Block 3 (everything)

The three phases of swallowing are:

1. Oral phase
2. Pharyngeal phase (involves the glossopharyngeal nerve)
3. Oesophageal phase

The gastroesophageal sphincter muscle prevents acid reflux. If there is a problem with this muscle, it can lead to acid reflux (heartburn), where gastric juice enters the oesophagus, potentially damaging the mucosa and leading to conditions like oesophageal cancer.

Chief cells in the stomach produce pepsinogen, which is an inactive precursor of the enzyme pepsin.

The stomach produces 2.5-3.5 liters of gastric juice per day, which is strongly acidic with a pH range of 1.5-3.

Damage to parietal cells can lead to macrocytic anemia, vitamin B12 deficiency, and a lack of intrinsic factor, which is essential for vitamin B12 absorption.

HCL activates pepsinogen, converting it to pepsin, which digests proteins. It is stimulated by gastrin, histamine, the vagus nerve, Ach, stomach stretching, and amino acids.

Gastrin, produced by G-cells, increases HCL production, enhances blood flow to the stomach, promotes pepsinogen production, increases digestive motility, and stimulates cell division in the stomach lining.

Gastrin production is stimulated by GRP, the vagus nerve (Ach), stomach stretching, and amino acids. It is inhibited by somatostatin and low pH as negative feedback.

The gastrocolic reflex is a physiological response that increases colon motility when the stomach stretches after eating. It is particularly strong in toddlers and dogs, helping to make room for food intake.

Secretin decreases HCL production in the stomach and increases bicarbonate release in pancreatic juice, making it alkaline. It also raises bicarbonate concentration in bile and regulates chloride ion channels.

CCK has several functions:

1. Inhibits gastric emptying
2. Relaxes the sphincter of Oddi
3. Stimulates pancreatic enzyme production
4. Promotes secretin functions
5. Enhances digestive motility of the small intestine
6. Induces satiety in the CNS.

CCK is mainly stimulated by lipids, followed by proteins and carbohydrates. It plays a crucial role in the enterogastric inhibitory reflex, which helps regulate gastric emptying when high osmolarity acidic chyme enters the duodenum.

Lipid-rich food stays in the stomach the longest because CCK, which is stimulated by lipids, inhibits gastric emptying, allowing more time for digestion and neutralization in the duodenum.

GIP decreases gastrin production, decreases HCl in the stomach, decreases digestive motility of the stomach, increases insulin production, and decreases blood flow to the stomach. It is secreted by the duodenum.

GRP is released by the parasympathetic ganglion fibers and increases gastrin production.

Motilin is a key hormone of interdigestive motility that activates the migrating myoelectric complex (MMC), stimulates gastric emptying, and increases interdigestive motility. It is important for cleaning the stomach and small intestines and removing bacteria.

The main function of the respiratory system is to provide oxygen to the tissues and remove carbon dioxide.

Minute ventilation is calculated as:

Minute ventilation = Tidal volume × respiration rate.

Alveolar ventilation is the total volume of new air entering the alveoli each minute. It is calculated as:

Alveolar ventilation = (Tidal volume – dead space) × respiration rate.

Tidal volume (TV) is the volume of air inspired or expired with each normal breath. The normal value is about 500 mL.

Inspiratory reserve volume (IRV) is the extra volume of air that can be inspired over and above the normal tidal volume at inspiration with full force. The normal value is about 2500 mL.

Expiratory reserve volume (ERV) is the maximum extra volume of air that can be expired forcefully after the end of a normal tidal expiration. The normal value is about 1000 mL.

Residual volume (RV) is the volume of air that remains in the lungs after the most forceful expiration. The normal value is approximately 1500 mL.

Inspiratory capacity is the amount of air a person can breathe in, beginning at the normal expiration level and distending the lungs to the maximum amount. It is calculated as:

IC = TV + IRV

The normal value is approximately 3000 mL.

Functional reserve capacity (FRC) is the amount of air that remains in the lungs at the end of normal expiration. It is calculated as:

FRC = ERV + RV

The normal value is approximately 2500 mL.

Vital capacity (VC) is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent. It is calculated as:

VC = IRV + TV + ERV

The normal value is about 4000 mL on average, usually 3100 mL in women and 4600 mL in healthy males.

Total lung capacity (TLC) is the maximum volume to which the lungs can be expanded with the greatest possible effort. It is calculated as:

TLC = VC + RV

The normal value in healthy adults is around 5500 mL.

Residual volume (RV)

Total lung capacity

Functional residual capacity (FRC)

Minimal air

Inspiratory capacity (IC)

VC = IC + ERV; where IC = IRV + TV and ERV = FRC - RV. Therefore, VC = 4L + 1L = 5L.

True

False. IC = TLC - FRC.

True.

The volume exhaled during the first second of forced expiratory movement started from the level of lung capacity.

Tiffeneau index = FEV1/FVC x 100.

The normal value is higher than 70%, with an optimal value above 80%.

