The small and large intestinal walls are composed of the following common layers:
1. Mucosa
2. Submucosa
3. Muscularis Externa
4. Adventitia

Intestinal villi are highly vascular projections of the mucosal surface that cover the entire small intestinal mucosa. They increase the lumen’s surface area, which aids in absorption and digestion, the primary functions of the small intestine. Villi are large and most abundant in the duodenum and jejunum.

In both the small and large intestines, the muscularis mucosae are found within the mucosa. The myenteric nerve plexus is found innervating the muscularis externa. The mucosa is lined with columnar epithelial cells, and goblet cells may be present to secrete mucins.

The hormone parathyroid hormone (PTH) and the receptor parathyroid hormone type 1 (PTH1-Rc) are important regulators of blood calcium homeostasis.

PTH can cause a rapid release of calcium from the matrix in bone, but it also affects long-term calcium metabolism by acting directly on bone-forming osteoblasts (by binding to PTH1-Rc) and indirectly on bone-resorbing osteoclasts.

PTH causes changes in the synthesis and/or activity of several proteins, including osteoclast-differentiating factor, also known as TRANCE or RANKL, when it acts on osteoblasts.

RANK receptors are found on the cell surfaces of osteoclast precursors. The osteoclasts are activated when RANKL binds to the RANK receptors. Osteoclasts lack PTH receptors, whereas osteoblasts do. Osteoclasts are activated indirectly when the RANK receptor binds to the RANKL secreted by osteoblasts, resulting in bone resorption. PTH1 receptors are found in osteoclasts, but they are few.

PTH activates G-protein coupled receptors in all target cells via adenylate cyclase.

The PTH2 receptor is most abundant in the nervous system and pancreas, but it is not a calcium metabolism regulator. It is abundant in the septum, midline thalamic nuclei, several hypothalamic nuclei, and the dorsal horn of the spinal cord, as well as the cerebral cortex and basal ganglia. Expression in pancreatic islet somatostatin cells is the most prominent on the periphery.

The distribution of the receptor is being used to test functional hypotheses. It may play a role in pain modulation and hypothalamic releasing-factor secretion control.

Dystonia is characterised by repetitive twisting movements or abnormal postures. They are classified as either primary or secondary.

Primary dystonia is a genetic disorder that is inherited in an autosomal dominant pattern.
Secondary dystonia can be caused by focal brain lesions, Parkinson’s disease, or certain medications.

The following drugs cause the most common drug-induced dystonic reactions:
Antipsychotics, antiemetics (especially prochlorperazine and metoclopramide), and antidepressants.

Following the administration of the neuroleptic prochlorperazine, 16 percent of patients experience restlessness (akathisia) and 4% experience dystonia.

Several published reports have linked the anaesthetics thiopentone, fentanyl, and propofol to opisthotonos and other abnormal neurologic sequelae. Dystonias following a general anaesthetic are uncommon. Tramadol has been linked to serotonin syndrome, while remifentanil has been linked to muscle rigidity.

The following are some of the risk factors:

Positive family history
Male
Children
An episode of acute dystonia occurred previously.
Dopamine receptor (D2) antagonists at high doses and recent cocaine use

Dystonia is treated in a variety of ways, including:

Benztropine (as a first-line therapy):

1-2 mg intravenous injection for adults
Child: 0.02 mg/kg to 1 mg maximum

Benzodiazepines are a type of benzodiazepine (second line treatment).

Midazolam:

1-2 mg intravenously, or 5-10 mg IV/PO diazepam

Antihistamines with anticholinergic activity (H1receptor antagonists):

Promethazine 25-50 mg IV/IM, or diphenhydramine 50 mg IV/IM (1 mg/kg in children) are used when benztropine is not available.

The patient is likely suffering from biliary colic since her pain is intermittent and comes and goes in waves. Biliary colic pain gets worse after eating, especially fatty food as bile helps digest fats. Gallstones are the most common cause of biliary colic and are usually located in the cystic duct or common bile duct. But since this patient has no signs of jaundice or steatorrhea, the duct most likely blocked is the cystic duct.

The cystic duct drains the gallbladder and combines with the common hepatic duct to form the common bile duct. The common bile duct then merges with the pancreatic duct and opens into the second part of the duodenum (major duodenal papilla).

