Metabolic acidosisis a process of:
- Accumulation and/or excess of non-respiratory H+.
- Deficiency of non-respiratory H+.
- Decresed CO2 partial pressure
- Increased CO2 partial pressure
- Increased bicarbonate concentration
Main pathogenetic mechanism for metabolic acidosis development is
- Excess production of H+ in the body.
- Decreased H+ excretion by kidneys.
- Increased bicarbonate production by kidneys.
- Activated Darrow– Kotlov mechanism
- 1, 2.
- 1, 3, 4.
Which process is characterized with accumulation of metabolic H+?
- Respiratory center depression.
- Diminished endogenous production of H+ donors.
- Exogenous intake of acid products.
- Reduced buffer capacity of extracellular space.
- Disturbed Starling equation.
- 3, 4
In which case the metabolic acidosis is NOT caused by increased production of H+?
- Diabetes mellitus
- Prolonged fasting.
- Renal failure.
- Acute intoxication.
- Shock.
- Severe hypoxia.
Hypoxic type lactic acidosis occurs when tissue pO2 falls:
- Under 70 mmHg
- Under 60 mmHg.
- Under 40 mmHg
- Under 20 mmHg.
- Under 10 mmHg.
- pO2 is not essential for lactic acidosis
Not-hypoxic lactic acidosis is most commonly observed in:
- Physical exercise.
- Enzyme defects in lactate metabolism.
- Hyperoxia.
- Respiratory acidosis.
- 1, 3.
Main pathogenetic unit in hypoalkaline metabolic acidosis is:
- Increased bicarbonate loss from extracellular space.
- Increased intracellular bicarbonates.
- Protein buffers deficiency.
- Disturbance in hemoglobin buffer system.
- Bicarbonates transfer into the cells.
Retention type metabolic acidosisis a result of:
- Retention of acid products.
- Impaired H+ secretory capacityof the kidney.
- Increased absorption of H+ ions.
- Development of renal H+ generator.
- 1, 2.
- 1, 3, 4.
Metabolic alkalosis is a process of:
- Accumulation and/or excess of non-respiratory H+
- H+ reduction and/or non-respiratory H+ deficiency.
- Cells and tissues H+ imbalance.
- Organic anions accumulation.
- Impaired hemoglobin buffering.
Main pathogenetic unit for metabolic alkalosis development is:
- Decreased bicarbonate concentration in extracellular space.
- Increased bicarbonate concentration in extracellular space.
- Bicarbonate transfer between cells and extracellular space.
- Decreased CO2 partial pressure.
- Increased CO2 partial pressure.
Main pathogenetic mechanism for metabolic alkalosis development is:
- Suppressed renal bicarbonate generation.
- Activated renal bicarbonate generation.
- Acids loss with subsequent chlor deficiency.
- 1, 2.
- 2, 3.
Trigger for metabolic alkalosis is:
- Synthesis or intake of bicarbonate.
- Increased renal bicarbonate affinity.
- Increased plasma-erythrocyte HCO3 translocation
- 1, 2.
- 1, 2, 3.
How can metabolic alkalosis be stabilized?
- Hypocapnia development.
- Compensatory glutamin lysis.
- Urea synthesis stimulation.
- Increased renal bicarbonate retention.
- Increased bicarbonate synthesis from monocyte-macrophage system.
How can metabolic alkalosis be divided?
- Hypoxic and non-hypoxic.
- Congenital and acquired.
- Calcium dependent andcalcium independent.
- Chlor dependent and chlor independent.
- Normo-, hypo- and hyperosmotic.
Which is the clinical breathing manifestations in metabolic alkalosis?
- Loud and deep breathing – Kussmaul’s respiration.
- Agonal breathing
- Slow and/ or shallow breathing.
- Biot’s respiration.
- Breathing is not changed.
What is the characteristic of respiratory acidosis?
- Decreased рСО2.
- Increased рСО2.
- Increased рО2.
- Decreased рО2.
- Decreased НbСО.
Main pathogenetic mechanism for respiratory acidosis development is:
- Alveolar hyperventilation.
- Alveolar hypoventilation.
- Disturbed gases diffusion in lungs.
- Isolated increase of CO2 production.
- 2, 4.
- 1, 3, 4.
Which of the followed does NOT lead to development of primary respiratory acidosis?
- Supressed respiratory center.
- Mechanical asphyxia.
- Inadequate dosed oxygen therapy.
- Airways spasm.
- Psycho-emotional excitement.
What is the compensation of respiratory acidosis?
- Tubular bicarbonate excretion.
- Activated tubular acid- and ammonia genesis.
- Activated ketone synthesis
- Suppressed ornithine cycle.
- Activated pentosephosphate cycle.
What is the characteristic of primary respiratory alkalosis?
- Increased bicarbonate level.
- Decreased bicarbonate level.
- Increased CO2 partial pressure.
- Decreased CO2 partial pressure.
- Mandatory presence of HbCO.
Main pathogenetic mechanism for respiratory alkalosis development is:
- Collateral alveolar ventilation.
- Alveolar hyperventilation.
- Alveolar hypoventilation.
- Decreased ventilation/perfussion ratio.
- Increased alveolar CO2 export.
What is the compensation of primary respiratory alkalosis?
- Hypercapnia development.
- Hypocapnia development.
- Chlorid deficiency development.
- Increased plasma bicarbonates.
- Decreased plasma bicarbonates.
What is the renal compensation of primary respiratory alkalosis?
- Decreased tubular H+ secretion.
- Increased tubular H+ secretion.
- Increased amino acid clearance.
- Activated renin-angiotensin system.
- Increased aldosteron effects.
Decreased plasma bicarbonate level in respiratory alkalosisis a result of:
- Supressed acido- and amonnia genesis.
- Hamburger’s effect.
- Increased cellular lactate production and secretion.
- 1, 2.
- 1, 2, 3.
Symptoms of "dizziness" and muscles tremor in respiratory alkalosis are associated with:
- Increased sodium level.
- Increased calcium level.
- Decreased sodium level.
- Decreased calcium level.
- Increased urea level.
The inadequacy in which processes leads to acid-base balance distublance?
- Production, transport and excretion of organic anions.
- Production, transport and excretion of lactate.
- Production, transport and excretion of electrolytes.
- Production, transport and excretion of CO2.
- Production, transport and excretion of H+.
The term “Hypoprotonemia”describes the presence of:
- Alkalosis.
- Bicarbonatemia.
- Alkalemia.
- Hyposmia.
- 1, 2, 3.
Which of the following is NOT a classification of acid-base disorders?
- Compensated, subcompensated and uncompensated.
- Mild, moderate, severe, life-threatening.
- Respiratory, metabolic, mixed.
- Local and general.
- Hereditary, congenital, acquired.
Neutralization of H+ excess /or deficiency/ in the extracellular space is achieved by:
- Extracellular buffering.
- Ion exchange in renal tubules.
- Metabolic transformations.
- Alterations of pulmonary ventilation.
- 1, 2, 3.
- 1, 2, 3, 4.
When an acid-base balanace disturbance can be definied as compensated?
- pH is in the references, but the other indexes are out if it.
- pH is out of the references, but the other indexes are normal.
- All the indexes are in the references.
- All the indexes are out of the references.
- All mentioned, but monitored in a timely manner.