The glomerular filtration membrane is composed of fenestrated capillary endothelium, basement membrane, and filtration slits. It is an organized, semipermeable membrane preventing the passage of most of the proteins into the urine.

The anatomical arrangement of the glomerular filtration membrane maximizes the surface area available for filtration. The arrangement of its arterioles results in high hydrostatic pressures and facilitates filtration.

Fenestrated capillary endothelium of the glomerular filtration membrane is with relatively large pores. It allows the free movement of plasma proteins and solutes but still restricts the movement of blood cells.

Filtration slits are the smallest filters and restrict the movement of plasma proteins but still allow free movement of ions and nutrients.

The glomerular basement membrane (GBM) is a critical component of the glomerular filtration membrane. Thus, it is not true that its absence will reduce the resistance of flow. The basement membrane is true to be more selective and contains negatively charged glycoproteins. However, it still allows free passage of water, nutrients, and ions. Severe structural abnormalities of the GBM can result in protein (albumin) leakage.

Raised platelet levels have emerged as a cancer risk marker, according to a large population-based study published in 2017(link is external). According to the study, 12 percent of men and 6% of women with thrombocytosis were diagnosed with cancer within a year. These figures increased to 18% in men and 10% in women if a second platelet count was taken within 6 months of the first and showed an increased or stable elevated platelet count.

The researchers discovered that thrombocytosis linked to cancer is most common in colorectal and lung cancers, and it is linked to a worse prognosis. Furthermore, one-third of the cancer patients in the study had no other symptoms that would have prompted an immediate cancer referral.

The exact mechanism by which these cancers cause thrombocytosis is unknown, but one theory proposes the existence of pathogenic feedback loops between malignant cells and platelets, with a reciprocal interaction between tumour growth and metastasis, as well as thrombocytosis and platelet activation. Another hypothesis is that thrombocytosis occurs independently of cancer but aids in its spread and progression.

The findings show that routinely testing for thrombocytosis could cut the time it takes to diagnose colorectal and lung cancer by at least two months. In the UK, this could result in around 5500 earlier cancer diagnoses per year.

Because the positive predictive value of thrombocytosis in middle age for cancer (10%) is higher than the positive predictive value for a woman in her 50s presenting with a new breast lump (8.5%), this is clearly an important research paper that should be used to adjust future clinical practise. The current NICE guidelines predate these new research findings, so we’ll have to wait and see how they affect cancer referral guidelines in the UK.

Because there are so many possible cancers associated with thrombocytosis, the treating clinician should take a thorough history and perform a thorough clinical examination if a patient is diagnosed with it. Further investigation and the most appropriate referral route should be aided by this information.

It’s worth noting that the patients in the study had their blood tests done for a medical reason rather than as a random screening test.

If there are no other symptoms to guide investigation and referral (one-third of the patients in the study had no other symptoms), keep in mind that the two most common cancers encountered were colorectal and lung cancer, so a chest X-ray and a faecal immunochemical test (FIT) for faecal blood may be reasonable initial investigations.

Clearance of a substance can provide an accurate estimate of the glomerular filtration rate (GFR) provided that the substance is:freely filterednot reabsorbed in the nephronnot secreted in the nephronnot synthesised or metabolised by the kidney

Damage to the long thoracic nerve results in weakness/paralysis of the serratus anterior muscle causing difficulty abducting the upper limb above 90 degrees and giving a ‘winged ‘ scapula appearance where the medial border, particularly the inferior angle, of the scapula moves laterally and posteriorly away from the thoracic wall (this becomes more pronounced if the patient presses the upper limb against a wall).

Gastrin is a peptide hormone that aids in gastric motility by stimulating the generation of gastric acid by the parietal cells of the stomach. G-cells in the stomach’s pyloric antrum, the duodenum, and the pancreas release it.

The following stimuli cause the release of gastrin:

Stimulation of the vagus nerve
Hypercalcaemia
stomach bloating
Proteins that have been partially digested, particularly amino acids.
The presence of acid and somatostatin inhibits the release of gastrin.
Gastrin’s main actions are as follows:
Gastric parietal cells are stimulated to release hydrochloric acid.
ECL cells are stimulated to produce histamine.
Gastric parietal cell maturation and fundal growth stimulation
Causes the secretion of pepsinogen by the gastric chief cells.
Improves antral muscle mobility
stimulates gastric contractions
Increases gastric emptying rate and stimulates pancreatic secretion
Gallbladder emptying is induced.

