A clinic in London, https://www.hah.co.uk/our-services/supported-hospital-discharge/ has this team goal for recovery plan:
Health stat in California
A writer wrote that public health costs have soared as one-third of California residents admitted to state hospitals for any causes suffer from diabetes, a sometimes-lethal disease often pre…
Source: Health stat in California
Health stat in California
A writer wrote that public health costs have soared as one-third of California residents admitted to state hospitals for any causes suffer from diabetes, a sometimes-lethal disease often predicated on poor diet, lack of exercise and excessive weight.
Connie’s Comments:
We can reallocate health resources better, build more roads and bridges, cut high housing costs, spend more on education, vocational skills schools, pattern technical degrees to current skill set needed by tech industries and have a universal health care with wellness promotion (insurance premiums goes toward incentives for those who exercise and good food choices).
——-
Viral Hepatitis
| Introduction |
| · Viral hepatitis is caused by viruses that cause inflammation to the liver Spectrum of clinical manifestations · Asymptomatic/ subclinical infection = serologic evidence · Acute hepatitis: symptoms are common to all viruses · Carrier state = asymptomatic individual but harbouring replicating virus · Chronic hepatitis → liver cirrhosis Systemic viral infections · Infectious mononucleosis (EBV) · CMV · Yellow fever · Dengue fever · Rubella · Haantan virus Immunological responses · Normal → acute hepatitis · Less adequate → chronic hepatitis · Inadequate → asymptomatic · Hyper → fulminant hepatitis |
| Acute hepatitis |
| 4 phases 1. Incubation period · Peak infectivity = last asymptomatic days of incubation period to early days of acute symptoms 2. Symptomatic pre-icteral phase · Usually precedes development of jaundice by a few days to 2 weeks · Non-specific prodromal illness : headache, myalgia, arthralgia, nausea and anorexia · Vomitting, diarrhea, RHC pain · May have dark urine and pale stools · May have physical signs: i. Liver is often tender but only minimally enlarged ii. Occasionally, mild splenomegaly and cervical lymphadenopathy (more frequent in children or EBV infx) 3. Symptomatic icteric phase · Mainly conjugated hyperbilirubinaemia · Common in actue HAV infection; absent in 50% of acute HBV infection; uncommon in acute HCV · Jaundice may be mild and the diagnosis may be suspected only after finding abnormal liver blood tests in the setting of non-specific symptoms. Symptoms rarely last longer than 3-6 weeks 4. Convalescence |
| Chronic hepatitis |
| · Symptomatic, biochemical or serological evidence of continuing hepatic disease > 6months with histological evidence of inflammation and necrosis Aetiology o Infective = viral hepatitis (HBV, HCV) o Drugs = chronic alcoholism, isonazid, methotrexate, methyldopa, nitrofurantoin o Autoimmune = autoimmune hepatitis (may be associate with primary biliary cirrhosis and primary sclerosing cholangitis) o Metabolic = Wilson’s disease, haemochromatosis, α1 –antitrypsin deficiency Clinical course unpredictable o Spontaneous remission o Indolent disease without progression o Rapidly progressive disease → cirrhosis Causes of death o Liver cirrhosis o Liver failure o Haematemesis o Hepatocellular carcinoma |
| Hepatitis A virus |
| · Epidemiology= usually found in developing world → substandard hygiene & sanitation; prevelance of seropositivity increases with age · Caused by picornavirus (ssRNA), 1 serotpe · Mode of transmission= o faecal oral route o food & water borne (e.g. eating partially cooked cockles & oysters/ contaminated food & water) o person-person (e.g. sexual oral-anal) · Incubation period = 4-6 weeks o HAV appears in faeces before clinical symptoms (usually 2-3 weeks before jaundice & 1 week after onset of jaundice) · Clinical presentation o Asymptomatic (most) = subclinical & milder than HBV infection o Acute hepatitis= usually bengn and self limiting o Worse if superimposed on chronic hepatitis o Does not cause chronic hepatitis or carrier state · Complications: Fulminant hepatitis (rare) · Serological picture: o Transient viraemia → blood borne transmission rare o IgM with acute infection → fecal shedding ends as IgM increases o IgG for long term immunity Prevention · Avoid eating contaminated food or drinks · Boiling 5 mins · Immunization o Passive immunization with Ig G § IgG collected from blood of persons who have been exposed to the hepatitis A § This method of immunization is getting obsolete because of the short supply of immune globulin and the potential risk of transmission of other infection through blood products o HAV vaccine § Inactivated virus § Given in 2 doses, with the second dose being given 6 – 12 months later. Immunity after vaccine lasts for 10 – 20 years. Protection against hepatitis A begins 4 weeks after vaccination People at risk of HAV · Persons travelling to or working in countries that have high or intermediate rates of hepatitis A · Persons who work with hepatitis A virus infected primates or with hepatitis A virus in a research laboratory should be vaccinated. · Persons with chronic liver disease eg. chronic hepatitis B carriers as these patients have been reported to have a higher mortality. |