First, calculate VC: VC = TLC - RV = 6L - 1L = 5L. Then, use the Tiffeneau index formula: 0.6 = FEV1/5L, thus FEV1 = 5L x 0.6 = 3L.

Residual volume (RV), total lung capacity (TLC), and functional residual capacity (FRC) cannot be measured by spirometer.

They can be measured by the helium dilution method.

Hutchinson's type spirometer is used for lung function examination.

Static examinations (for unhurried breathing) and dynamic examinations (for forced, rapid ventilation).

The main types of obstructive respiratory disorders include:

• Bronchial asthma
• Chronic bronchitis
• Emphysema

In obstructive respiratory disorders, the characteristic dynamic respiratory disturbance includes:

• Narrowed airways
• Increased airway resistance
• Main problem in expiration
• Decreased FEV1 in absolute value, leading to a decreased Tiffeneau index

In obstructive respiratory disorders, the residual volume (RV) is increased primarily due to the decreased expiratory reserve volume (ERV).

The main types of restrictive respiratory disorders include:

• Chest deformity
• Pulmonary fibrosis

In restrictive respiratory disorders, the characteristic changes in lung volumes include:

• Decreased Vital Capacity (VC)
• Decreased Total Lung Capacity (TLC)
• Decreased Inspiratory Capacity (IC)
• Decreased Relaxed Vital Capacity (RVC)
• Decreased Inspiratory Reserve Volume (IRV)
• Decreased Residual Volume (RV)
• Decreased FEV1

To imitate obstructive pulmonary disease in the lab, one could:

• Tape the spirometer tube and poke a hole through it.

To imitate restrictive pulmonary disease in the lab, one could:

• Place one belt over the chest and one belt over the abdomen of the test person.

This condition is considered obstructive disease due to the bronchoconstriction and inflammation of fluid in the bronchi/bronchioles.

Restrictive.

The equation for respiratory compliance is:

1/Respiratory compliance = 1/chest wall compliance + 1/pulmonary compliance

The dynamic lung function parameters include:

• Peak expiratory flow (PEF): L/min or L/sec, how fast you can exhale
• Peak inspiratory flow (PIF): L/min or L/sec, how fast you can inhale
• MEF75%: Maximal expiratory flow at 75% of vital capacity
• MEF50%: Maximal expiratory flow at 50% of vital capacity
• MEF25%: Maximal expiratory flow at 25% of vital capacity

The velocity of airflow can be determined by using a spirometer. The subject exhales forcefully after maximal inspiration, and the velocity of exhaled air is measured in relation to VC %. The velocity is highest when 20% of VC is exhaled, and it decreases gradually afterwards. The order of maximal expiratory flow is: MEF75% > MEF50% > MEF25%.

The flow measured at 50% and 25% of vital capacity (VC) is the best indicator of small airway diseases in an early reversible stage.

The different breathing patterns include:

• Apnoea: No breathing
• Apneusis: Prolonged inhalation and short exhalation (may stop during inhalation)
• Tachypnoea: High breathing rate
• Bradypnea: Low breathing rate
• Hyperventilation: Breathing more than needed
• Hypoventilation: Breathing less than needed

Hyperventilation causes a decrease in CO2 partial pressure in the blood, leading to hypocapnia and resulting in respiratory alkalosis.

Hyperventilation leads to low levels of H+ ions, causing plasma proteins to bind to calcium instead of H+, which results in decreased free calcium levels.

A common treatment is to have the patient breathe into a paper bag to 're-use' the CO2 they are exhaling.

The O2 partial pressure remains about normal because 98% of hemoglobin is already carrying oxygen, leaving no room for more oxygen transport, thus no hypoxia occurs.

Hypoventilation causes an increase in CO2 partial pressure, leading to hypercapnia and resulting in respiratory acidosis.

Hypoventilation increases the level of H+ ions, which leads to a higher concentration of free calcium in the blood.

The intrapleural pressure is always negative during a normal respiratory cycle, becoming more negative during inhalation and less negative during exhalation.

In the case of pneumothorax, the intrapleural pressure becomes positive, leading to lung collapse.

The Kussmaul breathing pattern is characterized by increased minute ventilation as a compensation for metabolic acidosis. It is often seen in conditions such as untreated diabetes mellitus (ketoacidosis), kidney failure, after consuming acidic substances (like cola), or in cases of severe diarrhoea.

The Cheyne-Stokes breathing pattern leads to an irregular breathing pattern with episodes of apnoea. It results in hypoventilation, which increases the CO2 partial pressure and consequently raises the concentration of hydrogen ions (H+).

