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The primary and most effective treatment for celiac disease is maintaining a strict gluten-free diet. Gluten is found in wheat, barley, rye, and their derivatives, so foods and products containing these ingredients must be avoided. Here are some key aspects of the nutrition plan for treating celiac disease:

1. Naturally Gluten-Free Foods: Focus on naturally gluten-free foods that are safe to consume. These include:

- Fruits and vegetables

- Meat and poultry (unprocessed)

- Fish and seafood

- Legumes (lentils, beans)

- Nuts and seeds (unseasoned)

- Dairy products (if you tolerate lactose; some individuals with celiac disease may also have lactose intolerance)

- Grains such as rice, corn, quinoa, and gluten-free oats (ensure they are certified gluten-free)

- Gluten-free flours like rice flour, almond flour, or coconut flour

2. Gluten-Free Grains and Starches: Examples include rice, corn, quinoa, millet, and gluten-free oats.

3. Gluten-Free Products: Gluten-free alternatives available in stores, including gluten-free bread, pasta, cereals, and baking mixes. Read labels carefully and look for gluten-free labels or certifications

4. Dining Out: When dining out, communicate your dietary needs to the restaurant staff, and choose restaurants that offer gluten-free options. Be cautious about cross-contamination in restaurant kitchens.

5. Nutrient Monitoring: Celiac disease can sometimes lead to nutrient deficiencies due to malabsorption in the damaged small intestine. Work with a healthcare professional to monitor and address any nutrient deficiencies, such as iron, calcium, vitamin D, and vitamin B12.

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Definition:
Also called celiac sprue or gluten-sensitive enteropathy. An immune reaction to eating gluten, a protein found in wheat, barley and rye. If you have celiac disease, eating gluten triggers an immune response in your small intestine. Over time, this reaction damages your small intestine's lining and prevents it from absorbing some nutrients (malabsorption). The intestinal damage often causes diarrhea, fatigue, weight loss, bloating and anemia, and can lead to serious complications.

Diagnosis:
blood tests:

Serology testing looks for antibodies in your blood. Elevated levels of certain antibody proteins indicate an immune reaction to gluten.

Genetic testing for human leukocyte antigens (HLA-DQ2 and HLA-DQ8) can be used to rule out celiac disease.

Endoscopy. This test uses a long tube with a tiny camera that's put into your mouth and passed down your throat (upper endoscopy). The camera enables your doctor to view your small intestine and take a small tissue sample (biopsy) to analyze for damage to the villi.

Capsule endoscopy. This test uses a tiny wireless camera to take pictures of your entire small intestine. The camera sits inside a vitamin-sized capsule, which you swallow. As the capsule travels through your digestive tract, the camera takes thousands of pictures that are transmitted to a recorder.

Symptoms:

Diarrhea

Fatigue

Weight loss

Bloating and gas

Abdominal pain

Nausea and vomiting

Constipation

Anemia, usually from iron deficiency

Loss of bone density (osteoporosis) or softening of bone (osteomalacia)

Itchy, blistery skin rash (dermatitis herpetiformis)

Mouth ulcers

Headaches and fatigue

Nervous system injury, including numbness and tingling in the feet and hands, possible problems with balance, and cognitive impairment

Joint pain

Reduced functioning of the spleen (hyposplenism)

Treatment:

A strict, lifelong gluten-free diet is the only way to manage celiac disease.
Vitamin and mineral supplements

If your anemia or nutritional deficiencies are severe, your doctor or dietitian might recommend that you take supplements.

Follow-up care
Medical follow-up at regular intervals can ensure that your symptoms have responded to a gluten-free diet. Your doctor will monitor your response with blood tests.

Medications to control intestinal inflammation

Celiac disease - Symptoms and causes - Mayo Clinic

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Risk Factors: Obesity, Hypertension, Hyperlipidemia, Metabolic syndrome, Diabetes mellitus, Chronic kidney disease, Dietary factors    Alcohol, Medications altering urate balance

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Risk Factors: Obesity, Hypertension, Hyperlipidemia, Metabolic syndrome, Diabetes mellitus, Chronic kidney disease, Dietary factors    Alcohol, Medications altering urate balance

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Florig

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Classification: It is classified into three types (overproduction, underexcretion and mixed types).

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Classification: It is classified into three types (overproduction, underexcretion and mixed types).

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Florig

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Symptoms: The two most common complaints associated with hyperuricemia are gout and uric acid nephrolithiasis. With gout, a patient will complain of a red hot, swollen joint, most commonly in the big toe. With nephrolithiasis, patients will complain of flank pain, hematuria, nausea/vomiting, and colicky pain (National library of medicine).

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Symptoms: The two most common complaints associated with hyperuricemia are gout and uric acid nephrolithiasis. With gout, a patient will complain of a red hot, swollen joint, most commonly in the big toe. With nephrolithiasis, patients will complain of flank pain, hematuria, nausea/vomiting, and colicky pain (National library of medicine).

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Florig

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Diagnosis: There will be no specific physical exam finding that will indicate hyperuricemia unless the patient is presenting with complaints of gout or nephrolithiasis (National library of medicine).

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Diagnosis: There will be no specific physical exam finding that will indicate hyperuricemia unless the patient is presenting with complaints of gout or nephrolithiasis (National library of medicine).

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Florig

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Definition: Hyperuricemia has been defined as serum uric acid (SUA) >6.0 mg/dL in women; >7.0 mg/dL in men; >5.5 mg/dL in children and adolescents [1], and is an independent risk factor of a strong non-linear concentration-dependent to the incident of gout (National library of medicine). 

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Definition: Hyperuricemia has been defined as serum uric acid (SUA) >6.0 mg/dL in women; >7.0 mg/dL in men; >5.5 mg/dL in children and adolescents [1], and is an independent risk factor of a strong non-linear concentration-dependent to the incident of gout (National library of medicine). 

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Florig

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Food high in fructose: Fruit in general, Juices, Jam, Dried and canned fruit, Soft Drinks with fructose-glucose-syrup, honey, Ice cream, cereal, cereal bars, fruit yoghurt

Improvement: Simultaneous intake of fat, protein and fibres as well as glucose and dextrose

Worsening: High amounts of starch or sugar and the simultaneous intake of liquids shorten the time food stays in the stomach. This makes it easier for complaints to arise. Certain sugar alcohols can block the absoprtion of fructose in the small intestine (e.g. sorbitol (E 420)).

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General:
- General renunciation of milk and dairy products usually not necessary -> because residual activity of the lactose-splitting enzyme is usually present: how much lactose is tolerated must be determined individually
- Milk and dairy products as part of a meal together with other foods is usually more tolerable
- Some research also suggests that people can become accustomed to lactose if they slowly and carefully increase their intake of lactose-containing products -> not verified yet

Possible nutrition:
- Lactose-free milk and dairy products
- selected types of cheese, e.g. hard and semi-hard cheeses such as Gouda, Edam and Tilsiter
- Acidified milk products, such as yogurt, kefir and sour milk, are also often well tolerated

Possibilities to be able to eat products containing lactose:
- Enzyme preparations containing lactase can be taken in consultation with the doctor or a nutritionist

source:
https://www.dge.de/presse/meldungen/2011-2018/essen-und-trinken-bei-lactoseintoleranz/
https://www.gesundheitsinformation.de/ernaehrung-bei-laktoseintoleranz.html

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(dge) Kakao, Milchkaffee oder Joghurt - kommt es bei Ihnen nach dem Verzehr dieser Lebensmittel auch zu Durchfall, Blähungen oder krampfartigen Bauchschmerzen? Nicht alle Menschen können Milch und Milchprodukte uneingeschränkt genießen: Etwa 15-20 % der Deutschen leiden an einer Lactoseintoleranz, einer Unverträglichkeit gegenüber Lactose (Milchzucker). Lactose ist natürlicherweise in Milch und Milchprodukten wie Quark, Sahne, Käse und Molke enthalten. Damit der Körper den Milchzucker verdauen kann, muss er mithilfe des Enzyms Lactase im Dünndarm in die Einzelbausteine Glucose oder Galactose zerlegt werden. Fehlt dieses Enzym oder ist seine Aktivität vermindert, gelangt die Lactose unverändert in den Dickdarm, wo Darmbakterien sie zu Milchsäure, Essigsäure und Kohlendioxid abbauen. Mögliche Folgen sind Durchfall, Blähungen, Magenkrämpfe, heftige Bauchschmerzen sowie Völlegefühl. Nicht immer muss allerdings ein Verzicht auf Milch und Milchprodukte, die wichtige Calciumlieferanten darstellen, die Konsequenz sein. Denn meist ist eine Restaktivität des Lactose spaltenden Enzyms vorhanden. Wie viel Lactose vertragen wird, muss individuell ermittelt werden.

Eine neue Infothek der Deutschen Gesellschaft für Ernährung (DGE) e. V. zeigt, wie eine Ernährungsumstellung die Beschwerden bei Lactoseintoleranz schnell und langfristig reduzieren kann: So sind beispielsweise Milch und Milchprodukte als Bestandteil einer Mahlzeit zusammen mit anderen Lebensmitteln meist verträglicher. Erlaubt sind bei Lactoseintoleranz auch lactosefreie Milch und Milchprodukte sowie ausgewählte Käsesorten, z. B. Hart- und Schnittkäse wie Gouda, Edamer und Tilsiter. Sauermilchprodukte wie Joghurt, Kefir und Sauermilch sind ebenfalls oft gut verträglich. Lactasehaltige Enzympräparate können in Absprache mit dem Arzt oder einer Ernährungsfachkraft bei einer Einladung zum Essen hilfreich sein.