Action potentials are initiated in nerves by activation of ligand-gated Na+channels by neurotransmitters. Opening of these Na+channels results in a small influx of sodium and depolarisation of the negative resting membrane potential (-70 mV). If the stimulus is sufficiently strong, the resting membrane depolarises enough to reach threshold potential (generally around -55 mV), at which point an action potential can occur. Voltage-gated Na+channels open, causing further depolarisation and activating more voltage-gated Na+channels and there is a sudden and massive sodium influx, driving the cell membrane potential to about +40 mV.

25-year-old receives immunoglobulin and vaccination after cutting her hand on a drinking glass and not knowing her vaccination history.

Because this is not a tetanus-prone wound, immunoglobulin is not recommended. Because you can’t be sure about her vaccination history, now is the best time to start a tetanus vaccination course to ensure coverage later in life. The first vaccination should be administered at the time of presentation; the patient’s own GP should then review the patient’s vaccination history and schedule the rest of the course as needed.

8-year-old whose hand was cut with a kitchen knife, received her first round of vaccinations as a baby and a booster at the age of four – receives vaccination:
The tetanus vaccinations for this child are up to date, and the next booster should not be given too soon. Immunoglobulin is not required because this is not a tetanus-prone wound.

80-year-old diabetic, a rusty nail went through his shoe and into his foot while walking in the woods, and he was uncertain of his vaccination history – he received vaccination and immunoglobulin:
A tetanus vaccination course may not have been completed by an 80-year-old UK resident (the vaccination was introduced in 1961). The vaccination should be given at a walk-in clinic, and the patient’s own GP should be contacted to confirm vaccination history and to schedule the rest of the course as needed. Because this is a tetanus-prone wound (puncture wound and potential soil contact), immunoglobulin would be recommended in a patient with incomplete tetanus vaccinations.

A 28-year-old Polish man cuts his leg while working in the garden, the wound is heavily contaminated with soil, and his vaccination history is unknown – he receives vaccination:
In a patient with an unknown vaccination history, this is a tetanus-prone wound. In this case, the best course of action would be to administer both the vaccination and immunoglobulin at the walk-in clinic, then contact the patient’s own GP to check his or her vaccination history and schedule the rest of the course as needed.

30-year-old with a large amount of devitalized tissue in the torso from an electrical burn – has had all vaccinations, so no need for vaccination or immunoglobulin:
Because this is a high-risk tetanus wound (with a lot of devitalized tissue), even if the patient has had a full course of vaccinations in the past, immunoglobulin is recommended. There is no need for any additional vaccinations.

Myosin is the major constituent of the thick filament.

Actin is the major constituent of the THIN filament.

Thin filaments consist of actin, tropomyosin and troponin in the ratio 7:1:1.

A daily calcium intake of 1,000 to 1,300 mg is advised for adults. Women have a slightly higher calcium need than men and are at a higher risk of developing osteoporosis as they age.

Calcium-rich foods include the following:
Milk, cheese, and butter as dairy products.
Broccoli, spinach, and green beans as green veggies.
Bread, rice, and cereals as whole grain foods.
Sardines, salmon, and other bony fish
Eggs
Nuts
The following foods have the least calcium:
Carrot
Fruits such as kiwis, raspberries, oranges, and papaya
Chicken and pork in meats.

The mitochondria is responsible for the production of the cell’s supply of chemical energy. It does this by using molecular oxygen, sugar and small fatty acid molecules to generate adenosine triphosphate (ATP) by a process ss known as oxidative phosphorylation. An enzyme called ATP synthase is required.