The duodenojejunal flexure is attached to the diaphragm by the ligament of Treitz and is not associated with any common pathology.
The fourth part of the duodenum passes very close to the abdominal aorta and can be compressed by an abdominal aortic aneurysm.
The third part of the duodenum can be affected by superior mesenteric artery syndrome, where the duodenum is compressed between the SMA and the aorta, often in cases of reduced body fat.
The first part of the duodenum is the most common location for peptic ulcers affecting this organ.

This patient has been shifted to a sulfonylurea drug whose most common side effect is hypoglycaemia. Similar symptoms can arise in a patient on insulin too. The signs and symptoms are consistent with a hypoglycaemic attack and include tachycardia, altered consciousness, and behaviour. This needs to be treated as an emergency with rapid correction of the blood glucose level using glucose or IV 20% dextrose.

In a hypoglycaemic attack, the body undergoes stress and releases hormones to increase blood glucose levels. These include:
Glucagon
Cortisol
Adrenaline

Adrenaline or epinephrine is the hormone responsible for this patient’s condition and is primarily produced in the medulla of the adrenal gland. It functions primarily to raise cardiac output and raise blood glucose levels in the blood.

Alpha-cells of the islets of Langerhans produce the hormone glucagon, which has opposing effects to insulin.

Follicular cells of the thyroid gland produce and secrete thyroid hormones. Thyroid hormones can cause similar symptoms, but it is unlikely with the patient’s medical history.

Post-ganglionic neurons of the sympathetic nervous system use norepinephrine as a neurotransmitter. Adrenaline can be made in these cells, but it is not their primary production site.

Zona fasciculata of the adrenal cortex is the main site for the production of cortisol.

The pH of CSF is 7.31 which is lower than plasma.

Compared to plasma, it has a lower concentration of potassium, calcium, and protein and a higher concentration of sodium, chloride, bicarbonate and magnesium.

CSF usually has no cells present but if white cells are present, there should be no more than 4/ml.

The pressure of CSF should be less than 20 cm of water.

The concentration of glucose is approximately two-thirds of that of plasma, and it has a concentration of approximately 3.3-4 mmol/L.

Unionised molecules are more likely than ionised molecules to cross membranes (such as the blood-brain barrier).

Because alfentanil and fentanyl are weak bases, the Henderson-Hasselbalch equation says that the ratio of ionised to unionised molecules is determined by the parent compound’s pKa in relation to physiological pH.

Alfentanil has a pKa of 6.5, while fentanyl has a pKa of 8.4.
At a pH of 7.4, 89 percent of alfentanil is unionised, whereas 9% of fentanyl is.

As a result, alfentanil has a faster onset than fentanyl.

Fentanyl is 83% plasma protein bound
Alfentanil is 90% plasma protein bound.

Alfentanil’s pharmacokinetics are affected by its higher plasma protein binding. Because alfentanil has a low hepatic extraction ratio (0.4), clearance is determined by the degree of protein binding rather than the time it takes to take effect.

Mid-shaft fractures of the humerus usually occur after a direct blow to the upper arm, which can occur after a fall or RTAs.
The most important clinical significance of a mid-shaft humeral fracture is an injury to the radial nerve. The radial nerve originates from the brachial plexus and has roots of C5-T1. It crosses the spiral groove on the posterior side of the shaft of the humerus.
On examination, the patient may have a wrist drop, loss or weakness of finger extension, and decreased or absent sensation to the posterior forearm, digits 1 to 3, and the radial half of the fourth digit.

The humeral shaft has two compartments:
1. Anterior:
Brachial artery and vein
Biceps brachii, brachialis, coracobrachialis
Musculocutaneous, median, and ulnar nerves
2. Posterior:
Radial nerve
Triceps

Other significant nerve injuries are:
1. Axillary nerve – surgical neck fracture of the humerus
2. Brachial Artery – supracondylar fracture of the humerus
3. Axillary artery – surgical neck fracture of the humerus, but is relatively uncommon

The Number Needed to Treat (NNT) is the number of patients you need to treat to prevent one additional bad outcome. For example, if a drug has an NNT of 5, it means you have to treat 5 people with the drug to prevent one additional bad outcome.

To calculate the NNT, you need to know the Absolute Risk Reduction (ARR); the NNT is the inverse of the ARR:

NNT = 1/ARR

Where ARR = CER (Control Event Rate) – EER (Experimental Event Rate).

NNTs are always rounded up to the nearest whole number.