Hintergrundinformation

Bei der Lactoseintoleranz werden verschiedene Formen unterschieden: der primäre Lactasemangel (Hypolactäsie), der genetisch bedingt ist, tritt am häufigsten auf. Bei dieser Form verringert sich die Aktivität des Enzyms im Laufe des Lebens. Eine Lactoseintoleranz kann auch die Folge anderer Krankheiten des Magen-Darm-Trakts sein, die zur Schädigung der Darmschleimhaut und zum Verlust der Dünndarmzotten geführt haben. Hierzu gehören beispielsweise die Glutenunverträglichkeit (Sprue, Zöliakie), chronisch entzündliche Darmkrankheiten (Morbus Crohn oder Colitis ulcerosa) und Infektionen. Die Verträglichkeit von Lactose verbessert sich in der Regel, wenn die Krankheiten behandelt werden. Der kongenitale Lactasemangel (Alactasie), bei dem von Geburt an das Enzym Lactase fehlt, tritt sehr selten auf und führt zu Entwicklungsstörungen bei Säuglingen. Eine konsequent lactosefreie Ernährung mit Spezialnahrungen ist in diesem Fall erforderlich.

Die Standardmethode für die Diagnose einer Lactoseintoleranz ist der sogenannte „Wasserstoff-Atemtest". Unter ärztlicher Aufsicht trinkt der Patient in Wasser aufgelösten Milchzucker. Über die Atemluft kann gemessen werden, ob die typischen Darmgase entstehen.

Lediglich die Alactasie macht eine lactosefreie Ernährung notwendig. Bei den anderen Formen der Lactoseintoleranz ist meist eine Restaktivität der Lactase vorhanden, sodass die Behandlung mit der Bestimmung der individuellen Verträglichkeit von Lactose beginnt. Empfehlenswert ist eine Ernährungsumstellung in drei Phasen. In der Karenzphase von zwei Wochen sollte Lactose weitestgehend gemieden werden, also Verzicht auf Milch und Milchprodukte und Lebensmittel und Getränke, die unter Verwendung von Milch hergestellt werden. Lactosefreie Milch und Milchprodukte, ausgewählte Käsesorten, z. B. Hart- und Schnittkäse sind erlaubt, da diese Käsesorten nahezu lactosefrei sind, denn durch den Reifungsprozess wird die enthaltene Lactose abgebaut. Nach Abklingen der Beschwerden werden in der zweiten Phase, der Testphase, nach und nach Milch und Milchprodukte wieder in den Speisenplan eingeführt. Sie sollten auf mehrere Portionen am Tag verteilt werden, um die verträgliche Lactosemenge zu ermitteln. Es ist empfehlenswert, Milch und Milchprodukte zusammen mit einer Mahlzeit aufzunehmen, z. B. Joghurt als Dessert. Nicht wärmebehandelte Sauermilchprodukte wie Joghurt und Kefir sowie probiotische Produkte werden häufig gut vertragen. Sie weisen zwar einen hohen Lactosegehalt auf, dieser wird aber durch die Milchsäurebakterien weitestgehend abgebaut. Diese Testphase geht fließend in die Dauerernährung über, die so gestaltet sein sollte, dass sie keine Beschwerden verursacht und den individuellen Ernährungsgewohnheiten entgegenkommt.

Diese und weitere Ratschläge sind in der neu aufgelegten DGE-Infothek „Essen und Trinken bei Lactoseintoleranz" der Deutschen Gesellschaft für Ernährung (DGE) e. V. zusammengestellt. Sie informiert über Ursachen, Formen, Symptomatik und Diagnostik der Lactoseintoleranz und gibt Ernährungsempfehlungen für die Praxis. Lebensmitteltabellen sowie Adressen von Ernährungsfachkräften runden die Broschüre ab. Die 20-seitige Infothek kann unter der Artikel-Nr. 123026 zum Preis von 1,00 € zzgl. Versandkosten beim DGE-MedienService bestellt werden, Tel.: 0228 9092626, Fax: 0228 9092610, www.dge-medienservice.de.

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(dge) Kakao, Milchkaffee oder Joghurt - kommt es bei Ihnen nach dem Verzehr dieser Lebensmittel auch zu Durchfall, Blähungen oder krampfartigen Bauchschmerzen? Nicht alle Menschen können Milch und Milchprodukte uneingeschränkt genießen: Etwa 15-20 % der Deutschen leiden an einer Lactoseintoleranz, einer Unverträglichkeit gegenüber Lactose (Milchzucker).

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Definition: People with fructose intolerance have an insufficient absorption of fructose in the small intestine.

2 Forms:
1. non-congenital form of fructose intolerance: fructose malabsorption
2. congenital form of fructose intolerance: hereditary fructose intolerance, in which the liver is permanently damaged

Symptoms: Stomach pain, somach cramps, diarrhea, bloating, nausea

Diagnosis: H2 breath test: A fructose solution is drunk and the breath is then analyzed. In the case of fructose intolerance, the measured value of hydrogen is increased.

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Lactose intolerance = lactose malabsorption

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Lactose intolerance = lactose malabsorption

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Definition:

It´s a clinical syndrome that symptoms after consuming food substances containing lactose which you can find in dairy products. Usually upon lactose consumption, the enzyme lactase hydrolyses the lactose into glucose and galactose. A deficiency of lactase due to primary or secondary causes results in symptoms.

Diagnosis:

- Hydrogen breath test: measures the hydrogen content of breath after lactose ingestion -> pos. if breath hydrogen value rises > 20 ppm

- Stool acidity test

- Milk tolerance test: ingest 500 ml milk -> obtain the blood glucose level -> rise in blood sugar of less than 9 mg/dl shows lactose intolerance

- Lactose tolerance test: determines lactose absorption after ingestion of a lactose-containing liquid -> measure serial blood glucose levels

Symptoms:

Come up 30 min to 1-2 hours after ingesting milk products -> presence of abdominal bloating, tenderness and pain, diarrhea, nausea and vomiting

Classification:

1) Primary Lactase Deficiency: most common cause of lactase deficiency -> with becoming older there is a decline in lactase enzyme activity

2) Secondary Lactase Deficiency: due to several infectious, inflammatory or other diseases

3) Congenital Lactase Deficiency: since birth due to autosomal recessive inheritance

4) Developmental Lactase Deficiency: premature infants born at 28 to 37 weeks of gestation

Risk factors:

- Increasing age -> more often in adolescents and young adults

- Diseases affecting the small intestine

References:
https://www.ncbi.nlm.nih.gov/books/NBK532285/

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- 5-6 small meals throughout the day (small quantities help the stomach heal by reducing the effect of stomach acid)

- INCLUDE: foods rich in fibre (apple, celery, carrots, beans), alkaline food, low fat meat, omega-3 fatty acids, vegetables low in acidity, probiotics (kombucha, kimchi, sauerkraut)

--> Goal is to prevent an increase in stomach acid, prevent further  inflammation

- EXCLUDE/AVOID: alcohol, coffee, carbonated drinks, citrus-based fruit juices, acidic foods (such as tomato), spicy food, fried and fatty foods --> impair gastritis

source: https://sydneygastroenterologist.com.au/blog/gastritis-diet-strategies-and-recommendations/

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Gastritis is a digestive condition that arises as a result of irritation, inflammation or erosion of the lining of the stomach. This is caused as a result of excessive acid in the stomach. As part of the long-term treatment strategies recommended by gastroenterologists, gastritis diet recommendations are important.

Given the long-term effects of this condition, including ulcers, ongoing pain, inflammation, bleeding, and even stomach cancer, individuals need to consider the benefits of food items that make up a gastritis diet.

This post identifies dietary recommendations deemed useful to manage gastritis symptoms and those that should be left out of these diets.

If patients are already on a special diet or are suffering from other health conditions, medical guidance from a gastroenterology specialist is required before dietary changes are made.

Food items to be included in a gastritis diet

Dietary changes can help patients experience relief from gastritis symptoms by eliminating H.pylori, which is a type of bacteria that causes this condition.

Yoghurt is also considered a beneficial food item for a gastritis diet. In a study conducted by the American Journal of Clinical Nutrition, the probiotics in yoghurt demonstrated a stronger health benefit (when combined with medication) in terms of eliminating H.pylori, compared to individuals who took medication alone.

Yoghurt also contains good bacteria that improve the body's ability to fight off unwanted bacteria in the stomach .

Other items recommended for a gastritis diet include high-fibre additions such as apples, celery, berries, carrots, and beans. Low-fat meat items including fish, chicken, and turkey breast are similarly beneficial for patients.

Vegetables that are low in acidity and other probiotics including kombucha, kimchi, and sauerkraut are also believed to provide relief from gastritis symptoms in the long run.