The decreasing order of O2 partial pressure is as follows:

1. Atmospheric air pressure - 760 mmHg (21% O2)
2. Exhaled air
3. Alveolar air (350 ml alveolar air, 150 ml dead space)
4. Arterial blood (100-150 mmHg)
5. Venous blood

The decreasing order of CO2 partial pressure is as follows:

1. Venous blood (46 mmHg)
2. Capillaries
3. Arterial blood (40 mmHg)
4. Alveolar air (40 mmHg)
5. Exhaled air (35 mmHg)
6. Atmospheric air

CO2 is transported in the blood in three main forms:

• Bound to hemoglobin
• As bicarbonate
• In physically dissolved form

B: You are at sea level and in the arterial blood the O2 - partial pressure is 92 mmHg and the CO2 42 mmHg.

In the femoral vein, as CO2 can be transported as bicarbonate and the CO2 pressure is higher in veins.

The pulmonary artery.

The pulmonary vein.

Hyperventilation.

In the alveolar air (46 mmHg). Exhaled air is a mix of alveolar air and dead space, which contains very little CO2.

In exhaled air.

In exhaled air.

Because blood pressure is low, and the hydrostatic pressure of the capillaries in the pulmonary circulation is low.

The sympathetic nervous system, through epinephrine and norepinephrine, binds to B-2 adrenergic receptors in the lungs, leading to bronchodilation and decreased airway resistance during 'fight or flight' mode.

The parasympathetic nervous system releases acetylcholine via the vagus nerve, which binds to muscarinic acetylcholine receptors in the lungs.

The vagus nerve leads to bronchoconstriction, which increases airway resistance.

Surfactant reduces surface tension and keeps the alveoli open, preventing collapse.

Surfactant production begins in the 3rd trimester, specifically around week 24 of embryonic development.

Surfactant production is stimulated by the vagus nerve and glucocorticoids (stress hormones, e.g., cortisol).

A normal birth compresses the baby's head, causing stress that stimulates surfactant production. In a C-section, this stress is absent, potentially leading to lower surfactant levels and increased risk for the baby.

During inhalation, the surfactant layer becomes thinner.

During exhalation, the surfactant layer becomes thicker.

Surfactant is more important in small alveoli, as they have a higher tendency to collapse according to Laplace's law.

The Herring-Breuer reflex protects the lung from overfilling by initiating a response when the pulmonary tissues are stretched during inhalation. This stretch is detected by mechanoreceptors, which activate the sensory (afferent) vagus nerve. The vagus nerve inhibits the I-neurons in the medulla oblongata, leading to exhalation. During inhalation, the heart rate (HR) increases, and during exhalation, it decreases.

When the afferent vagus nerve is stimulated, the tidal volume decreases. This is because the vagus nerve inhibits the I-neurons, blocking breathing and resulting in a smaller tidal volume.

If the vagus nerve is cut (vagotomy), the tidal volume will increase. This is due to the removal of inhibition on the I-neurons, allowing for greater breathing capacity.

The primary stimulus for breathing is hypercapnia (increased CO2), while the secondary stimulus is hypoxia (decreased O2). The primary respiratory center is located in the medulla oblongata, where I-neurons are active during inhalation and E-neurons during exhalation.

The pneumotaxic center, located in the upper part of the pons, inhibits the apneustic center, which is located in the lower pons. This regulation helps control the rhythm and pattern of breathing.

The cortex can voluntarily change the respiratory breathing pattern, while the limbic system can affect breathing patterns based on emotions.

Cutting the brain in the middle of the pons would disrupt the normal regulation of breathing, likely leading to irregular or abnormal respiratory patterns due to the loss of coordination between the pneumotaxic and apneustic centers.

Hypercapnia stimulates breathing due to increased CO2 levels in the blood. In scenario A, inhaling 5% CO2 leads to hypercapnia, causing dyspnoea. In scenario B, a CO2 partial pressure of 45 mmHg indicates hypercapnia, stimulating breathing. In scenario C, a CO2 partial pressure of 52 mmHg in venous blood also indicates hypercapnia, leading to increased breathing effort.

The Valsalva manoeuvre involves forceful exhalation against a closed glottis, leading to positive intrapleural pressure. This results in:

1. Decreased venous return (almost zero)
2. Decreased stroke volume (SV)
3. Decreased cardiac output (CO)
4. Decreased blood pressure (BP), activating the pressor reflex, increasing heart rate (HR) and total peripheral resistance (TPR).

The Müller manoeuvre is performed by forced inspiration with a closed glottis, creating significant negative intrapleural pressure. This leads to:

1. Increased venous return
2. Decreased stroke volume (SV) due to increased wall tension (Frank-Starling law)
3. Decreased cardiac output (CO)
4. A weak radial pulse due to overstretch in the ventricular wall, affecting pump function.

Decreased blood pressure activates the pressor reflex, leading to an increase in heart rate (HR) and total peripheral resistance (TPR).

The pulse is very weak and may even disappear during the Valsalva/Müller manoeuvre.

Pulmonary compliance is the capability of the lungs and chest to distend under pressure, measured by the pulmonary volume change per unit pressure change. In the lab, it was measured using an isolated rat lung connected to a cmH2O pressure meter and a 10 ml syringe, where air was pushed into the lungs and the water level difference was recorded.

