulation of the pancreas caused by food intake. If a patient has a digestive enzyme deficiency, enzyme supplements help food to be better absorbed, which improves nutritional intake. Avoiding the stimulation of the pancreas also helps to reduce pain associated with pancreatitis.
Pain Management:
Many patients take a regimen of more than one kind of medication. Oral medications include narcotics such as Percocet and oxycodone, and these may be used in conjunction with non-narcotic medicines such as muscle relaxants and antidepressants.
Surgery:
Depending on the cause of pancreatitis, the patient’s anatomy, level of pain, and other factors, surgery may be an appropriate treatment.
If gallstones are the cause of pancreatitis, surgery to remove the gallstones and possibly the gallbladder may be required.
References
1. “Pancreatitis”. Mayo Clinic. Mayo Foundation for Medical Education and Research (MFMER). 2018. Retried on 12 Jun 2018 from 7 https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227
2. “Pancreas”. The American Heritage Dictionary of “The English Language, 5th Edition”. Houghton Mifflin Harcourt Publishing Company. 2016. Retrieved on 7 Jun 2018 from http://www.yourdictionary.com/pancreas
3. http://columbiasurgery.org/pancreas/symptoms-pancreatitis
Weather is to lose weight, to adhere to a healthy diet or even to take their medications every day. It often seems like most of my patients make little progress in controlling their diabetes or high blood pressure. Thinking I was doing a good job by reviewing the complications of diabetes and high blood pressure, IT MIGHT HAVE BEEN DOING THE OPPOSITE. We are told to educate patients regarding complications which often results in scaring patients. We are told that by scaring patients, will lead patients to make the right decisions. But the sad reality is that it doesn’t work. Why was I not able to motivate patients into making better decisions based on what could happened in the future? Why is it so hard to motivate patients?
If you try to stop yourself from snacking, we will tell our self you will be fat. If some one is smoking you will tell them, you will die of cancer. We have a deep-rooted belief that by scaring ourselves or others we will do the right thing. Except that science shows that warnings have limited impact on behavior. Graphic images on cigarette packets, do not deter people from smoking. (Ruite & Kok, 2005; Taubman Ben-Ari, Florian & mikulincer, 1999’ Trenholm et al, 2007; Ennett et al, 10994)
Warning and treats work but have a very limited impact in motivating people into action.
When animals get scared, they have two reactions, freezing or fleeing. Human beings are animals and have the same responses to fear or being scared. When something is scary, we try to eliminate what is scaring us using rationalization. We could tell ourselves, I had my blood sugars high for a while now and nothing has happened. The process makes you feel stronger than before and makes it harder to do the right thing.
Many of us will act like the Ostridge and place our head on the ground. We ignore what is front of us, people avoid negative information because it makes us feel bad. People will start facing reality when is too late, when we have bad outcomes or complications that can not be ignored. People will avoid worrying about something that might or might not happen in the future now, they choose to worry about it when it does happen.
Studies show that people prefer to go along with the better or positive outcome. People listen to the positive information. Ability to learn from positive information remains the same throughout life, where learning from bad news is less in the young and elder but better with those right before midlife.
How can we use this information to motivate ourselves and others?
Using positive information uses three principles that drive peoples’ decision and behavior. The first is:
*Social incentives (response to opinion of others that lead to change, Edelson, Sharot, Dolan & Dudai, 2011=science). We are social people, we want to know what others are doing and we want to do it better.
*Immediate reward Values rewards you can get now more than rewards you can get in the future. Choose something tangible now rather than something is insure in the future. Can you reward people now for actions that are good for them in the future? Actions become associated with the rewards, leading to the desire outcomes.
*Progress monitoring highlight progress not the decline.
Do we need to stop communicating risks? No but we might want to re-think how to approach motivating ourselves and others. Because fear of loosing your health will lead to inaction or freezing. While positive information will lead to action.
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