In this case, the NNT can be computed as follows:

ARR = 10% – 5% = 0.05

NNT = 1/0.05 = 20

The shaft of the humerus has two prominent features:
1. Deltoid tuberosity – attachment for the deltoid muscle
2. Radial or spiral groove – The radial nerve and profunda brachii artery lie in the groove

Mid-shaft fractures of the humerus usually occur after a direct blow to the upper arm, which can occur after a fall or RTAs. The most important clinical significance of a mid-shaft humeral fracture is an injury to the radial nerve. The radial nerve originates from the brachial plexus and has roots of C5-T1. It crosses the spiral groove on the posterior side of the shaft of the humerus.
On examination, the patient may have a wrist drop, loss or weakness of finger extension, and decreased or absent sensation to the posterior forearm, digits 1 to 3, and the radial half of the fourth digit.

The following parts of the humerus are in direct contact with the indicated
nerves:
Surgical neck: axillary nerve.
Radial groove: radial nerve.
Distal end of humerus: median nerve.
Medial epicondyle: ulnar nerve.

Bell’s palsy is facial muscle weakness or paralysis that arises from idiopathic damage to the facial nerve. It can occur at any age but is commonly associated with some conditions:
1. pregnancy
2. diabetes
3. upper respiratory ailment
4. GBS
5. Toxins

The common symptoms of Bell’s palsy are:
1. Abnormal corneal reflex as the facial nerve controls the motor aspect of the corneal reflex.
2. The loss of control of facial muscles and eyelids leads to decreased tear production.
3. mild weakness to total paralysis on one side of the face, occurring within hours to days.
4. Bell’s palsy is a lower motor neuron lesion that usually spares the forehead while the upper motor near lesions, like stroke, involves the entire face.
5. The anterior two-thirds of the tongue is supplied by the chorda tympani branch of the facial nerve, thus resulting in loss of taste.
6. Ptosis can be a feature of Bell’s palsy but Bell’s palsy would typically show unilateral symptoms rather than bilateral.

When drugs are bound to proteins, drugs cannot cross membranes and exert their effect. Only the free (unbound) drug can be absorbed, distributed, metabolized, excreted and exert pharmacologic effect. Thus, when amide local anaesthetics are bound to ?1-glycoproteins, their duration of action are reduced.

The potency of local anaesthetics are affected by lipid solubility. Solubility influences the concentration of the drug in the extracellular fluid surrounding blood vessels. The brain, which is high in lipid content, will dissolve high concentration of lipid soluble drugs. When drugs are non-ionized and non-polarized, they are more lipid-soluble and undergo more extensive distribution. Hence allowing these drugs to penetrate the membrane of the target cells and exert their effect.

Tissue pKa and pH will determine the degree of ionization.

The diaphragm has three opening through which different structures pass from the thoracic cavity to the abdominal cavity:

Inferior vena cava passes at the level of T8.

Oesophagus, oesophageal vessels and vagi at T10.

Aorta, thoracic duct and azygous vein through T12.

Sympathetic trunk and pulmonary branches of vagus nerve form a posterior pulmonary plexus at the root of the lung. Fibres continue posteriorly from superficial cardiac plexus to form Anterior pulmonary plexus. It contains vagi nerves and superficial cardiac plexus. These fibres then follow the blood vessel and bronchi into the lungs.

The lower border of the pleura is at the level of:

8th rib in the midclavicular line

10th rib in the lower level of midaxillary line

T12 at its termination.

Both lungs have oblique fissure while right lung has transverse fissure too.

The trachea expands from the lower edge of the cricoid cartilage (at the level of the 6th cervical vertebra) to the carina.

Refractometers measure the degree to which the light changes direction, called the angle of refraction. A refractometer takes the refraction angles and correlates them to refractive index (nD) values that have been established. Using these values, you can determine the concentrations of solutions.

Tracheal tubes are made of either disposable plastic or reusable red rubber.

The tube size refers to the internal diameter (ID) in mm which is marked on the outside of the tube (some manufacturers mark the external diameter on the outside).

Plastic tubes have a radiopaque line spanning the entire length of the tube, which allows their position to be identified on x-rays. The bevel located at the end of the tube is left-facing and oval in shape, which improves the view of the vocal cords during intubation.

Oxford tubes are L-shaped and have a bevel that faces posteriorly. They have thick walls that increase the external diameter, making for a wider internal diameter.