Dietary habits that reduce symptoms of gastritis

Patients may be recommended to start consuming around 5-6 small meals throughout the day, as opposed to 3 big meals. Eating meals in small quantities can help the stomach heal by reducing the effect of stomach acid.

Patients are also asked to drink plenty of water. Those who consume alcohol frequently must reduce their intake, given that it increases the content of acid in the stomach, leading to inflammation.

Certain nutritional supplements may be recommended by doctors including Omega-3 fatty acids and probiotics. Any vitamins or nutritional supplements should be cleared with a GP prior to their incorporation in a gastritis diet.

Food items to be excluded from a gastritis diet

Certain food items need to be excluded from these types of diets to ensure that stomach acid isn't increased, inadvertently. While these don't necessarily pose negative health effects, they may trigger symptoms of gastritis in those with this condition.

Certain beverages such as coffee, alcohol, carbonated drinks, and citrus-based fruit juice are known to exacerbate gastritis.

Acidic food including tomatoes and certain types of fruit, spicy food, allergenic or symptomatic food, fried and fatty food should also be avoided if patients wish to prevent pain and discomfort.

Patients require professional medical guidance to create a personalised diet for gastritis.

A diet for gastritis includes food items that can provide long-term relief to symptoms of gastritis. Patients suffering from this condition must receive guidance from a trained gastroenterologist specialist to receive recommendation suited to his/her lifestyle and health.

For the right recommendations, patients can request further information from Dr Suhirdan Vivekanandarajah; an interventional gastroenterologist and hepatologist in Sydney.

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Gastritis Diet Strategies | Dr. Suhirdan Vivekanandarajah

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With the right diet, you may be able to get gastritis symptoms under control. Here are recommendations and strategies to help you create a gastritis diet.

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Consume more potassium-rich foods, e.g. coconut water, bananas, peeled potatoes.
Drink or eat some high-sodium foods, e.g crackers, pretzels.

Refenrences
https://stanfordhealthcare.org/content/dam/SHC/programs-services/cancer-nutrition/docs/diarrhea-during-chemo-and-radiation-nutrition-facts.pdf

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- high fiber intake
(at least 30 g of dietary fiber as a guideline for daily intake)

-> Good Sources: whole grain cereal products such as whole grain bread, cereal flakes, whole grain pasta and brown rice, as well as vegetables, fruits, legumes, nuts and seeds, Flaxseed

- Increase fluid and mineral intake (drinks without sugar)

Literature:
https://www.ernaehrungs-umschau.de/news/23-12-2014-aktualisierte-dge-infothek-essen-und-trinken-bei-chronischer-verstopfung/
(Altmann)

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1. Balanced Macronutrient Intake: Maintain a balanced intake of carbohydrates, proteins, and fats, focusing on healthy fats like monounsaturated and polyunsaturated fats.

2. Omega-3 Fatty Acids: Include sources like fatty fish, chia seeds, flaxseeds, and walnuts for their heart-healthy benefits.

3. Dietary Fiber: Consume whole grains, legumes, fruits, vegetables, and nuts to help regulate cholesterol levels.

4. Plant Sterols and Stanols: Include foods fortified with these compounds, such as margarines and yogurts, to help lower LDL cholesterol.

5. Antioxidants: Eat colorful fruits and vegetables like berries, tomatoes, spinach, and broccoli for their antioxidant properties.

6. Limit Added Sugars and Refined Carbohydrates: Reduce intake of sugary beverages, sweets, processed snacks, and refined grains.

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Several healthy diets such as Mediterranean diet or approches to stop hypertension (DASH) diets are recommended. Obese/overweight people should also lose weight as cardiometabolic risk factors and outcomes improve as a result.
Less meat and seafood consumtion, more legumes instead. Avoide alcohol and sugar-sweetened beverages as they increase urid acid.

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-The best diet for preventing heart disease is one that is full of fruits and vegetables, whole grains, nuts, fish, poultry, and vegetable oils.
- Omega-3 consumption is really important for CVD patients.
-They have to choose more vegetables, nuts especillay unsaturated fatty acids source.
- Mediterian diet style is really effective on the CVD nutrition.
-Sodium and potassium are two interrelated minerals that play major roles in regulating blood pressure and a healthy heart. Eating less salty foods and more potassium-rich foods may significantly lower the risk of cardiovascular disease.

AYSE MERVE UYAR

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Definition

“Diffuse inflammation of gastric mucosa” (Taylor, 1969, p. 818)

Diagnosis

Clinical examination, gastroscopy.

Symptoms

Symptoms are abdominal pains (upper part), postprandial fullness, nausea, vomiting and loss of appetite.

Classification

Sipponen & Maaroos (2015) classify gastritis as being caused by the bacterium Helicobacter pylori or by autoimmune issues, however there are many more classifications for example into chronic or acute gastritis. For more classifications; https://flexikon.doccheck.com/de/Gastritis

Risk factors

Lifestyle choices (especially nicotine, caffeine and alcohol abuse). Furthermore Sipponen & Maaroos (2015) suggest that lacking hygiene and lower socioeconomical status influence the settlement of unfavorable bacteria like H. pylori in childhood.

Literature

Sipponen, P., & Maaroos, H. I. (2015). Chronic gastritis. Scandinavian journal of gastroenterology, 50(6), 657–667. https://doi.org/10.3109/00365521.2015.1019918

Taylor K. B. (1969). Gastritis. The New England journal of medicine, 280(15), 818–820. https://doi.org/10.1056/NEJM196904102801507

https://flexikon.doccheck.com/de/Gastritis

(Tim Salomon)

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Definition is based on the symptoms and includes at least one of the following criteria:

Too frequent defecation: ≥3 unformed stools in 24 h.

Decreased stool consistency: water content of stool >75%.

Increased stool weight:>250 g daily.

Diagnosis

Diagnosis is difficult due to the many possible causes. Possibilities are:

anamnesis

laboratory tests

imaging procedures

endoscopy

functional tests

Classification

Acute diarrhea: duration ≤4 weeks (usually a few days).

Chronic diarrhea: duration >4 weeks.

By pathomechanisms:

Secretory diarrhea

Malassimilatory diarrhea

Functional diarrhea

Risk factors

Diarrhea can be caused by many different factors:

Microorganisms

viruses

Food intolerances

Autoimmune diseases

Medications

Tumors

Functional factors

Endocrine disorders

Operations

Physical noxious agents

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Definition:
The body lacks the ability to pass gas and stool due to obstruction in the intestines.

Diagnosis:
- physical examination of the rectum  to watch for any signs of obstruction
- blood check for signs of inflammation
- CT to get a clear picture of the gastrointestinal system
- Ultrasound to locate the site of obstipation including the causes of obstipation
- Colonoscopy to detect any damage to the tissues and A biopsy is also done to detect colon cancer

Symptomes:
- The patient is constipated
- A feeling of fullness or bloating
- There is an abnormal increase in bowel sounds
- The patient does not have the appetite to eat which leads to generalized body malaise (weakness)
- Abdominal pain
- Change in stool excretion pattern (decreased frequency, decreased stool volume)
- Hard, formed stool
- Severe flatulence
- Dehydration
- fast/rapid pulse

Classification:
Constipation can be classified according to different dimensions:
1. according to course

acute constipation

chronic constipation

2. according to causative intestinal segment

colonic constipation

anorectal constipation

3. by cause

travel constipation

diabetic constipation

idiopathic constipation

Risk factors:
- insufficient physical activity
- emotional stress
- medication
- Neurological impairments
- rectal changes
- Altered eating habits
- Inadequate fiber intake
- Inadequate fluid intake

Literature:
https://flexikon.doccheck.com/de/Obstipation
https://www.onkopedia.com/de/onkopedia-p/guidelines/obstipation-verstopfung/@@guideline/html/index.html
(Altmann)

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Definition:
Heart failure (HF) is a clinical syndrome characterised by a constellation of symptoms and signs often caused by a structural and/or functional cardiac abnormality resulting in reduced cardiac output and/or elevated intracardiac pressures

Diagnosis:

Elevated jugular venous pressure

Pulmonary congestion

Symptoms:

Dyspnoea

Orthopnoea

Lower limb swelling

Classification
based on symptoms and calculated left ventricular ejection fraction (LVEF).

heart failure with reduced ejection fraction (HFrEF)

heart failure with preserved ejection fraction (HFpEF)

heart failure with mid-range ejection fraction (HFmrEF)

Risk factors

Smoking tobacco

Eating foods high in fat, cholesterol, and sodium

Not getting enough physical activity

Excessive alcohol intake

References
https://www.ncbi.nlm.nih.gov/books/NBK430873/
https://link.springer.com/article/10.1007/s11897-017-0351-y
https://www.cdc.gov/heartdisease/heart_failure.htm

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Continuing Education Activity

Heart failure is a complex clinical syndrome in which the heart cannot pump enough blood to meet the body's requirements. It results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with fatigue and dyspnea, reduced exercise tolerance, and fluid retention (pulmonary and peripheral edema). This activity reviews the evaluation and management of congestive heart failure and highlights the role of the healthcare team in improving care for patients with this condition.

Objectives:

Review the pathophysiology of congestive heart failure.

Describe the diagnostic approach to patients presenting with clinical features of congestive heart failure.

Outline the management of congestive heart failure.