Lung compliance is decreased in cases of fibrosis, oedema, pneumonia, and atelectasis, while it is increased in emphysema.

The Donders model demonstrates the basic principles of human respiratory function, showing correlations between lung volumes, intrapleural pressure, and intrapulmonary pressure changes. It illustrates diaphragm function using an isolated heart-lung preparation.

Pneumothorax can be simulated in the Donders model by opening the valve of the plug of the Donders bell.

The GI tract is the passageway that includes the organs through which food and liquids travel when swallowed, digested, absorbed, and excreted as feces. The main organs include the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus, with the pancreas, gall bladder, and liver assisting in digestion.

The parasympathetic nervous system, primarily through the vagus nerve and sacral parasympathetic fibers, increases digestive motility, enhances gastrointestinal juice production, and increases blood flow to the gastrointestinal tract.

The sympathetic nervous system decreases digestive motility, reduces gastrointestinal juice production, and decreases blood flow to the gastrointestinal tract, which is important for sphincter constriction.

On average, we produce 1 liter of saliva per day. This amount can increase with food intake or decrease during fasting.

The primary functions of saliva include:

1. Digestion
2. Lubrication
3. Wash-out (taste buds)
4. Moistening (mucous)
5. Cleaning (teeth and tongue)
6. Antibacterial properties
7. Secretory functions (heavy metals)

Saliva contains:

• H2O
• Ions
• IgA (mucosal defense)
• Lysosome (antibacterial effect)
• Mucin
• Amylase (digests carbohydrates - polysaccharides)
• Lipase (small amount, digests lipids)

The pH of saliva is slightly acidic (alkaline) compared to blood pH, which ranges from 7.35 to 7.45.

Aldosterone is important for the reabsorption of sodium (Na2+) ions in saliva, which results in lower sodium concentration in saliva compared to blood plasma.

In saliva, the concentrations of sodium ([Na2+]) and chloride ([Cl-]) ions are less than in blood plasma, while potassium ([K+]), bicarbonate ([HCO3-]), hydrogen ([H+]), and cyanide ([CN-]) concentrations are greater in saliva than in blood plasma.

When the rate of salivation increases, there is less time for Na+ and Cl- reabsorption, and secretion of K+, HCO3-, F, and H+ ions. As a result, the ion concentrations in the blood plasma and saliva become more similar to each other.

Renin activates angiotensinogen to become angiotensin I, which plays a crucial role in regulating blood pressure and fluid balance.

1250 ml/minute

Somatostatin inhibits gastrin production, HCl secretion, anterior pituitary hormone production, insulin, glucagon, and VIP, leading to a higher pH of gastric juice.

In the stomach.

In the mouth.

In the cecum, as there are no enzymes present there.

There is no production of enzymes in the stomach, but the enzyme is swallowed to aid in carbohydrate digestion.

Gastric juice contains HCL, intrinsic factor, pepsin, gelatinase, chymosin, gastrin lipase, and mucin.

The cephalic phase is triggered by thinking about, seeing, smelling, or tasting food.

The gastric phase is the most important phase, producing more than 50% of gastric juice, stimulated by food entering the stomach and stretching of the gastric wall.

During the intestinal phase, chyme arrives in the duodenum, and a feedback mechanism regulates gastric juice production based on the chyme's components.

The primary function of pancreatic juice is to neutralize gastric juice entering the duodenum, and it has an alkaline pH around 8-8.9.

The hormone secretin regulates the bicarbonate secretion to the pancreatic juice and also regulates the chloride channels.

Pancreatic enzymes are produced in an inactive form to prevent them from digesting the pancreas itself, as their active forms have substrates in the pancreas.

Trypsinogen is activated in the duodenum to trypsin by enteropeptidase, and it is significant for protein digestion as it can activate other trypsinogen molecules.

Chymotrypsinogen is activated by trypsin to chymotrypsin, which is important for protein digestion.

Prophospholipase is activated by trypsin to phospholipase, which is important for phospholipid digestion.

Procarboxypeptidase is activated by trypsin to carboxypeptidase, and it is important for protein digestion.

Proelastase is activated by trypsin to elastase, which is important for the digestion of collagen and elastic tissues.

The active enzymes of the pancreas include:

• Lipase: lipid digestion
• Amylase: carbohydrate digestion
• DNA-ase: DNA digestion
• RNA-ase: RNA digestion

Trypsinogen is activated by enteropeptidase or trypsin.

In case of pancreatic failure, the clotting time and prothrombin time will increase due to Vitamin K deficiency, which is caused by the lack of fat absorption. This condition is associated with the disease called Jaundice.

The liver produces about 0.5-1L of bile per day, which is stored and concentrated in the gallbladder.

The different types of bile include:

Bile contains:

• H2O
• Bile pigments (e.g., bilirubin)
• Bile salts
• Lecithin (phospholipid)
• Cholesterol
• Triglycerides
• Mucin
• Electrolytes

The primary function of bile is the emulsification of lipids, which makes fats available for lipase action.