| Hepatitis B virus |
| · Epidemiology: endemic in Africa and Asia; Microbiology · Belongs to the Hepadnavirus family · Has 3 well characterized antigens: o HBsAg (surface) → stimulates anti-HBs o HBcAg (core) → stimulates anti-HBc o HBeAg (core associated) → stimulates anti-HBe · Dane particle = infectious spherical HBsAg particle containing HBcAg core · HBeAg arises from the same gene as HBcAg o c gene has 2 initiation codons= precore and core region o translation intitated at precore region = HBeAg → signal peptide that facilitates secretion (can be used as surrogate marker for presence of HBcAG) o translation initiated at core region = HBcAg → no signal peptide →not secreted into serum · Nucleocapsid o circular partially ds DNA o DNA polymerase with reverse transcriptase activity o HBcAg → remains in hepatocytes for complete assembly of virions, only detected in liver biopsy samples · Incubation period = 3-4months · Pathogenesis o Cell-mediated mechanisms = destruction of hepatocytes with viral/ modified surface antigens o Humoral-mediated mechanisms = GN/ vasculitis from circulating immune complex · Mode of transmission o Vertical transmission o Sexual transmission o Parententral transmission: blood transfusion, organ transplant, needle-stick injury, IV drug abuser · Clinical presentation: o Asymptomatic disease (90%) o Acute hepatitis § Fulminant hepatitis rare o Carrier status (10-15%) o Chronic hepatitis (5%) o Liver cirrhosis (3%) o HCC (1%) |
| Serology 1) Acute infection with recovery · HBsAg= appears before onset of symptoms, peaks and declines rapidly, undetectable at 3-6months · HBeAg= appears just after HbsAg, indicates active replication (infectiousness) i. anti-HBe appears after disappearance of HBeAg (indicates waning infection) · anti-HBc= IgM appears just prior to the onset of infection (indicates acute infection); replaced by IgG i. does not protect against re-infection ii. serves as a surrogate marker for natural HBV infection· anti-HBs IgG= appears after acute disease is over 2) Acute infection with progression to chronic disease · Carrier state = presence of HBsAg > 6 months · Chronic replication of HBV virions = persistent HBsAg, ±HBeAg and HBV DNA · Chronic sequel: cirrhosis & HCC · High risk of becoming a carrier: i. Age at time of infection · Perinatal: 85-95% · Infants: 40-50% · Children: 30-40% · Adults: 5-10% ii. Sex – male: female 3:1 iii. Ethnicity – Chinese> Malays> Indians; related to prevalence of female carriers and periantal infx iv. Impaired immune responses – transplants, drugs Markers of past infectivity · Anti-HBs IgG · Anti-HBc IgG · Anti- HBe HBV mutants · Pre-core mutant: variant C gene fails to produce HBeAg (–ve HBeAg viraemia); still infections because of HBcAG o HBV DNA necessary to detect presence of disease activity · S mutants: mutation at ‘a’ epitope (HBsAg –ve viraemia) → vaccine not effective; low frequency in Singapore Treatment · Anti-virals: lamivudine, adefovir · Interferon-α · Vaccination |
| Hepatitis C virus |
| · · Caused by Flavivirus, ssRNA · Transmission: blood-borne, sexual intercourse · Incubation period: 6-12 weeks · Clinical presentation Mainly asymptomatic Acute hepatitis = general milder than HBV; no effective immunity
· Chronic hepatitis = hallmark of HCV infection 60-80% develop chronic hepatitis 20% go on to develop liver cirrhosis Acute infection with recovery · HCV RNA detectable for 1-3 weeks during active infection, · HCV RNA frequently persists despite neutralizing antibodies (Abs present in 50-70% of acute infection; 30-50% have anti-HCV Abs after 3-6 weeks) Chronic Infection · Persistence of HCV RNA despite neutralising Ab · Episodic elevations of HCV RNA and transminases Treatment · Ribavirin and IFNα combination therapy → partial efficacy · No vaccine available; difficult to cover agains the 6 major genotypes |
| Hepatitis D virus |