RAE (Ring, Adair, and Elwyn) tubes are preformed and can either be north or south facing and cuffed or uncuffed. The cuffed RAE tubes have one Murphy eye, whereas the uncuffed has two Murphy eyes. Uncuffed tubes are primarily used in paediatric anaesthesia and the two Murphy eyes ensure adequate ventilation- should the tube be too long.

Superior vena cava is the main vein bringing blood back to the heart. It can get partially or completely blocked by various causes, the most common being due to malignant tumours of the mediastinum.

There are collateral pathways that form in long-standing cases with 60% or more stenosis and continue venous drainage in cases of superior vena obstruction. The collaterals are classified into four as follows:

1. The azygos-hemiazygos pathway
Azygos, hemiazygos, intercostal, and lumbar veins.

2. The internal and external mammary pathway
internal mammary, superior epigastric, and inferior epigastric veins and superficial veins of the thorax.

3. The lateral thoracic pathway
Lateral thoracic, thoracoepigastric, superficial circumflex, long saphenous, and femoral veins to collateralize to the IVC.

4. The vertebral pathway
Innominate, vertebral, intercostal, lumbar, and sacral veins to collateralize to the azygos and internal mammary pathways.

Nitric oxide (NO), an endothelial-derived relaxant factor (EDRF), is a powerful vasodilator. Its cell-signalling molecule is calcium-dependant and generated endogenous by nitric oxide synthetases from the precursor L-arginine, oxygen and NADPH. Three main isoforms have been isolated and they are inducible (iNO), neuronal (nNO) and endothelial (eNO).

Endothelial NO stimulates intracellular guanylyl cyclase which generates cyclic GMP (cGMP) from its action on guanylyl tri-phosphate (GTP). The cGMP goes on to activate protein kinase G (PKG). PKG phosphorylates cell membrane proteins that regulate intracellular calcium concentrations and level of calcium sensitisation.

Smooth muscle vasodilatation results from:

1. Light chain phosphatase activation.
2. Inhibition of calcium entry into the cell (reducing Ca2+ concentrations) and
3. Hyperpolarisation of cells by activation of H+ channels.

Systemic vascular resistance (SVR), also known as total peripheral resistance (TPR), is the amount of force exerted on circulating blood by the vasculature of the body. Three factors determine the force: the length of the blood vessels in the body, the diameter of the vessels, and the viscosity of the blood within them. The most important factor that determines the systemic vascular resistance (SVR) is the tone of the small arterioles.

These are otherwise known as resistance arterioles. Their diameter ranges between 100 and 450 µm. Smaller resistance vessels, less than 100 µm in diameter (pre-capillary arterioles), play a less significant role in determining SVR. They are subject to autoregulation.

Any change in the viscosity of blood and therefore flow (such as due to a change in haematocrit) might also have a small effect on the measured vascular resistance.

Changes of blood temperature can also affect blood rheology and therefore flow through resistance vessels.

Systemic vascular resistance (SVR) is measured in dynes·s·cm-5

It can be calculated from the following equation:

SVR = (mean arterial pressure − mean right atrial pressure) × 80 cardiac output

Correctly used, antibiotic prophylaxis can reduce
the total use of antibiotics.
There is strong scientific support that antibiotic
prophylaxis reduces the development of infection after:

• Operations and endoscopic procedures in the large intestine,
  the rectum, and the stomach (including appendectomies and
  penetrating abdominal trauma), and after percutaneous endoscopic gastrostomy (PEG)
• Cardiovascular surgery, and insertion of pacemakers
• Breast cancer surgery
• Hysterectomy
• Reduction of simple fractures and prosthetic limb surgery
• Complicated surgery for cancer in the ear, nose, and throat
  regions
• Transrectal biopsy and resection of the prostate (febrile urinary
  tract infection and blood poisoning).

In most cases the scientific evidence is inadequate to determine
which type of antibiotic is most effective for antibiotic prophylaxis.

The most common cause of hypoparathyroidism is injury or removing the parathyroid glands. They can be injured accidentally during surgery to remove the thyroid as they are located posterior to the thyroid gland.

A result of both low parathyroid hormone and low calcium is likely to mean that the parathyroid glands are not responding to hypocalcaemia. The hypocalcaemia can cause confusion, and the stay in the hospital is likely to refer to her surgery.

While a parathyroid adenoma is fairly common and can cause hypoparathyroidism, it much more likely causes hyperparathyroidism.

Chronic kidney disease is likely to cause hypocalcaemia, which would increase parathyroid hormone production in an attempt to increase calcium levels, causing hyperparathyroidism. Vitamin D is activated by the kidneys and then binds to calcium to be absorbed in the terminal ileum so that a deficiency would cause hyperparathyroidism.