Bile pigments can be detected using Rosenbach's test, which involves:

1. Passing diluted bile through filter paper several times.
2. Allowing the paper to dry.
3. Applying a drop of nitric acid (HNO3) on top of the dried paper. As the HNO3 oxidizes bilirubin, colored rings develop in the order: green, blue, violet, red, and yellow.

After hemoglobin degradation in the spleen, indirect bilirubin, which is not water soluble, is transported to the liver by albumin. The liver then converts it to bilirubin diglucuronide, making it water soluble.

In the case of a bile duct obstruction (bilestone):

• The color of the feces will be lighter.
• The level of urobilinogen in the urine will be lower.
• The concentration of bilirubin in the blood will increase.

Vagus nerve, histamine, and gastrin.

A reflex which stretches the stomach and makes room for food in the stomach.

1 primary peristaltic movement, and several secondary peristaltic movements.

3-10 seconds, depending on how solid the bolus is.

Secretin, GIP (Gastrin inhibitory peptide), CCK (cholecystokinin), Somatostatin, VIP.

Chloride channels.

By increasing the secretion of bicarbonate, which is a base, secretin can increase the bicarbonate concentration. It also works on the chloride channels, lowering chloride ion concentration in the pancreas.

Similar.

The small intestine juice has a pH of about 7.5-8 and a daily volume of approximately 1.8 L.

Enteropeptidase activates trypsinogen and is especially important in protein digestion.

Brush border enzymes finish the digestion of polysaccharides and polypeptides, which cannot be absorbed until fully digested.

In the proximal part, folate, calcium (Ca2+), iron (Fe2+), sugar molecules (glucose, fructose), and amino acids are absorbed.

In the middle part (jejunum), fat-soluble vitamins (A, D, E, K) and long-chain lipids are absorbed, while short-chain lipids go directly to the bloodstream.

The distal part (ileum) is primarily responsible for the absorption of vitamin B12 and the early absorption of bile pigments and bile salts.

The large intestine juice constitutes about 0.2 L per day and has a pH of approximately 7.5-8.

The main functions of the large intestine include water absorption, electrolyte absorption, feces storage, and vitamin production (such as vitamin K and B by bacteria).

The normal daily amount of feces is 60-250 g per day, with a water content of 100-150 ml/day.

In the proximal large intestine, there are both peristaltic movements (towards the anus) and antiperistalsis movements (towards the oral cavity). From the transverse colon to the sigmoid colon, only peristaltic movements occur.

The three nerve systems involved in the defecation reflex are:

1. Sacral parasympathetic fibers - Increases motility of the distal colon.
2. Sympathetic nervous system - Regulates the internal sphincter.
3. Somatic nervous system - Regulates the external anal sphincter.

Blood in the feces can be determined by:

• Black tarry feces indicating bleeding from the upper part of the digestive tract.
• Benzidine test: A small piece of feces mixed with acetic acid and ether, then combined with hydrogen peroxide; a dark green color indicates blood.
• FOBT test: Human hemoglobin in stool binds to monoclonal antibodies; two stripes (red and blue) indicate a positive test, while one blue stripe is negative, and one red stripe or no stripes means the test is invalid.

Basal gastric secretion (BAO) represents the amount of acid secreted by the stomach in one hour in the morning, without any stimulation. It is a reliable measure of the secretory function of gastric mucosa.

Maximal acid output (MAO) is the highest rate of gastric acid secretion that can be achieved in an individual after injection of gastric stimulant (gastrin, histamine, or histamine-like structures), usually Penta gastrin, which stimulates gastric acid secretion maximally in the same manner as gastrin.

MAO (Maximal Acid Output) indicates the total amount of hydrochloric acid produced in one hour after stimulation. There is a significant correlation between MAO and the number of parietal cells, suggesting that MAO can be considered a possible indicator of parietal cell quantity.

PAO (Peak Acid Output) is calculated as the sum of the two highest 15-minute fractions of maximal acid secretion. Its normal value is typically 10-12 mmol/30 min.

1. Introduce a gastric probe into the fasting patient's stomach and remove the gastric juice produced overnight, measuring its volume (normally 10-15 ml).

2. Titrate 10 ml of this gastric juice with 0.1 mol/L NaOH using phenol red as an indicator until the color changes from yellow to violet to determine HCl concentration.

3. Administer penta gastrin to stimulate gastric juice secretion after 1 hour.

4. Collect gastric juice every 15 minutes for 1 hour, measuring the volume of each fraction and titrating 10 ml aliquots.

BAO (Basal Acid Output) indicates the amount of H+ secreted in the stomach without any stimulating agent. Normal BAO is about 4 mmol/hour:

• BAO < 4 mmol/hour = hypacid gastric juice
• BAO > 4 mmol/hour = hyperacid gastric juice

Hypersecretion of gastric acidity, or hyperchlorhydria, is indicative of conditions such as duodenal ulcers (basal acidity > 20 mmol/l), Zollinger-Ellison syndrome (basal secretion > 30 mmol/l), and peptic ulcer.