Explain the importance of collaboration and communication among the interprofessional team to educate the patients on the importance of medication compliance to improve outcomes for those with congestive heart failure.

Access free multiple choice questions on this topic.
Introduction

Heart failure is a complex clinical syndrome that results from a functional or structural heart disorder impairing ventricular filling or ejection of blood to the systemic circulation. It is by definition a failure to meet the systemic demands of circulation. Heart failure remains a highly prevalent disorder worldwide with a high morbidity and mortality rate. It has an estimated prevalence of 26 million people worldwide and contributes to increased healthcare costs worldwide.[1] Multiple different diseases can cause heart failure. The etiology of heart failure varies the treatment plan to some degree; however, most of the treatment recommendations are based on the presence of heart failure alone, regardless of the cause.

Classification of heart failure is based on symptoms and calculated left ventricular ejection fraction (LVEF). Heart failure due to left ventricular dysfunction is categorized into heart failure with reduced ejection fraction (HFrEF), heart failure with preserved ejection fraction (HFpEF), and heart failure with mid-range ejection fraction (HFmrEF). The latter may consist of mixed left ventricular dysfunction (a combination of systolic and diastolic heart failure). The definition of HFrEF has varied among different studies and guidelines but is generally defined as an ejection fraction (EF) of less than 40%. Heart failure with preserved ejection fraction (HFpEF) is generally defined as heart failure with an EF of greater than 50%. HFmrEF is defined as heart failure with an EF of 40% to 50%.[2]

Heart failure can severely decrease the functional capacity of a patient and increase mortality risk. It is imperative to diagnose and effectively treat the disease to prevent recurrent hospitalizations, improve quality of life, and enhance patient outcomes. The treatment of heart failure requires a multifaceted approach involving patient education, optimal medical regimen to improve cardiac contractility, and prevention/limitation of exacerbations. An interprofessional team approach is warranted to optimize patient care.

Etiology

Congestive heart failure is caused by structural abnormalities of the heart, functional abnormalities, and other triggering factors. Historically, an overwhelming majority of the cases were due to coronary artery disease and myocardial infarction. Over time, coronary artery disease and diabetes mellitus have become the predominant predisposing factors for heart failure. Other structural causes of congestive heart failure (CHF) include hypertension, valvular heart disease, uncontrolled arrhythmia, myocarditis, and congenital heart disease. Diastolic heart failure with impaired ventricular filling can be caused by restrictive cardiomyopathies and constrictive pericarditis, in addition to the etiologies identified above.[3]

It is important to identify etiologies of decompensated heart failure, as they contribute to most of the morbidity and mortality associated with the disease. The most common cause of decompensated congestive heart failure is inappropriate drug treatment, dietary sodium restriction, and decreased physical activity. Uncontrolled hypertension is the second most common cause of decompensated heart failure.[4] Uncontrolled tachyarrhythmias in patients with underlying congestive heart failure can promptly lead to CHF exacerbations.

Another group of diseases associated with "congestive heart failure" leads to high-output cardiac failure. This, by definition, is not an impairment in cardiac function but a failure of the heart to meet the increased systemic demands due to extracardiac diseases. Common etiologies of this type of congestive heart failure include severe anemia, thyrotoxicosis, obesity, nutritional deficiencies (thiamine deficiency, etc.), and pregnancy.[5]

The above-mentioned list of etiologies is not an all-inclusive list but a broad categorization of various etiologies.

Epidemiology

Approximately 6.2 million people in the United States had clinically manifested heart failure from 2013 to 2016.[6] By some reports, the incidence rate has plateaued; however, the prevalence increases as more patients receive therapy. This has not translated to improved quality of life or a decrease in the number of hospitalizations for patients with heart failure. According to the Global Health Data Exchange registry, the current worldwide prevalence of CHF is 64.34 million cases. This translates to 9.91 million years lost due to disability (YLDs) and 346.17 billion US dollars in healthcare expenditure. Age is a major determinant of HF. Regardless of the cause or the definition used to classify patients with heart failure (HF), the prevalence of HF increases steeply with age. The registry also notes a predilection for race with a 25% higher prevalence of HF in patients of African-American descent than Caucasians. According to the American Heart Association, heart failure is still the primary cause of hospitalization in the elderly population and accounts for 8.5% of cardiovascular-related deaths in the United States.[7] The report states a higher incidence and prevalence of heart failure among African Americans, Hispanic Americans, Native Americans, and recent immigrants from developing nations. According to the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM program), the prevalence of HF is relatively greater in younger patients, which was attributed to obesity as the cause.[8] The incidence of heart failure in men doubles with each 10-year age increase after the age of 65, whereas in women, for the same age cohort, the incidence triples.[7]

International statistics regarding the epidemiology of HF are similar to those of the United States. The incidence increases dramatically with age, and metabolic risk factors along with a sedentary lifestyle are major risk factors. Ischemic cardiomyopathy, along with hypertension, is a major cause of HF in developing countries.[9] The notable difference based on a review of small cohort studies from these nations is a higher prevalence of isolated right heart failure. The theoretical cause of this is thought to be due to the higher prevalence of tuberculous, pericardial disease, and lung disease. There is a lack of robust data to verify these claims.

Pathophysiology

The adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance.

In the initial stages of congestive heart failure, cardiac physiology attempts to adapt via several compensatory mechanisms to maintain cardiac output and meet the systemic demands. These include the Frank-Starling mechanism, changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility. With increased wall stress, the myocardium attempts to compensate via eccentric remodeling, which further worsens the loading conditions and wall stress.[10]

A decrease in cardiac output stimulates the neuroendocrine system with a release of epinephrine, norepinephrine, endothelin-1 (ET-1), and vasopressin. They cause vasoconstriction leading to increased afterload. There is an increase in cyclic adenosine monophosphate (cAMP), which causes an increase in cytosolic calcium in the myocytes. This increases myocardial contractility and further prevents myocardial relaxation.

An increase in afterload and myocardial contractility with impaired myocardial relaxation leads to increased myocardial oxygen demand. This paradoxical need for increased cardiac output to meet myocardial demand eventually leads to myocardial cell death and apoptosis. As apoptosis continues, a decrease in cardiac output with increased demand leads to a perpetuating cycle of increased neurohumoral stimulation and maladaptive hemodynamic and myocardial responses.[10]

A decrease in cardiac output also stimulates the renin-angiotensin-aldosterone system (RAAS), leading to increased salt and water retention, along with increased vasoconstriction. This further fuels the maladaptive mechanisms in the heart and cause progressive heart failure. In addition to this, the RAAS system releases angiotensin II, which has been shown to increase myocardial cellular hypertrophy and interstitial fibrosis. This maladaptive function of angiotensin II has been shown to increase myocardial remodeling.[11]

In HFpEF, there is a decrease in myocardial relaxation and an increase in the stiffness of the ventricle due to an increase in ventricular afterload. This perpetuates a similar maladaptive hemodynamic compensation and leads to progressive heart failure.[12]

History and Physical

The diagnosis and classification of heart failure are primarily based on the presence/severity of symptoms and physical exam findings. It is imperative to obtain a detailed history of symptoms, underlying medical conditions, and functional capacity/exercise tolerance to adequately treat the patient. The most commonly reported symptom is shortness of breath. Further qualification of this symptom is essential to help elucidate potential causes of heart failure and to determine the plan of care for the patient. Shortness of breath must further be classified to determine if it is related to exertion, positional changes (orthopnea), and whether it is acute or chronic. Other commonly reported symptoms of HF include chest pain, palpitations, anorexia, and fatigue. Some patients may present with a recumbent cough which may be due to orthopnea.

Physical examination of patients with heart failure requires a comprehensive assessment. The general appearance of patients with severe, chronic heart failure or those with acutely decompensated heart failure will include anxiety, diaphoresis, and poor nutritional status. The classical finding of pulmonary rales translates to heart failure of moderate to severe intensity. Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary congestion increases, frothy and blood-tinged sputum may be seen. It is important to note that the absence of rales does not exclude pulmonary congestion. Jugular venous distention is another classical finding which must be assessed in all patients with HF. A paradoxical increase in jugular venous distention with respiration (Kussmaul sign) may be seen. In patients with elevated left-sided filling pressures, hepatojugular reflux (distention of the jugular vein after applying pressure over the liver with the patient lying at a 45° angle) will be seen. Peripheral edema is present in severe heart failure and will be seen if a substantial degree of volume overload is present.[13]

Cardiac findings in patients with HF include S3 gallop, pulsus alternans, and accentuation of P2. An S3 gallop is the most significant and early finding associated with HF.[14] In decompensated dilated cardiomyopathy, mitral and tricuspid regurgitation murmurs will be noted.