A passive leg raise can lead to transient increases in blood pressure and stroke volume as it increased the amount of venous return to the heart. Venous return increases in this situation as it transfers a larger volume of blood from the lower limbs to the right heart. It therefore mimics a fluid challenge. However its effects are short lasting and often lead to minimal increases in blood pressure. It therefore should not be used to treat shock in isolation. The passive leg raise is useful in determining the likelihood that a patient with shock will respond to fluid resuscitation.

Stroke volume (via a cardiac monitor) and/or pulse pressure (via an arterial line) should be measured to assess the effects of a passive leg raise. An increase in stroke volume by 9% or in pulse pressure by 10% are considered indicative of fluid responsiveness.

Blood that enters the ventricles during diastole causes stretching of sarcomeres within cardiac muscle. The extent to which they stretch is proportional to the strength of ventricular muscle contraction. Therefore, the venous return (amount of blood returned to the heart) is proportional to stroke volume. The end diastolic volume is determined by venous return and is also proportional to stroke volume.

Cardiac muscle contraction strength is dependent on the action of adrenaline and noradrenaline, but these hormones contribute to cardiac contractility, not to stroke volume.

Hypoxic Pulmonary vasoconstriction (HPV) reflects the constriction of small pulmonary arteries in response to hypoxic alveoli (.i.e.; PO2 below 80-100mmHg or 11-13kPa).

These blood vessels become independent of the nerve stimulus, when blood with a high PO2 flows through the lung which contains a low alveolar PO2.

Thus a low PO2 within the alveoli has been shown to impact on hypoxic pulmonary vasoconstriction (HPV) more than a low PO2 within the blood.

HPV results in the blood flow being directed away from poorly ventilated areas of the lung and helps to reduce the ventilation/perfusion mismatch (not increase).

In animals, volatile anaesthetic agents can diminish HPV, while in adults, the evidence proves less persuading, in spite of the fact that it certainly doesn’t strengthen the effects.

HPV response will be suppressed by 20 parts per million (ppm) of nitric oxide.

A thermocouple, or a thermal junction, is temperature measuring device consisting of a pair of dissimilar metal (bimetallic) wires or strips joined together. Typically, copper and constantan (an alloy of 55% copper and 45% nickel) are used. When there is contact between these metals, a small voltage is generated in the order of millivolts. The magnitude of the thermojunction electromotive force (emf) is proportional to applied temperature (the Seebeck effect). This physical principle is applied in the measurement of temperature. The electromotive force at the measuring junction is proportional to temperature.

Two wires with different coefficients of expansion, joined together, can be used as a switch for thermostatic control.

Semiconductors are NOT used in thermocouple. The resistance of the measuring junction of a thermocouple is irrelevant.

Drug interactions can be seen in the following examples:

Additive interaction (summation).

Additive effects are described for intravenous drug combinations such as ketamine and thiopentone or ketamine and midazolam. Different mechanisms of action are used by them. Thiopentone and midazolam are GABAA receptor agonists, whereas ketamine is an NMDA receptor antagonist. Nitrous oxide and halothane are two other examples.

Synergism is a supra-additive interaction.

Refers to the administration of two drugs with similar pharmacological properties and closely related sites of action, resulting in a combined effect that is greater than the sum of the contributions of each component. The construction of an isobologram can be used to interpret and understand these. The best example is the hypnotic effect of benzodiazepines and intravenous induction agents like propofol. As part of a co-induction technique, midazolam is frequently given before propofol.

Potentiation

In a dose-dependent manner, volatile agents enhance the effects of neuromuscular blocking agents. Electrolyte disturbance (hypomagnesaemia), Penicillin, and probenecid can all increase the effects of neuromuscular blocking agents (the latter has no similar pharmacological activity).

Infra-additive interaction (antagonism).

This can be subdivided into the following categories:

-Pharmacokinetic interference occurs when one drug affects the absorption of another through the gastrointestinal tract or when hepatic microsomal enzyme induction influences metabolism.
-Heparin and protamine, for example, or heavy metals and chelating agents, are examples of chemical antagonists.
-Competitive reversible antagonistic antagonism of receptors, such as opioids and naloxone, and irreversible antagonistic antagonism of receptors

As there is no brachiocephalic artery on the left side, the artery is entered by the catheter on the right side.