Hyposecretion of gastric acidity (hypochlorhydria) or absence of gastric acidity (achlorhydria) is associated with hypochromic anemia, pernicious anemia, atrophic gastritis, and gastric carcinoma.

The BAO results can demonstrate the HCl content of night secretion, which helps in diagnosing various gastric conditions based on acidity levels.

Metabolism is the sum of energy and chemical substances occurring in a living organism. It is primarily measured through two methods: direct measurement, which involves a heat isolated room and measuring temperature changes, and indirect measurement, which relies on measuring O2 consumption.

The basal metabolic rate for women is 150 kJ/m² * h, which is 10% lower than that of men, which is 170 kJ/m² * h.

The normal oxygen energy/heat equivalent used in calculations is approximately 20 kJ/L, although it can vary between 19-21 kJ/L depending on dietary intake.

In indirect measurement, the metabolic rate is calculated using the formula: Metabolic rate = (O2 consumed per hour) × (O2 heat equivalent) / (body surface area). For example, if 1L of O2 is consumed in 3 minutes, the hourly consumption is 20L, which can be used in the calculation.

The metabolic rate is 300 kJ/m² x h, calculated from the oxygen consumption of 30 L in one hour.

The respiratory quotient (RQ) is calculated as RQ = produced CO2 / consumed O2.

The normal Body Mass Index (BMI) is between 19 and 25.

Body Mass Index (BMI) is calculated using the formula: BMI = body weight (kg) / height (m)².

The body mass index (BMI) is calculated as follows:

• BMI = weight (kg) / (height (m))^2
• BMI = 80kg / (2m)^2 = 20

This indicates that the patient is in the normal weight range.

The metabolic rate can be influenced by ambient temperature in the following ways:

• High ambient temperature: Increases metabolic rate due to the body's need to dissipate heat through sweating.
• Low ambient temperature: Also increases metabolic rate as the body needs to produce heat (e.g., through shivering).

Factors that can increase metabolic rate include:

In high ambient temperatures, the sympathetic nervous system (SNS) is activated to help the body cool down by:

• Activating sweat glands to promote sweating, which helps dissipate heat.
• Increasing the metabolic rate to support these physiological processes.

The metabolic rate increases because the body needs to produce heat to counteract the cold.

Protein increases the metabolic rate more than carbohydrates or lipid-rich food.

The metabolic rate increases the least during studying.

1. 12 hours fasting before examination
2. No physical exercise before and during examination
3. No medication before examination
4. No sleeping during examination
5. Patient should be laying down
6. Normal body temperature (no fever)
7. Thermoneutral ambient temperature

1. Conduction: Gaining or losing heat by touching something warm or hot.
2. Convection: Gaining or losing heat through cold weather or warm ambient temperature.
3. Radiation: Gaining or losing heat from the sun or radiating heat to a cold environment.
4. Evaporation: This method is used only to lose heat.

The main way to lose heat in a hot climate is through evaporation.

No, it is not possible for the body to gain and lose heat at the same time.

The kidneys consist of the renal parenchyma (cortex and medulla) and the renal sinus. The functional unit of the kidneys is the nephrons, which include the renal corpuscle and the renal tubules.

The renal corpuscle is located in the cortex and consists of the glomerulus (for filtration) and the Bowman's capsule (which has fenestrated epithelium).

The filtration layers in the kidneys include:

1. Fenestrated epithelium
2. Basement membrane with a negative charge
3. Podocyte layer (with nephrin in between)

The primary functions of the kidneys include:

• Excretion of waste products
• Endocrine function (producing erythropoietin, thrombopoietin, calcitriol, and renin)
• Regulation of water and electrolytes balance
• Regulation of arterial blood pressure
• Regulation of acid/base balance

RBF = RPF / (1 - Htc)

670 ml/minute

1 ml/min

120 - 125 ml/minute

0.2

The protein concentration; plasma has 60-80 g/L while primary filtrate has almost zero protein concentration.

Around 2 million nephrons

About 99% of the primary filtrate is reabsorbed.

Effective filtration pressure = hydrostatic pressure of glomerulus - colloid osmotic pressure of plasma - hydrostatic pressure of the Bowman's capsule

Dilation of the afferent arteriole increases effective filtration pressure because more blood can enter the glomerulus, raising the hydrostatic pressure.

Constriction of the efferent arteriole increases effective filtration pressure as more blood is trapped in the glomerulus, leading to more filtration.

In liver failure, the concentration of plasma proteins decreases, leading to lower colloid osmotic pressure and increased effective filtration pressure.

High intrarenal pressure, which indicates high pressure in the Bowman's capsule, decreases effective filtration pressure, resulting in less filtration.

The effective filtration pressure is highest close to the afferent arteriole due to the filtration of water and ions in the glomerulus, while plasma proteins remain in the blood.

