75. Heartburn, eructation, nausea, vomiting.

Heartburn (pyrosis) – burning or heat feeling alongside oesophagus.

Its development can be delt with oesophagus receptors irritation at stomach content reflux to oesophagus. It can be caused by:

1. large amount of formed stomach juice;

2. cardial sphincter functional insufficiency.

Eructation is sudden inarbitrary gas releasing from stomach or oesophagus sometimes with stomach juice little portions.

Gases content in stomach can be caused by 2 reasons:

1. big gas amounts coming with food (drinking) (food with cellulose, aerated drink), gas swallowing (aerophagy);

2. gases formation in stomach especially at food prolonged lack in it (ulcer disease, gastric cancer).

Gases content increasing in stomach leads to intragastral pressure rising up. It cause by reflex:

1. stomach wall muscles contraction;

2. pylorospasm;

3. oesophageal-gastral sphincter muscles relaxation.

Consequent result – gases coming from stomach cavity to oesophagus, then pharynx and oral cavity.

Nausea – hard feeling in epigastral area, thorax and oral cavity sometimes followed by vomiting and often expressed in general weakness, sweat-releasing, hypersalivation, extremities coldness, skin palor, arterial pressure diminishing id est parasympathetic nervous system activation. Base – vomiting center activation (in medulla oblongata) but insufficient for vomiting appearance.

Vomiting – conditionally-reflectory act leading to stomach expulsion outside through mouth. Base: vomiting center excitement.

Types:

1. central – due to vomiting center excitability increasing; reasons: meningitis, encephalitis, brain tumors; at exciting impulses coming from brain cortex (conditionally-reflectory vomiting) or from labirhynthium receptors (vestibulary vomiting);

2. hematogenic-toxic – due to direct action of toxic substances in blood to vomiting center chemoreceptors: CO, alcohol, medicines, bacterial toxins or toxic products of own metabolism accumulating at uremia, renal insufficiency, decompensated diabetes mellitus;

3. visceral (reflectory) – from reflexogenic zones in stomach, pharyngeal mucosa, coronary vessels, peritoneum, biliary ducts.

76. Hepatic failure. Classification. Functional hepatic tests.

Hepatic failure – pathological state at which liver activity can not allow organism homeostasis constancy due to its recquirements.

1. a) relative –at primary load increasing to liver when organism recquirements of homeostasis support dominant over liver functional abilities;

b) absolute – at primary liver injury due to which its functional abilities are reduced and it can not support homeostasis constancy under normal conditions.

Relative insufficiency can be transformed into absolute one: load increasing to liver→releative insufficiency→homeostasis disorder→liver secondary injury→absolute insufficiency.

2. Dependently on injury reasons absolute insufficiency can be:

   1. hepato-cellular;

   2. cholestatic;

   3. hepatic-vascular.

3. Dependently on quantity of functions disturbed at liver injuries:

   1. total (all functions types are suffered);

   2. partial (one or several functions are injured).

4. By clinical course:

   1. acute;

   2. chronic.

Functional tests:

Proteinic exchange:

1. Total blood protein – hypoproteinemia <65 g/l.

2. Hypoalbuminemia <35-55 g/l.

3. Thymole probe more than 4 units. It reflects colloid resistance of blood and sharply positive at hypoalbuminemia (thymol sediments globulines); >expressed increasing is observed before bilirubin increasing in pre-jaundice period.

4. Albumine/globuline co-efficient (N=1,5-2,3) – less than 1,5 because of hypoalbuminmia.

5. NH₄ (ammonia) amount increasing in blood – hyperammmoniemia (N=21-47 mcmol/l) which leads to hepatic encephalopathy.

6. Urea (N=3,3-8,3 mmol/l) is decreased because of ATP decreasing.

7. Free aminoacids level in blood plasma is sharply increased because proteins are not synthesized and aminoacids decomposition is disordered→hyperaminoacidemia.

8. For cellular integrity assessment or cytolytic syndrome enzymatic diagnostics is applied: lactatedehydrogenase (LDG) more than N (N=4-5 units), AlAT ↑; AsAT ↑; gamma-glutamyltransferase. Hepatocytes have protein biosynthesis threshold as well as other functions. At hard insufficiency and hepatitis 8 enzymes levels are rised up.

Carbohydrate exchange:

1. Galactose probe: load with galactose 50 g -to detect galactosuria: under norm in 4 hours galactosuria must disappear – probe “-“ transforming in glucose and in glycogen; at hard form of hepatic insufficiency – probe will be still “+” in 4-24 hours.

2. Adrenaline probe (for glycogenoses diagnostics) allows to make differential diagnostics of hereditary glycogenoses: adrenaline is injected in antebrachium→phosphorylase increasing)→glucose level increasing (to determine in 30 min) (at hepatic insufficiency or negative probe); under physiological conditions glycogenolysis takes place, glucose level is unchanged and probe is “+”.

Lipid metabolism:

1. Phospholipids decreasing (N=2,0-4,6 mmol/l).

2.Alpha-lipoproteins (highly-densed) decreasing (N=1,5-4,5 g/l).

3. Cholesterol etherification occurs only in liver tha is why co-efficient which reflects free cholesterol correlation to etherificated noe reflects hepatic insufficiency. Free cholesterol does not reflext hepatic failure (because both cholesterol biosynthesis and its decomposition takes place in liver).