The brachiocephalic artery branches into the common carotid and the right subclavian artery, so the catheter is most likely to enter the right subclavian artery, or also possibly the right carotid.

The superficial inguinal ring is an opening in the aponeurosis of the external oblique muscle, just above and lateral to the pubic crest.

The superficial ring resembles a triangle more than a ring with the base lying on the pubic crest and its apex pointing towards the anterior superior iliac spine. The sides of the triangle are crura of the opening in the external oblique aponeurosis. The lateral crura of the triangle is attached to the pubic tubercle. The medial crura of the triangle is attached to the pubic crest.

The external oblique aponeurosis forms the anterior wall of the inguinal canal and also the lateral edge of the superficial inguinal ring. The rectus abdominis lies posteromedially, and the transversalis posterior to this.

Barbituric acid is the barbiturates’ pharmacologically inactive precursor. A pyrimidine heterocyclic nucleus is formed by the condensation of urea and malonic acid. Its pharmacological activity can be influenced by minor structural changes (structure function relationship).

The duration of action and potency as a sedative are influenced by the length of the side chains at C5. Barbiturates with three carbon atoms in their chain last longer than those with two. Anticonvulsant properties are enhanced by branched chains.

The addition of a methyl group at N1 causes a faster onset/offset of action, but it also causes excitatory phenomena (twitching/lower convulsive threshold).

The addition of oxygen and sulphur to C2 increases the molecule’s lipid solubility and thus its potency. Thiopentone (thiobarbiturate) has sulphur groups at C2, making it 20-200 times more lipid soluble than oxybarbiturates.

Haemorrhage, including intracranial bleeding, is a common and potentially fatal side effect of warfarin therapy, and reversing anticoagulation quickly and completely can save lives. When complete and immediate correction of the coagulation defect is required in orally anticoagulated patients with life-threatening haemorrhage, clotting factor concentrates are the only viable option.

For rapid reversal of vitamin K anticoagulants, prothrombin complex concentrates (PCC) are recommended. They contain the vitamin K-dependent clotting factors II, VII, IX, and X and are derived from human plasma. They can be used as an adjunctive therapy in patients with major bleeding because they normalise vitamin K dependent clotting factors and restore haemostasis.

The most common treatments are fresh frozen plasma (FFP) and vitamin K. The efficacy of this approach is questioned due to the variable content of vitamin K-dependent clotting factors in FFP and the effects of dilution. Significant intravascular volume challenge, as well as the possibility of rare complications like transfusion-associated lung injury or blood-borne infection, are all potential issues.

To avoid anaphylactic reactions, vitamin K should be given as a slow intravenous infusion over 30 minutes. Regardless of the route of administration, the reversal of INRs with vitamin K can take up to 24 hours to reach its maximum effect.

Reversal of anticoagulation in patients with warfarin-associated intracranial haemorrhage may be considered with factor VIIa (recombinant), but its use is controversial. There are concerns about thromboembolic events following treatment, as well as questions about assessing efficacy in changes in the INR. If the drug is to be administered, patients should be screened for an increased risk of thrombosis before the drug is given.

Staphylococcus aureus colonizes the nasopharynx in >20% of the general population.

Methicillin-resistant Staphylococcus aureus (MRSA) is resistant to flucloxacillin.

Trimethoprim binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF) to tetrahydrofolic acid (THF). THF is an essential precursor in the thymidine synthesis pathway and interference with this pathway inhibits bacterial DNA synthesis.

All ?-lactam antibiotics like penicillin interfere with the synthesis of the bacterial cell walls. The ?-lactam antibiotics inhibit the transpeptidases so that cross-linking (which maintains the close-knit structure of the cell wall) does not take place

Observation bias occurs when the behaviour of an individual changes that results from their awareness of being observed.

Recall bias introduced when participants in a study are systematically more or less likely to recall and relate information on exposure depending on their outcome status.

Attrition bias is a systematic error caused by unequal loss of participants from a randomized controlled trial (RCT). In clinical trials, participants might dropout due to unsatisfactory treatment or efficacy, intolerable adverse events, or even death.

Selection bias introduced when the individuals are not chosen randomly to take a part in the study. It usually occurs when the research decides who is going to be studied, they are not the representative of the population.

Lead-time bias occurs when a disease is detected by a screening test at an earlier time point rather than it would have been diagnosed by its clinical appearance. In this bias, earlier detection improves the survival time in the intervention group.