Framingham Diagnostic Criteria for Heart Failure

The commonly used Framingham Diagnostic Criteria for Heart Failure requires the presence of 2 major criteria or 1 major and 2 minor criteria to make the diagnosis of heart failure. This diagnostic tool is highly sensitive for the diagnosis of heart failure but has a relatively low specificity. The Framingham Diagnostic criteria are as follows:.[13]

Major Criteria

Paroxysmal nocturnal dyspnea or orthopnea

Third heart sound (S3 Gallop)

Weight loss of 4.5 kg or more in 5 days in response to treatment

Central venous pressure greater than 16 cm of water

Radiographic cardiomegaly

Minor Criteria

Tachycardia (heart rate greater than 120 beats per minute)

A decrease in vital capacity by one third the maximal value recorded

New York Heart Association Functional Classification

Based on symptoms, the patients can be classified using the New York Heart Association (NYHA) functional classification as follows: [11]

Class I: Symptom onset with more than ordinary level of activity

Class II: Symptom onset with an ordinary level of activity

Class III: Symptom onset with minimal activity

Class IV: Symptoms at rest

Evaluation

A comprehensive laboratory analysis, including assessment for anemia, iron deficiency, renal dysfunction, and liver dysfunction, is needed to help elucidate the cause and/or severity of heart failure. Cardiac-specific testing and prognostic factors for HF are outlined below.

Serum sodium levels have prognostic value as predictors of mortality in patients with chronic HF. They also play a role in the prediction of short-term mortality for patients admitted with decompensated heart failure. The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) trial demonstrated a significantly increased risk of in-hospital mortality as well as 30-day mortality in patients with HF who presented with hyponatremia. The mean serum sodium for patients enrolled in the study was 134 mEq/L. The highest mortality risk was seen in patients in the lowest quintile of serum sodium levels on presentation.[15]

Serum B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) levels can aid in differentiating cardiac from noncardiac causes of dyspnea in patients with ambiguous presentations. BNP is an independent predictor of increased left ventricular end-diastolic pressure, and it is used for assessing mortality risk in patients with heart failure. BNP levels correlate with New York Heart Association (NYHA) classification, and the utility is primarily as a marker to assess treatment efficacy. According to the American Heart Association (AHA) and the American College of Cardiology (ACC) recommendations from 2013 and 2017, predischarge natriuretic peptide levels are strong predictors of the risk of death and hospital readmission in patients with HF. In patients with true clinical presentation of HF, natriuretic peptides should not be used to drive treatment plans. It is important to remember that BNP and NT-proBNP levels can be elevated in patients with renal dysfunction, atrial fibrillation, and in older patients. Conversely, BNP levels can be falsely low in patients with obesity, hypothyroidism, and advanced heart failure (due to myocardial fibrosis).[16][17]

Chest radiographs are used to assess the degree of pulmonary congestion and cardiac contour (to determine the presence of cardiomegaly). Findings indicative of congestive heart failure on chest radiographs include enlarged cardiac silhouette, edema at the lung bases, and vascular congestion. In florid heart failure, Kerley B lines may be seen on chest radiographs. The absence of these findings in patients with clinical features of HF does not rule out CHF.[13]

Echocardiography is the most commonly used test for the diagnosis of HF. It can assess for systolic and diastolic dysfunction and help elucidate the presence of focal wall motion abnormalities or valvular pathology. Traditional 2D transcutaneous echocardiography is the most commonly utilized form of testing. However, in patients with severe obesity, pregnancy, or mechanical ventilation, it may be difficult to obtain adequate acoustic windows. Transesophageal echocardiography (TEE) is an alternative for these patients. Adequate rate control in patients with tachyarrhythmias is necessary to obtain adequate echocardiographic images.[13]

Computed tomography (CT) and magnetic resonance imaging (MRI) in patients with HF are used principally for the diagnosis of congenital cardiac abnormalities. Cardiac MRI is also the gold standard test for evaluating right ventricular (RV) function.[18]

Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for the evaluation of left ventricular (LV) and right ventricular (RV) function. MUGA scan is, in fact, the most accurate scan to assess for ejection fraction (EF) and is used in patients when there is a disparity of EF measurements from other studies.[19]

Electrocardiogram (ECG)-gated myocardial perfusion imaging is another diagnostic tool for assessing the EF, regional wall motion, and regional wall thickening. EF measurement with this study may be affected in patients with an irregular heart rate, low count density, and extracardiac radiotracer uptake. ECG-gated images are also useful in recognizing artifactual defects seen on SPECT imaging, such as breast tissue and diaphragmatic attenuation.[19]

Iobenguane scanning is scintigraphic imaging using iobenguane I-123 injection. It has been used for cardiac risk stratification in patients with New York Heart Association (NYHA) class II to III and an LVEF of 35% or less. Iobenguane I-123 is a norepinephrine analog. The test can show the amount of norepinephrine uptake in the cardiac sympathetic nervous system. Improved reuptake of norepinephrine is associated with a better prognosis.[20]

Other tests used in evaluating patients with HF include cardiac catheterization, stress testing, and electrocardiograms. However, they are used in patients with HF to determine the underlying cause of the disease. They do not play any specific role in the diagnosis of HF or its prognostication. In patients with severe systolic CHF, abnormalities of the electrocardiogram (ECG) are certain. However, in patients with HFpEF, the ECG may be normal.

Treatment / Management

The goal of therapy for chronic CHF is to improve symptom management and quality of life, decrease hospitalizations, and decrease overall mortality associated with this disease. The goal of pharmacologic therapy is to give all indicated agents rather than single agents because the aggregate effect of these therapies is better than monotherapy from any of the agents.

The primary combination therapy for HFrEF includes diuretics, a renin-angiotensin system inhibitor (such as an angiotensin receptor neprilysin inhibitor (ARNI), angiotensin-converting enzyme (ACE) inhibitor, or angiotensin II receptor blockers (ARB)), and a beta-blocker. The combination of hydralazine and nitrate is an alternative to an angiotensin system blocker for primary therapy if ACE inhibitor, ARNI, and ARB therapies are contraindicated. The nitrate and hydralazine combination is also indicated to reduce mortality and morbidity in African American patients with symptomatic HFrEF, currently receiving optimal medical therapy.[21] The combination therapy of ARB-ARNI significantly reduced cardiovascular death and HF hospitalizations when compared to ACE inhibitors alone.[22]

Mineralocorticoid receptor antagonists such as spironolactone or eplerenone are indicated in patients with NYHA functional class II to IV and an LVEF of less than or equal to 35%. They are also indicated in patients with symptomatic HF after a myocardial infarction (MI) and an LVEF of less than 40%. However, in patients with recent MI and a low EF without symptoms of HF, these medications did not show any benefit.[23]

Ivabradine selectively inhibits the funny current (I-f) in the sinoatrial node. According to the AHA/ACC, ivabradine is indicated in patients with persistently symptomatic HF and an EF of less than or equal to 35% in sinus rhythm. The resting heart rate should be greater than 70 beats/min despite goal-directed beta-blocker therapy.[24]

Vericiguat is an agent that stimulates the intracellular receptor for endogenous NO, which is a potent vasodilator. It was recently approved by the FDA in 2021 to reduce the risk of mortality and HF hospitalizations in adults admitted with HF exacerbation who have chronic symptomatic HF and an EF of less than 45%.[25]

Digoxin may be considered in symptomatic patients in sinus rhythm despite adequate goal-directed therapy to reduce the all-cause rate of hospitalizations, but its role is limited.

An implantable cardioverter-defibrillator (ICD) is indicated for primary prevention of sudden cardiac death in patients with HF who have an LVEF of less than or equal to 35% and an NYHA functional class of II to III while on goal-directed medical therapy. It is also indicated if a patient has NYHA functional class II and an EF of less than or equal to 30% on adequate medical therapy.[26]

Cardiac resynchronization therapy (CRT) with biventricular pacing is indicated in patients with HFrEF and an NYHA functional class of II to IV with an LVEF less than or equal to 35% and QRS duration of greater than 150 ms.[26] According to the European Society of Cardiology (ESC), CRT is not recommended in patients with a QRS duration of less than 130 ms as multiple studies have shown potential harm. The ESC recommends CRT for patients with non-left bundle branch block (LBBB) morphology who meet the criteria for CRT; however, the ACC/AHA guidelines limit it to those with LBBB morphology on ECG. There is ongoing debate as to whether QRS morphology versus QRS duration should be the primary determinant for the selection of CRT.[16]

In patients with refractory HF, despite optimized pharmacologic therapy, intravenous vasodilator therapy and intravenous inotropes have been considered in the past. However, according to the AHA/ACC 2013 and 2017 guidelines, this should be restricted to palliative symptom relief in patients with end-stage disease who cannot get relief with standard medical therapy.[16]

In patients with HFpEF, none of the current therapies have a definitive improvement in mortality or hospitalization. However, medical management with the above therapies is indicated.[27]

Patients with progressive HF or those with acute, severe refractory HF may be considered for heart transplantation.

It is also important to address potential triggers for HF exacerbation once the diagnosis of HF is made. Drugs that should be avoided in patients with HF include nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers (CCBs) except vasoselective CCBs, and most antiarrhythmic drugs (except those in class III).[28]

Differential Diagnosis

Diseases that may present with clinical features of volume overload and/or dyspnea are in the differential for HF. These include:

Staging

ACC/AHA Heart Failure Stages[16]

Stage A: Patients at high risk for HF but have no symptoms or structural heart disease

Stage B: Patients have structural heart disease but are asymptomatic

Stage C: Patients have structural heart disease plus symptoms

Stage D: Patients have refractory HF that requires modified interventions

Management Recommendations by ACC/AHA According to HF Stages[16]

Stage A: Reduction of risk factors and aggressive treatment of comorbidities

Stage B: Aggressive risk factor reduction and treatment with an angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker (ACEI/ARB) and/or beta-blocker.