Renal clearance refers to how quickly a particular substance is removed from the plasma by the kidney and excreted in urine. A high renal clearance indicates that the substance is quickly removed from the blood, while a low clearance indicates slower removal.

Inulin clearance is used to determine the glomerular filtration rate (GFR) because inulin is freely filtered and is neither reabsorbed nor secreted in the tubular segments. The amount filtered is reflected in the urine, making it a reliable measure of GFR.

Clearance is calculated using the formula:

Clearance = (UxV)/P

Where:

• U = concentration of the substance in the urine
• V = urine flow rate (1 ml/minute)
• P = concentration of the substance in the plasma

The normal filtration fraction is approximately 20%.

A glucose clearance of 0 ml/min indicates that glucose does not appear in the urine, meaning it is completely reabsorbed by the kidneys and not excreted.

Filtration fraction = GFR / RPF = Inulin clearance / PAH clearance. It represents the fraction of plasma that is filtered through the glomeruli into the renal tubules.

The fluid entering the proximal convoluted tubule is isosmotic, with an osmolarity of 280-300 mOsm/L, meaning its ion concentration is similar to that of blood plasma.

The primary active transporter in the proximal convoluted tubule is the Sodium-potassium ATPase (Na+/K+).

When plasma glucose exceeds the transport maximum of 9 mmol/L for the Na+/Glc cotransporter, glucose can appear in the urine, a condition known as glycosuria.

In untreated diabetes mellitus, glucose appears in urine due to the saturation of the Na+/Glc cotransporter, leading to osmotic diuresis.

The transport maximum of the Na+/Glc cotransporter is 9 mmol/L.

The Na+/phosphate cotransporter (1 Na+/1 Phosphate) facilitates the reabsorption of phosphate in the proximal convoluted tubule.

PTH injection increases urine phosphate concentration while decreasing phosphate concentration in blood plasma.

Na+/amino acid cotransporters reabsorb amino acids to prevent their loss in urine.

The Na+/H+ antiporter reabsorbs sodium and secretes hydrogen, which is important for bicarbonate reabsorption.

Angiotensin II stimulates sodium reabsorption and hydrogen secretion in the proximal convoluted tubule.

Aquaporin I, III, and IV facilitate water reabsorption in the proximal convoluted tubule and are ADH-independent.

Bicarbonate is reabsorbed indirectly in the proximal convoluted tubule.

The total concentration of Ca2+ in the proximal convoluted tubule is 1.25 mmol/L, with 50% bound to plasma proteins.

The Na+/Glc antiporter and Aquaporin II are not present in the proximal convoluted tubules.

The osmolarity doesn't change because the same ratio of water and ions is reabsorbed.

The concentration of urea increases because more water (2/3) is reabsorbed than urea, leading to a higher concentration of urea in the tubular fluid.

Urine phosphate concentration increases (phosphaturia) while plasma phosphate concentration decreases, as phosphate is excreted in urine.

Urine volume will increase due to inhibited reabsorption of Na+, K+, and 2x Cl-, leading to decreased blood volume and blood pressure.

About 2/3 of Ca2+ is reabsorbed in the distal convoluted tubule, which is stimulated by PTH (parathyroid hormone).

Injecting Thiazide increases urine volume, while blood volume and blood pressure decrease.

Injecting PTH results in a decrease in urine calcium concentration and an increase in plasma calcium concentration.

ADH is produced in the hypothalamus, specifically in the supraoptic and paraventricular nuclei, and is transported to the posterior pituitary gland via axonal transport.

ADH has two main functions: it promotes water reabsorption in the kidneys and helps regulate blood pressure by constricting blood vessels.

V1 receptors mediate the vasoconstrictor effect of ADH, which increases total peripheral resistance (TPR) and consequently raises blood pressure.

ADH makes the collecting ducts water permeable by placing aquaporin II molecules on the luminal surface, allowing for water reabsorption and conservation.

In the absence of ADH, a large amount of diluted urine is produced.

ADH production is stimulated by:

1. High osmolarity of the blood
2. Angiotensin II
3. Low blood volume and low blood pressure
4. Stress
5. Pain
6. Nausea

ADH production is inhibited by:

• Alcohol
• Coffee (sometimes)

In central diabetes insipidus, there is no production or release of ADH. In nephrogenic diabetes insipidus, ADH is present but the kidneys are not sensitive to it, leading to excessive urine production (about 15 L a day).

Nephrogenic diabetes insipidus is more severe because, although ADH is present, the kidneys do not respond to it. In contrast, central diabetes insipidus can be treated with intranasal ADH.

ANP is produced by the atrium when there is a stretch in the atrial wall, which occurs when blood volume is increased.

Aldosterone increases sodium reabsorption and increases potassium and hydrogen ion secretion in the collecting ducts.

After aldosterone injection, sodium concentration decreases ([Na+] ↓), while potassium ([K+] ↑) and hydrogen ion concentrations ([H+] ↑) increase in the urine.