Transcription of ribosomal RNA occurs in the nucleolus

Production of messenger RNA occur in the nucleus

Production of lysosome occurs in the Golgi apparatus

The post-translational processing of newly made proteins occurs in the endoplasmic reticulum

Common side effects include diarrhoea, dizziness, headache, nausea and vomiting.
Other adverse effects include: Tendon damage (including rupture), Seizures (in patients with and without epilepsy), QT-interval prolongation, Photosensitivity and Antibiotic-associated colitis

The loop of Henle consists of three functionally distinct segments: the thin descending segment, the thin ascending segment, and the thick ascending segment. About 20 percent of the filtered water is reabsorbed in the loop of Henle and almost all of this occurs in the thin descending limb. Na+ and Cl-ions are actively reabsorbed from the tubular fluid in the thick ascending limb via the Na+/K+/2Cl-symporter on the apical membrane. Because the thick ascending limb is water-impermeable, ion reabsorption lowers tubular fluid osmolality while raising interstitial fluid osmolality, resulting in an osmotic difference. Water moves passively out of the thin descending limb as the interstitial fluid osmolality rises, concentrating the tubular fluid. This concentrated fluid descends in the opposite direction of fluid returning from the deep medulla still higher osmolality areas.

Chronic kidney disease (CKD) is a disorder in which kidney function gradually deteriorates over time. It’s fairly prevalent, and it typically remains unnoticed for years, with only advanced stages of the disease being recognized. There is evidence that medication can slow or stop the progression of CKD, as well as lessen or prevent consequences and the risk of cardiovascular disease (CVD).

CKD is defined as kidney damage (albuminuria) and/or impaired renal function (GFR 60 ml/minute per 1.73 m2) for three months or longer, regardless of clinical diagnosis.

A prolonged decline in GFR of 25% or more with a change in GFR category within 12 months, or a sustained drop in GFR of 15 ml/minute/1.73 m² per year, is considered accelerated CKD progression.
End-stage renal disease (ESRD) is defined as severe irreversible kidney impairment with a GFR of less than 15 ml/minute per 1.73 m² and a GFR of less than 15 ml/minute per 1.73 m².

The brachialis muscle is a prime flexor of the forearm at the elbow joint. It is fusiform in shape and located in the anterior (flexor) compartment of the arm, deep to the biceps brachii. The brachialis is a broad muscle, with its broadest part located in the middle rather than at either of its extremities. It is sometimes divided into two parts, and may fuse with the fibres of the biceps brachii, coracobrachialis, or pronator teres muscles. It also functions to form part of the floor of the cubital fossa.

The brachialis is primarily supplied by the musculocutaneous nerve (C5, C6). In addition, a small lateral portion of the muscle is innervated by the radial nerve (C7).

The NICE guidelines do NOT recommend isolating a patient with viral conjunctivitis from others or skipping school or work. The disease is contagious, but the spread of the disease can be controlled by maintaining good hygiene practices such as:
1. frequent hand washing
2. use of separate flannels and towels
3. Avoid close contact with others

Antibiotic prescriptions are not part of the NICE guidelines for viral conjunctivitis as they will not affect the course of the disease. Most cases of viral conjunctivitis are self-limiting and resolve within one to two weeks.

The NICE guidelines recommend that symptoms may be eased with self-care measures such as:
1. Bathing/cleaning the eyelids with cotton wool soaked in sterile saline or boiled and cooled water to remove any discharge
2. Cool compresses applied gently around the eye area
3. Use of lubricating drops or artificial tears

Paroxysmal supraventricular tachycardia is an intermittent tachycardia (HR > 100 bpm) and has the following characteristics:
1. Sudden onset/offset (Contrast with sinus tachycardia)
2. Electrical activity originates above the ventricle (Contrast with ventricular tachycardia)
3. Produces narrow QRS complex (<120ms) The most common cause of PSVT is Atrioventricular nodal re-entrant tachycardia (AVNRT), most common in young women with a mean age onset of 32 years old. There are recurrent episodes of palpitations, and most of the episodes spontaneously. Sometimes, some vagal manoeuvres are required:
1. Valsalva manoeuvre
2. immersing the face in ice-cold water
3. carotid sinus massage.

If PSVT keeps persisting or is causing severe symptoms, the treatment of choice is intravenous adenosine. The patient’s ECG should be continuously monitored throughout the treatment.

The recommended doses in adults are as follows:
– Initial dose of adenosine is 6 mg by rapid IV bolus
– If unsuccessful, give another dose of adenosine 12 mg by rapid IV bolus
– If unsuccessful, give a further dose of adenosine 12 mg by rapid IV bolus
The latest ALS guidelines advocate 18 mg for the third dose, whereas the BNF/NICE guidelines advocate 12 mg.