Stage C: Combination goal-directed therapy with ACEI/ARBs or angiotensin receptor-neprilysin inhibitors (ARNIs), beta-blockers, and loop diuretics for fluid retention. The most recent AHA/ACC update from 2017 added a class IIa recommendation for ivabradine in patients with stage C HF.[28]

Stage D: Goal-directed medical therapies indicated for stage C and consideration for heart transplantation. In patients with advanced disease and decreased life expectancy, palliative care discussions and advance directive planning should be considered.

Prognosis

According to the Centers for Disease Control and Prevention (CDC), in December 2015, the rate for heart failure-related deaths decreased from 103.1 deaths per 100,000 population in 2000 to 89.5 in 2009 but subsequently increased to 96.9 in 2014. They note that the trend correlates with a shift from coronary heart disease as the underlying cause of heart failure deaths to metabolic diseases and other noncardiac causes of HF such as obesity, diabetes, malignancies, chronic pulmonary diseases, and renal disease. The mortality rate following hospitalization for heart failure is estimated at around 10% at 30 days, 22% at 1 year, and 42% at 5 years. This can increase to greater than 50% for patients with NYHA class IV, stage D heart failure.[29]

Ottawa Heart Failure Risk Score[30]

The Ottawa Heart Failure Risk Score is a useful tool for prognosis determination in patients with HF who present to the emergency department with symptoms of HF. It determines the 14-day risk of mortality, hospital readmission, and acute coronary syndrome in patients who presented to the emergency department with symptoms of HF to help arrive at safe disposition planning. Patients with a score of 0 are considered low risk. A score of 1-2 is considered moderate risk, a score of 3-4 is considered high risk, and a score of 5 or higher is considered very high risk. The scoring criteria are as follows:

One point for each of the following

History of stroke or transient ischemic attack

Oxygen saturation less than 90%

Heart rate greater than 110 beats per minute on the 3-minute walk test

Acute ischemic ECG changes

An NT-proBNP level of greater than 5000 ng/L

Two points for each of the following

Prior history of mechanical ventilation for respiratory distress

Heart rate greater than 110 beats/min on presentation

Blood urea nitrogen (BUN) greater than 33.6 mg/dl (12 mmol/L)

Serum bicarbonate greater level than 35 mg/d

Complications

Clinical complications of HF include decreased quality of life, decreased functional capacity, unintentional weight loss (cardiac cachexia), renal dysfunction (cardiorenal disease), and liver dysfunction (hepatic congestion).[31] Adverse cardiac events associated with HF include valvular dysfunction with dilated cardiomyopathy, MI, and ventricular arrhythmias. Sudden cardiac death is a potential complication for patients with HFrEF and requires primary prevention with ICD placement, as discussed above. Complications of the treatment for HF include renal failure, hypotension, and recurrent nosocomial infections due to frequent hospitalizations and central venous access.[32]

Deterrence and Patient Education

Risk factor reduction and aggressive management of comorbid conditions in patients with high-risk HF is key to preventing the associated morbidity and mortality of this disease. In addition to appropriate medical therapy, patients need guidance on self-monitoring of symptoms/signs of heart failure and adopting healthy lifestyle habits such as weight loss, smoking cessation, regular exercise, and alcohol cessation. These strategies can help prevent the development of HF in patients at high risk for the disease and slow the progression in those who are already diagnosed with it. Recent data suggests that in high-risk patients with diabetes mellitus type 2, sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of heart failure in patients with coronary artery disease. It also noted a decrease in hospitalizations and other adverse cardiovascular events with the use of SGLT2 inhibitors in this group of patients.[33]

The ACC/AHA and ESC recommend patient education to facilitate self-care and compliance. Close supervision, including surveillance by the patient and family, home-based visits, telephone support, and/or remote monitoring, is recommended by both of these associations to prevent adverse outcomes and progression of the disease. Dietary sodium restriction to 2-3 g/day and fluid restriction to 2 L/day are recommended if patients have hyponatremia and evidence of volume overload despite medical therapy. Patients require frequent in-depth education and re-evaluation to ensure they can adhere to the recommendations to have optimal outcomes.[16][26]

Pearls and Other Issues

Summary of Recommendations for Pharmacotherapy in HF by the 2013 ACC/AHA Guideline Update[16][28]

Class I Recommendations

Evidence-based specific beta-blockers (carvedilol, bisoprolol, and metoprolol succinate) with one of the following:

Angiotensin-converting enzyme inhibitors (ACEIs)

Angiotensin receptor blockers (ARBs)

Angiotensin receptor-neprilysin inhibitor (ARNI)

Chronic symptomatic HFrEF NYHA class II or III, replace an ACEI or ARB with an ARNI

Class IIa

Ivabradine for patients with symptomatic HF while on goal-directed medical therapy for chronic HFrEF with LVEF less than or equal to 35% and in sinus rhythm with a heart rate of at least 70 bpm at rest.

Class III

ARNI should not be given with or within 36 hours of the last dose of an ACEI or in patients with a history of angioedema

The Heart Failure Society of America (HFSA) Guidelines for Management of Acute Decompensated HF[34]

Oral therapy should be continued in most patients with HFrEF and up titrated as needed.

Continue angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) and beta-blockers during treatment of acute exacerbations.

Only consider withholding beta-blockers in patients hospitalized after a recent beta-blocker initiation.

Loop diuretics remain the cornerstone of therapy. (Class I recommendation)

Vasodilators (e.g., nitroprusside, nitroglycerin, or nesiritide) can be used as adjuvant therapies in patient with systolic blood pressure above 90 mmHg.

Inotropic agents can be used short-term in patients with hypotension (SBP < 90 mmHg) and the patient is symptomatic from hypotension.

Enhancing Healthcare Team Outcomes

Heart failure is a complex clinical syndrome with high morbidity and mortality. It requires a multifaceted treatment approach, including patient education, pharmacologic management, and surgical interventions to optimize clinical outcomes. Specialty trained HF nurses are essential to the interprofessional team caring for patients with HF. They educate the patient on the importance of lifestyle modifications and medical compliance to help improve morbidity and mortality for the patient. They also educate the patient on symptom and weight management to prevent HF exacerbations and hospital admissions. The HF-trained social worker and case manager can help evaluate the patient in community settings/in-home visits to help the patient adhere to the lifestyle modifications recommended by the medical team. The clinical pharmacists assist the medical providers by reviewing patient medication lists and decreasing potential adverse drug-drug interactions. Primary care medical providers and cardiologists must coordinate care to minimize any adverse outcomes of medical therapy and prevent the progression of this disease. A collaborative interprofessional team can greatly improve the quality of life for patients with HF and decrease mortality.[Level 5]

References

# data[].attributes.attachment_link.description
Heart failure is a complex clinical syndrome that results from a functional or structural heart disorder impairing ventricular filling or ejection of blood to the systemic circulation. It is by definition a failure to meet the systemic demands of circulation. Heart failure remains a highly prevalent disorder worldwide with a high morbidity and mortality rate.

# data[].attributes.body
Definition:
It occurs when the blood supply of the brain (or part of it) is damaged or interrupted, and it prevents the brain tissue from getting oxygen.

Symptoms:

Headache

trouble walking

Paralysis

Trouble speaking or understanding

Seeing problems in one or both eyes

Diagnosis:
It is important to seek immediate medical attention if a person suffers from any form of a stroke. The method "FAST" helps to determinate some symptoms of a stroke:

Face = Ask the person to smile. Does one side of the face drops?

Arms = Ask the person to raise both arms. Does one arm drift downward or is unable to rise one arm?

Speech = Ask the person to repeat a simple phrase. Is his or her speech strange or slurred?

Time = if the person presents any of these signs, it is important to call immediately a doctor or sick for medical help

Classification:
Stroke can be classified in two categories depending on the cause of it:

1. Ischemic Stroke = or thrombotic stroke happens due to "blood clots", which blocks the brain's blood vessels, causing reduced blood flow. This leads to hypoxia to a certain part of the brain. It is the most common type of stroke.

2. Hemorrhagic Stroke = or bleeding stroke happens when a blood vessel in the brain ruptures or leaks and results in bleeding into the brain. Factors related to hemorrhagic stroke includes:

Trauma

Aneurysms

Uncontrolled high blood pressure

Risk factors:
Lifestyle

Overweight or obese

physical inactivity

Heavy drinking

Use of drugs

Medical

high blood pressure

Diabetes

high colesterol

Smooking

Obstructive sleep apnea

Cardiovascular diseases

Genetic (familiar history of stroke)

Other factors include

Age = 55 and older people have a higher risk

Sex = Men have a higher risk than women

Hormones = birth control pills and hormone therapies increases the risk

Literatur
https://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/syc-20350113

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427029/#:~:text=Traditionally%2C%20stroke%20has%20been%20classified,and%20thrombotic%20(ischemic)%20stroke.

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Overview

What is a stroke? A Mayo Clinic expert explains

Learn more from neurologist Robert D. Brown, Jr. M.D., M.P.H.