| · Defective ssRNA virus → requires HBsAg coat to infect cells · HBV serves as helper virus Clinical presentation 1. Super infection: chronic HBV carrier exposed to HDV → severe hepatitis 2. Co-infection: exposed to HBV & HDV at the same time a. HBV must become established first to provide HBsAg required for HDV virion production b. Chronic hepatitis rare c. Higher rates of fulminant hepatitis (3-4%) Serology · HDV RNA appears just before and during early acute symptomatic infection · IgM anti-HDV = recent HDV exposure · To differentiate co-infectin and super infection = correlate with HBV markers |
| Hepatitis E virus |
| · Calicivirus, ssRNA · 4 genotypes, endemic in India and the Middle East · Transmission: faecal-oral, water borne · Incubation period= 4-6 weeks Clinical presentation · Acute hepatitis o Usually self-limiting and benign o Abs are non-protective · No chronic state or chronic hepatitis · High rate of fulminant hepatitis in pregnant women (25% fatal); foetal mortality also high · No vaccines Serology · HEV RNA and HEV virions present in stool and liver before onset of symptoms · IgM anti-HEV present with rising transaminase → IgG |
| Hepatitis Screen |
| · HAV= o Anti- HAV IgM (acute) o Anti- HAV IgG (previous infection) · HBV= o HBsAG, HBeAG, anti-HBc, IgM (acute) o Anti-HBs IgG, anti-HBe, anti-HBc IgG (previous infection) · HCV= o Anti-HCV IgM (acute) o Anti-HCV IgG (previous infection) · CMV = anti-CMV IgM · EBV = anti EBV IgM · HSV = anti-HSV IgM, HSV PCR (if patient presents with acute liver failure) |
| HAV | HBV | HCV | HDV | HEV | HGV | |
| Agent | Icosohedral capsid, ssRNA Picornavirus | Enveloped dsDNA Hepadnavirus | Enveloped ssRNA Flavivirus | Enveloped ssRNA | Unenveloped ssRNA Calicivirus | ssRNA Flavivirus |
| Transmission | Faecal-oral | Parenteral, close contact, vertical | Parenteral, close contact | Parenteral, close contact | Waterborne | Parenteral |
| Incubation period | 2 – 6 weeks | 4 – 26 weeks | 2 – 26 weeks | 4 – 7 weeks (superinfection) | 2 – 8 weeks | Unknown |
| Carrier state | None | 0.1 – 1% of blood donors; 90 – 95% of those infected at birth (vertical transmission); 1 – 10% infected as adults (esp. If immune-compromised) | 0.2 – 1% of blood donors; <1% are healthy carriers | 1 – 10% of drug addicts, haemophiliacs | Unknown / none | 1 – 2% of blood donors |
| Chronic hepatitis | None | 5 – 10% of acute infections (adults); 90% in infected neonates | >60%; half then progress to cirrhosis | <5% if co-infection with HBV; 80% upon super infection with HBV | None | None |
| Fulminant hepatitis | 0.1 – 0.4% | <1% | Rare | 3 – 4% in co-infection | 0.3 – 3% 20% in pregnant females | Unknown |
| Hepatocellular Ca | No | Yes + (but most common cause in Singapore due to high prevalence from vertical transmission) | Yes ++(but less common in Singapore due to lower prevalence) | No increase above HBV | Unknown, but unlikely | Probably not |
| Vaccine available | Yes | Yes | No | No | No | No |
| Others | Acute hepatitis (symptomatic, asymptomatic) | Fulminant hepatitis almost never occurs with HCV | At present, not considered pathogenic |
How can I bring out the best from a baby boy?
How can I bring out the best from a baby boy? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Healthy food, massage, breastmilk, empowering parenting (not saying NO all the time, encouraging, forgiving,loving), opportunities of learning, of exercise and play and love from both parents.
Is there any legitimate treatments for cancer when radiation/chemo fails?
Is there any legitimate treatments for cancer when radiation/chemo fails? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Immunotherapy
Is there any legitimate treatments for cancer when radiation/chemo fails?
What are ways to shorten your period?
What are ways to shorten your period? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Heavy bleeding in my 40s made me seek an herbalist. I use the herbs on the third day from http://www.getwellinternational and I have a discount , email motherhealth@gmail.com
Is belly dancing beneficial for a woman’s health? Is it bad for women’s health? How?
Is belly dancing beneficial for a woman's health? Is it bad for women's health? How? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
All music and dancing are beneficial for all especially for women. The happiness hormones, oxytocin and dopamine (neurotransmitter) are increased. Pelvic exercises are important as we age to control urination. Music can reduce symptoms of Parkinson's and Alzheimer (tango, waltz, mozart). The calming rhythms of music calms the multi-tasking mind of women.
Is belly dancing beneficial for a woman's health? Is it bad for women's health? How?
How can I get rid of oestrogen dominance?
How can I get rid of oestrogen dominance? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Increase progesterone, take B vitamins and E. Sleep more with calcium and magnesium. Get a massage and have a nature walk. Surround yourself with less toxic environment.