Conn's syndrome, also known as primary aldosteronism, is a rare disease characterized by overproduction of aldosterone, leading to hypokalaemia and metabolic alkalosis. Patients typically have elevated blood pressure due to increased sodium reabsorption.

In high blood pressure, sodium reabsorption is increased, leading to water retention, which subsequently increases blood volume and blood pressure.

In Conn's syndrome, the plasma potassium concentration is decreased, resulting in hypokalaemia.

In Conn's syndrome, free calcium concentration decreases due to alkalosis, where plasma proteins bind to calcium instead of hydrogen ions, reducing free calcium levels.

Renin is a protease enzyme that converts angiotensinogen into angiotensin I by cutting ten amino acids from it, initiating the angiotensin-renin-aldosterone system.

Angiotensin II increases blood volume and blood pressure by:

1. Vasoconstriction (increases TPR)
2. Increasing thirst sensation
3. Increasing salt hunger
4. Increasing ADH production
5. Increasing Na+ reabsorption in the proximal convoluted tubule
6. Increasing aldosterone production
7. Reducing GFR (less is filtered, less is urinated)

Renin formation is stimulated by the sympathetic nervous system, particularly during low blood volume and low blood pressure conditions.

Concentration of Na+/Cl- detected by macula densa cells in the distal convoluted tubule, high intrarenal pressure, and low blood pressure in the afferent arteriole stimulate renin production.

Renin production can be increased by sympathetic activation (e.g., scare the patient) or by constricting the renal artery, which lowers blood pressure in the afferent arteriole.

Aldosterone acts in the collecting ducts of the kidneys, sweat glands, colon, saliva, and gallbladder.

When the atrial wall is stretched, indicating high blood volume, renin production decreases due to inhibition of the sympathetic nervous system.

Renin production increases after significant blood loss to help increase blood volume; blood pressure decreases, angiotensin II and aldosterone levels increase, while ANP decreases, ADH increases, urine volume decreases, and urine osmolarity increases.

Renin production decreases due to the brain perceiving high blood pressure (false signal), leading to inhibition of the sympathetic nervous system.

Hematocrit levels decrease in kidney failure due to reduced erythropoietin production, leading to decreased red blood cell formation and anemia.

In kidney failure, potassium concentration in the blood plasma typically increases due to the kidneys' reduced ability to excrete potassium.

In kidney failure, potassium levels in the blood increase due to the kidneys' inhibited ability to secrete potassium into the urine.

Creatinine levels in the blood plasma increase during kidney failure because the kidneys are unable to secrete creatinine effectively.

In kidney failure, calcitriol levels in the blood decrease because the final step of its synthesis occurs in the kidneys, which are not functioning properly.

In a hot climate with no fluid intake, blood volume and blood pressure decrease, while renin and aldosterone production increase. Angiotensin II production also increases, ADH increases, urine volume decreases, and urine osmolarity increases.

After drinking 1.5 L of water quickly, blood volume and blood pressure increase, urine volume increases, urine osmolarity decreases, and ANP, renin, angiotensin II, ADH, and aldosterone levels decrease.

Parathyroid hormone (PTH) increases blood plasma calcium concentration and reduces blood plasma phosphate concentration.

The normal pH of arterial blood is 7.35-7.45.

The main buffers in the blood are:

• Hemoglobin (140-180 g/L in males, 120-160 g/L in females)
• Plasma proteins (60-80 g/L)
• Bicarbonate (22-28 mmol/L)
• Phosphate (1 mmol/L)

The most important buffer in the blood is hemoglobin because it has the highest concentration and contains an imidazole group that can easily bind and release hydrogen ions.

A positive base excess (BE) indicates that there are more base (alkaline) molecules, such as HCO3-, in the blood.

In respiratory acidosis, the pH is low and the pCO2 is high.

In acute respiratory acidosis:

• pH is decreased (pH↓)
• pCO2 is increased (pCO2↑)
• Base excess (BE) is normal.

In chronic/compensated respiratory acidosis:

• If fully compensated, the pH can be normal.
• If partly compensated, the pH remains low (pH↓↓).

• pH: High (↑)
• pCO2: Low (↓)
• Base Excess (BE): Normal

• Fully compensated: pH is normal
• Partly compensated: pH is high (↑)
• pCO2: Low (↓)
• Base Excess (BE): Decreased (↓)

• pH: Low (↓)
• pCO2: Normal
• Base Excess (BE): Decreased (↓)

• Kussmaul breathing: A respiratory pattern used to compensate for metabolic acidosis.
• Fully compensated: pH is normal
• Partly compensated: pH is still low (↓)
• pCO2: Decreased (↓)
• Base Excess (BE): Decreased (↓)

• pH: High (↑)
• pCO2: Normal
• Base Excess (BE): Increased (↑)

Metabolic acidosis.

Respiratory alkalosis.

Respiratory acidosis.

Metabolic alkalosis.