I'm Dr. Robert Brown, neurologist at Mayo Clinic. In this video, we'll cover the basics of a stroke. What is it, who it happens to, the symptoms, diagnosis, and treatment. Whether you're looking for answers for yourself or someone you love, we're here to give you the best information available. You've likely heard the term stroke before. They affect about 800,000 people in the United States each year. Strokes happen in two ways. In the first, a blocked artery can cut off blood to an area of the brain. And this is known as an ischemic stroke. 85% of strokes are of this type. The second type of stroke happens when a blood vessel can leak or burst. So the blood spills into the brain tissue or surrounding the brain. And this is called a hemorrhagic stroke. Prompt treatment can reduce brain damage and the likelihood of death or disability. So if you or someone you know is experiencing a stroke, you should call 911 and seek emergency medical care right away.

Anyone can have a stroke, but some things put you at higher risk. And some things can lower your risk. If you're 55 and older, if you're African-American, if you're a man, or if you have a family history of strokes or heart attacks, your chances of having a stroke are higher. Being overweight, physically inactive, drinking alcohol heavily, recreational drug use. Those who smoke, have high blood pressure or high cholesterol, have poorly controlled diabetes, suffer from obstructive sleep apnea, or have certain forms of heart disease are at greater risk as well.

Look for these signs and symptoms if you think you or someone you know is having a stroke: Sudden trouble speaking and understanding what others are saying. Paralysis or numbness of the face, arm or leg on one side of the body. Problems seeing in one or both eyes, trouble walking, and a loss of balance. Now many strokes are not associated with headache, but a sudden and severe headache can sometimes occur with some types of stroke. If you notice any of these, even if they come and go or disappear completely, seek emergency medical attention or call 911. Don't wait to see if symptoms stop, for every minute counts.

Once you get to the hospital, your emergency team will review your symptoms and complete a physical exam. They will use several tests to help them figure out what type of stroke you're having and determine the best treatment for the stroke. This could include a CT scan or MRI scan, which are pictures of the brain and arteries, a carotid ultrasound, which is a soundwave test of the carotid arteries which provide blood flow to the front parts of the brain, and blood tests.

Once your doctors can determine if you're having an ischemic or hemorrhagic stroke, they'll be able to figure out the best treatment. If you're suffering an ischemic stroke, it's important to restore blood flow to your brain as quickly as possible, providing the oxygen and other nutrients your brain cells need to survive. To do this, doctors may use an intravenous clot buster medicine, dissolving the clot that is obstructing the blood flow or they may perform an emergency endovascular procedure. This involves advancing a tiny plastic tube called a catheter up into the brain arteries, allowing the blockage in the artery to be removed directly. Unlike ischemic strokes, the goal for treating a hemorrhagic stroke is to control the bleeding and reduce pressure in the brain. Doctors may use emergency medicines to lower the blood pressure, prevent blood vessel spasms, encourage clotting and prevent seizures. Or, if the bleeding is severe, surgery may be performed to remove the blood that is in the brain.

Every stroke is different, and so every person's road to recovery is different. Management of a stroke often involves a care team with several specialties. This may include a neurologist and a physical medicine and rehabilitation physician, among others. Now, in the end, our goal is to help you recover as much function as possible so that you can live independently. A stroke is a life-changing event that can affect you emotionally as much as it can physically. You may feel helpless, frustrated, or depressed. So look for help and support from friends and family. Accept that recovery will take hard work and most of all time. Strive for a new normal and remember to celebrate your progress. If you'd like to learn even more about strokes, watch our other related videos or visit mayoclinic.org. We wish you all the best.

An ischemic stroke occurs when the blood supply to part of the brain is blocked or reduced. This prevents brain tissue from getting oxygen and nutrients. Brain cells begin to die in minutes. Another type of stroke is a hemorrhagic stroke. It occurs when a blood vessel in the brain leaks or bursts and causes bleeding in the brain. The blood increases pressure on brain cells and damages them.

A stroke is a medical emergency. It's crucial to get medical treatment right away. Getting emergency medical help quickly can reduce brain damage and other stroke complications.

The good news is that fewer Americans die of stroke now than in the past. Effective treatments also can help prevent disability from stroke.

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Symptoms

If you or someone you're with may be having a stroke, pay attention to the time the symptoms began. Some treatments are most effective when given soon after a stroke begins.

Symptoms of stroke include:

Trouble speaking and understanding what others are saying. A person having a stroke may be confused, slur words or may not be able to understand speech.

Numbness, weakness or paralysis in the face, arm or leg. This often affects just one side of the body. The person can try to raise both arms over the head. If one arm begins to fall, it may be a sign of a stroke. Also, one side of the mouth may droop when trying to smile.

Problems seeing in one or both eyes. The person may suddenly have blurred or blackened vision in one or both eyes. Or the person may see double.

Headache. A sudden, severe headache may be a symptom of a stroke. Vomiting, dizziness and a change in consciousness may occur with the headache.

Trouble walking. Someone having a stroke may stumble or lose balance or coordination.

When to see a doctor

Seek immediate medical attention if you notice any symptoms of a stroke, even if they seem to come and go or they disappear completely. Think "FAST" and do the following:

Face. Ask the person to smile. Does one side of the face droop?

Arms. Ask the person to raise both arms. Does one arm drift downward? Or is one arm unable to rise?

Speech. Ask the person to repeat a simple phrase. Is the person's speech slurred or different from usual?

Time. If you see any of these signs, call 911 or emergency medical help right away.

Call 911 or your local emergency number immediately. Don't wait to see if symptoms stop. Every minute counts. The longer a stroke goes untreated, the greater the potential for brain damage and disability.

If you're with someone you suspect is having a stroke, watch the person carefully while waiting for emergency assistance.

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Causes

There are two main causes of stroke. An ischemic stroke is caused by a blocked artery in the brain. A hemorrhagic stroke is caused by leaking or bursting of a blood vessel in the brain. Some people may have only a temporary disruption of blood flow to the brain, known as a transient ischemic attack (TIA). A TIA doesn't cause lasting symptoms.

Ischemic stroke

This is the most common type of stroke. It happens when the brain's blood vessels become narrowed or blocked. This causes reduced blood flow, known as ischemia. Blocked or narrowed blood vessels can be caused by fatty deposits that build up in blood vessels. Or they can be caused by blood clots or other debris that travel through the bloodstream, most often from the heart. An ischemic stroke occurs when fatty deposits, blood clots or other debris become lodged in the blood vessels in the brain.

Some early research shows that COVID-19 infection may increase the risk of ischemic stroke, but more study is needed.

Hemorrhagic stroke

Hemorrhagic stroke occurs when a blood vessel in the brain leaks or ruptures. Bleeding inside the brain, known as a brain hemorrhage, can result from many conditions that affect the blood vessels. Factors related to hemorrhagic stroke include:

High blood pressure that's not under control.

Overtreatment with blood thinners, also known as anticoagulants.

Bulges at weak spots in the blood vessel walls, known as aneurysms.

Head trauma, such as from a car accident.

Protein deposits in blood vessel walls that lead to weakness in the vessel wall. This is known as cerebral amyloid angiopathy.

Ischemic stroke that leads to a brain hemorrhage.

A less common cause of bleeding in the brain is the rupture of an arteriovenous malformation (AVM). An AVM is an irregular tangle of thin-walled blood vessels.

Transient ischemic attack

A transient ischemic attack (TIA) is a temporary period of symptoms similar to those of a stroke. But a TIA doesn't cause permanent damage. A TIA is caused by a temporary decrease in blood supply to part of the brain. The decrease may last as little as five minutes. A transient ischemic attack is sometimes known as a ministroke.

A TIA occurs when a blood clot or fatty deposit reduces or blocks blood flow to part of the nervous system.

Seek emergency care even if you think you've had a TIA. It's not possible to tell if you're having a stroke or TIA based only on the symptoms. If you've had a TIA, it means you may have a partially blocked or narrowed artery leading to the brain. Having a TIA increases your risk of having a stroke later.

Risk factors

Many factors can increase the risk of stroke. Potentially treatable stroke risk factors include:

Lifestyle risk factors

Being overweight or obese.

Physical inactivity.

Heavy or binge drinking.

Use of illegal drugs such as cocaine and methamphetamine.

Medical risk factors

High blood pressure.

Cigarette smoking or secondhand smoke exposure.

High cholesterol.

Diabetes.

Obstructive sleep apnea.

Cardiovascular disease, including heart failure, heart defects, heart infection or irregular heart rhythm, such as atrial fibrillation.

Personal or family history of stroke, heart attack or transient ischemic attack.

COVID-19 infection.

Other factors associated with a higher risk of stroke include:

Age - People age 55 or older have a higher risk of stroke than do younger people.

Race or ethnicity - African American and Hispanic people have a higher risk of stroke than do people of other races or ethnicities.

Sex - Men have a higher risk of stroke than do women. Women are usually older when they have strokes, and they're more likely to die of strokes than are men.

Hormones - Taking birth control pills or hormone therapies that include estrogen can increase risk.

Complications

A stroke can sometimes cause temporary or permanent disabilities. Complications depend on how long the brain lacks blood flow and which part is affected. Complications may include:

Loss of muscle movement, known as paralysis. You may become paralyzed on one side of the body. Or you may lose control of certain muscles, such as those on one side of the face or one arm.