I took an herbal supplement from getwellinternational. I have a discount, email motherhealth@gmail.com
How can I tell if I have a male yeast infection?
How can I tell if I have a male yeast infection? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
A white discharge. Wash with diluted vinegar and eat pickled veggies, avoid sugar and cheese, take acidophilus, wash with guava leaves or comfrey leaves, gargle with diluted hydrogen peroxide and up Vitamin C rich food or supplement.
How does one alleviate period cramps?
How does one alleviate period cramps? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Magnesium and Vitamin C before the menstruation starts.
In which areas of the world can the largest variety of crops be produced?
In which areas of the world can the largest variety of crops be produced? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
In the dessert areas of Israel and Egypt , they use drip irrigation (night time, few drops at a time) to water the plants. In small pots in California, tomatoes are growing. In Taiwan, rice and veggie production are up as they hired Filipino rice scientists. In Switzerland, they do crop rotation. In the Philippines, families leave their farms to work overseas to earn dollars that they can send back home.
In which areas of the world can the largest variety of crops be produced?
In which areas of the world can the largest variety of crops be produced?
In which areas of the world can the largest variety of crops be produced? by Samuel Lickiss
Answer by Samuel Lickiss:
This is quite an interesting question, but I think we need to introduce some constraints first.
With modern technology you can grow any crops anywhere, just not naturally. For example, a surprising amount of tropical fruit is grown in Iceland, of all countries! Have a watch of this video (in Icelandic, but there’s lots of photographs and annoying music):
https://www.youtube.com/watch?v=bIlzzXFD140
Iceland has the advantage of plentiful cheap energy to heat the greenhouses and provide extra lighting in the dark winter months, but you could do this anywhere.
So I think we should limit ourselves to looking at areas of the world where the greatest variety of crops can be grown naturally, i.e. out in the open air with minimal usage of modern technology.
However, it isn’t that easy. Crops are increasingly selectively bred (and genetically modified). This means new strains of crops can increase the range in which they can be grown. Rice makes an interesting example. Rice likes wet weather, but it can’t tolerate being submerged for long periods of time. They’ve already developed flood-resistant rice, useful in countries like China and India where rapid urbanisation, deforestation and construction of hydroelectric schemes increases flood risk and magnitude. More recently, a lot of work has been going into drought-resistant rice. See this article from the Financial Times for more information: Asia races to find drought-resistant rice – FT.com
The vast majority of crops that we eat today have been selectively bred in some way. New strains and varieties are being developed constantly, and there are practically infinite examples of this.
The point in all this is to say that more and more types of crop can be grown in more and more places.
My answer, therefore, is probably quite boring. We can quickly eliminate extreme climates, such as those of Antarctica, the Himalaya and the Sahara Desert. On balance, the areas of the world that have the best range of climactic conditions are the world’s temperate regions.
They have plentiful rainfall, warm (not hot) summers and cool (not cold) winters. They do not tend to experience any kind of extreme events, like forest fires, hurricanes and severe floods.
Much of Europe falls into this category, as do parts of the USA, Brazil, Argentina, China, Japan, India, South Africa, Australia and New Zealand. Basically anywhere coloured in light green on this map:
I live in the UK. Outside of my house I have an olive tree. Olives are usually grown in the Middle East and Mediterranean, where of course it is a lot warmer than the UK. My tree still manages to provide yields every year (though admittedly not very consistent ones), despite receiving frost in the winter and abundant rainfall.
I also grow tomatoes outside (i.e. not in a greenhouse). They grow better in a greenhouse, but I still manage to grow plenty of fresh tomatoes. I’ve grown chillies before as well.
You can even grow citrus fruits outside in the UK with some modern varieties. Here’s a guide someone wrote on growing these fruits in the UK: Growing Citrus Fruits | Lemons | Limes | Oranges | How To Grow | Grow Your Own
All these crops grow best in much warmer conditions, but they do manage in the cooler temperate regions.
I also grow cold-loving vegetables in my garden like carrots, leeks and parsnips. I’ve also grow plums and, right now, my raspberry bush is producing lots of delicious raspberries. Many of these crops would not survive in much warmer climates.
As I’ve already said, the tolerance ranges of different crops are increasing year on year. Technology increases these ranges even further.
In which areas of the world can the largest variety of crops be produced?
If medicine conquered cancer and heart disease, what would be the average human life expectancy?
If medicine conquered cancer and heart disease, what would be the average human life expect… by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
122 yrs of age based on latest data of older women from around the world who reached this age. Medicine conquered bacteria (with antibiotics). Cancer and heart disease are disease of the modern world.
If medicine conquered cancer and heart disease, what would be the average human life expectancy?