Trouble talking or swallowing. A stroke might affect the muscles in the mouth and throat. This can make it hard to talk clearly, swallow or eat. You also may have trouble with language, including speaking or understanding speech, reading or writing.

Memory loss or trouble thinking. Many people who have had strokes experience some memory loss. Others may have trouble thinking, reasoning, making judgments and understanding concepts.

Emotional symptoms. People who have had strokes may have more trouble controlling their emotions. Or they may develop depression.

Pain. Pain, numbness or other feelings may occur in the parts of the body affected by stroke. If a stroke causes you to lose feeling in the left arm, you may develop a tingling sensation in that arm.

Changes in behavior and self-care. People who have had strokes may become more withdrawn. They also may need help with grooming and daily chores.

Prevention

You can take steps to prevent a stroke. It's important to know your stroke risk factors and follow the advice of your healthcare professional about healthy lifestyle strategies. If you've had a stroke, these measures might help prevent another stroke. If you have had a transient ischemic attack (TIA), these steps can help lower your risk of a stroke. The follow-up care you receive in the hospital and afterward also may play a role.

Many stroke prevention strategies are the same as strategies to prevent heart disease. In general, healthy lifestyle recommendations include:

Control high blood pressure, known as hypertension. This is one of the most important things you can do to reduce your stroke risk. If you've had a stroke, lowering your blood pressure can help prevent a TIA or stroke in the future. Healthy lifestyle changes and medicines often are used to treat high blood pressure.

Lower the amount of cholesterol and saturated fat in your diet. Eating less cholesterol and fat, especially saturated fats and trans fats, may reduce buildup in the arteries. If you can't control your cholesterol through dietary changes alone, you may need a cholesterol-lowering medicine.

Quit tobacco use. Smoking raises the risk of stroke for smokers and nonsmokers exposed to secondhand smoke. Quitting lowers your risk of stroke.

Manage diabetes. Diet, exercise and losing weight can help you keep your blood sugar in a healthy range. If lifestyle factors aren't enough to control blood sugar, you may be prescribed diabetes medicine.

Maintain a healthy weight. Being overweight contributes to other stroke risk factors, such as high blood pressure, cardiovascular disease and diabetes.

Eat a diet rich in fruits and vegetables. Eating five or more servings of fruits or vegetables every day may reduce the risk of stroke. The Mediterranean diet, which emphasizes olive oil, fruit, nuts, vegetables and whole grains, may be helpful.

Exercise regularly. Aerobic exercise reduces the risk of stroke in many ways. Exercise can lower blood pressure, increase the levels of good cholesterol, and improve the overall health of the blood vessels and heart. It also helps you lose weight, control diabetes and reduce stress. Gradually work up to at least 30 minutes of moderate physical activity on most or all days of the week. The American Heart association recommends getting 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous aerobic activity a week. Moderate intensity activities can include walking, jogging, swimming and bicycling.

Drink alcohol in moderation, if at all. Drinking large amounts of alcohol increases the risk of high blood pressure, ischemic strokes and hemorrhagic strokes. Alcohol also may interact with other medicines you're taking. However, drinking small to moderate amounts of alcohol may help prevent ischemic stroke and decrease the blood's clotting tendency. A small to moderate amount is about one drink a day. Talk to your healthcare professional about what's appropriate for you.

Treat obstructive sleep apnea (OSA). OSA is a sleep disorder that causes you to stop breathing for short periods several times during sleep. Your healthcare professional may recommend a sleep study if you have symptoms of OSA. Treatment includes a device that delivers positive airway pressure through a mask to keep the airway open while you sleep.

Don't use illicit drugs. Certain illicit drugs such as cocaine and methamphetamine are established risk factors for a TIA or a stroke.

Preventive medicines

If you have had an ischemic stroke, you may need medicines to help lower your risk of having another stroke. If you have had a TIA, medicines can lower your risk of having a stroke in the future. These medicines may include:

Anti-platelet drugs. Platelets are cells in the blood that form clots. Anti-platelet medicines make these cells less sticky and less likely to clot. The most commonly used anti-platelet medicine is aspirin. Your healthcare professional can recommend the right dose of aspirin for you.

If you've had a TIA or minor stroke, you may take both an aspirin and an anti-platelet medicine such as clopidogrel (Plavix). These medicines may be prescribed for a period of time to reduce the risk of another stroke. If you can't take aspirin, you may be prescribed clopidogrel alone. Ticagrelor (Brilinta) is another anti-platelet medicine that can be used for stroke prevention.

Blooding-thinning medicines, known as anticoagulants. These medicines reduce blood clotting. Heparin is a fast-acting anticoagulant that may be used short-term in the hospital.

Slower acting warfarin (Jantoven) may be used over a longer term. Warfarin is a powerful blood-thinning medicine, so you need to take it exactly as directed and watch for side effects. You also need regular blood tests to monitor warfarin's effects.

Several newer blood-thinning medicines are available to prevent strokes in people who have a high risk. These medicines include dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis) and edoxaban (Savaysa). They work faster than warfarin and usually don't require regular blood tests or monitoring by your healthcare professional. These medicines also are associated with a lower risk of bleeding complications compared to warfarin.

Stroke care at Mayo Clinic

Show references

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# data[].attributes.attachment_link.description
Promptly spotting stroke symptoms leads to faster treatment and less damage to the brain.

# data[].attributes.body
Definition:
A persistend elevated blood pressure above 140/90 mmHg resulting from either an elevated cardiac output, elevated peripheral vascular resistance, or a combination of both.

Diagnosis:
Blood pressure measuring: At least three measurements should be made on each of several days, with 1–2 minutes between measurements and with a 3–5 minute pause before blood pressure is measured with the patient sitting for some time before the measurement. Some additional factors should be considered aswell, for example no caffeine should be consumed prior. Additionally a 24hr measurement can be conducted and the patient should measure his blood pressure at home regularly.

Risk Factors:
-positive family anamnesis
-other cardiovascular diseases
-male sex
-higher age
-high salt intake
-high alcohol intake
-high saturated and trans fat intake
-smoking
-obesity
-hyperuricemia
-high blood cholesterol
-sedentary lifestyle

Symptomps:
often none or only starting with a severe hypertension
-headaches
-dizziness
-chest pain
-difficulty breathing
-nausea
-nose bleeding

Non-nutritional treatment:
blood pressure medicines like
ACE-inhibitors
Angiotensin-2-receptor blockers
Calcium channel blockers
Diuretics

Sources:
https://www.aerzteblatt.de/int/archive/article/199598
https://www.who.int/news-room/fact-sheets/detail/hypertension

# data[].attributes.body
Definition:
Lipid metabolism disorders are conditions that involve disturbances in the synthesis, transport, utilization, or clearance of lipids in the body, leading to abnormal lipid levels in the blood.

Diagnosis:
The diagnosis of a lipid metabolism disorder is typically made through a combination of medical history assessment, physical examination, and laboratory tests. Blood tests are performed to measure lipid levels, including total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides. Genetic testing may also be conducted in some cases to identify specific genetic mutations associated with certain lipid disorders.

Symptoms:
Lipid metabolism disorders may not always present with specific symptoms. However, individuals with severe or uncontrolled lipid disorders may experience symptoms such as:

1. Xanthomas: Yellowish deposits of cholesterol under the skin, commonly found on the eyelids, elbows, knees, or buttocks.

2. Xanthelasma: Yellowish plaques around the eyelids.

3. Pancreatitis: Inflammation of the pancreas, which can cause abdominal pain.

4. Chest pain or angina.

5. Symptoms of peripheral artery disease, such as leg pain or numbness during physical activity.

6. Fat deposits in the tendons and joints, leading to tendonitis or joint pain.

Classification:
Lipid metabolism disorders can be classified into several types, including:

1. Hypercholesterolemia: High levels of LDL cholesterol in the blood.

2. Hypertriglyceridemia: High levels of triglycerides in the blood.

3. Mixed hyperlipidemia: Elevated levels of both LDL cholesterol and triglycerides.

4. Familial hypercholesterolemia: A genetic disorder characterized by high LDL cholesterol levels.

5. Familial combined hyperlipidemia: Elevated levels of both LDL cholesterol and triglycerides, often with a family history of lipid disorders.

6. Dysbetalipoproteinemia: Abnormal levels of beta-lipoproteins in the blood.

Risk factors:
Several factors can increase the risk of developing a lipid metabolism disorder, including:

1. Genetics: Certain lipid disorders have a strong genetic component and may be inherited from parents.

2. Diet: Consumption of a diet high in saturated fats, trans fats, and cholesterol can contribute to abnormal lipid levels.

3. Obesity: Excess body weight, particularly abdominal obesity, can disrupt lipid metabolism.

4. Sedentary lifestyle: Lack of physical activity can affect lipid metabolism and lead to imbalances.

5. Diabetes: Poorly controlled diabetes can adversely affect lipid levels.

6. Hypothyroidism: Underactive thyroid function can impact lipid metabolism.

7. Certain medications: Some medications, such as certain types of antipsychotics, immunosuppressants, and diuretics, can influence lipid levels.