If adenosine fails or is contraindicated, intravenous verapamil can be used as an alternative, but it should be avoided in patients recently treated with beta-blockers.

Synchronized electrical cardioversion will be necessary with signs of hemodynamic instability or if drug treatment has failed to restore sinus rhythm.
Recurrent episodes of paroxysmal supraventricular tachycardia can be treated by catheter ablation or prevented with drugs such as flecainide, sotalol, diltiazem, or verapamil.

Aspirin inhibits cyclo-oxygenase irreversibly by covalently acetylating the cyclo-oxygenase active site in both COX-1 and COX-2. The production of prostaglandin and thromboxane is reduced as a result. As a result, platelet activation and aggregation are reduced. A single dose of aspirin has a half-life of 7-10 days, which is the time it takes for the bone marrow to produce new platelets.

Aspirin only inhibits COX-1, the enzyme that produces thromboxane A2, at low doses (75 mg per day), and thus has a primarily anti-thrombotic effect.

Aspirin inhibits both COX-1 and COX-2 at medium to high doses (500-5000 mg per day). COX-2 is involved in the production of prostaglandins, so it has an anti-inflammatory effect at these concentrations.

Aspirin, when used as an antipyretic for a viral illness in children, can cause Reye’s syndrome. Reye’s syndrome is a potentially fatal liver disease that causes encephalopathy and liver failure.

The inability of aspirin to reduce platelet production of thromboxane A2, and thus platelet activation and aggregation, is known as aspirin resistance. Although the exact frequency and mechanism of aspirin resistance are unknown, it is thought to affect about 1% of users. Women are more likely than men to experience this phenomenon.

According to new research, taking aspirin on a regular basis lowers the risk of colorectal cancer. It may also protect against cancers of the breast, bladder, prostate, and lungs.

Polydipsia is the feeling of extreme thirstiness. It is often linked to polyuria, which is a urinary condition that causes a person to urinate excessively. The cycle of these two processes makes the body feel a constant need to replace the fluids lost in urination. In healthy adults, a 3 liter urinary output per day is considered normal. A person with polyuria can urinate up to 15 liters of urine per day. Both of these conditions are classic signs of diabetes.

The other options are also types of diabetes, except for psychogenic polydipsia (PPD), which is the excessive volitional water intake seen in patients with severe mental illness or developmental disability. However, given the patient’s previous head injury, the most likely diagnosis is cranial diabetes insipidus.

By definition, cranial diabetes insipidus is caused by damage to the hypothalamus or pituitary gland after an infection, operation, brain tumor, or head injury. And the patient’s history confirms this diagnosis. To define the other choices, nephrogenic diabetes insipidus happens when the structures in the kidneys are damaged and results in an inability to properly respond to antidiuretic hormone.

Kidney damage can be caused by an inherited (genetic) disorder or a chronic kidney disorder. As with cranial diabetes insipidus, nephrogenic diabetes insipidus can also cause an elevated urine output.

Diabetes mellitus is classified into two types, and the main difference between them is that type 1 diabetes is a genetic disorder, and type 2 diabetes is diet-related and develops over time. Type 1 diabetes is also known as insulin-dependent diabetes, in which the pancreas produces little or no insulin. Type 2 diabetes is termed insulin resistance, as cells don’t respond customarily to insulin.

Because the anterior ends of the ribs are inferior to the posterior ends, when the ribs are elevated, the anterior end moves upwards and forwards, moving the sternum upwards and forwards in turn. This ‘pump handle’ upwards and forwards movement changes the anteroposterior (AP) dimension of the thorax.

Following a myocardial infarction scar tissue formation will take place at the site of the damaged muscle. This places increased load on the rest of the myocardium causing it to hypertrophy. The left ventricle will hypertrophy first as it is pumping blood against a greater afterload as compared to the right ventricle.

There are three types of cells in the body with regards to the cell cycle: 1. permanent
2. labile
3. stable cells

Permanent cells do not re-enter the cell cycle and remain in G0. If there is a pool of stem cells the stem cells will enter the cell cycle to form more cells. Myocardial cells are a type of permanent cell and there is no pool of stem cells in the heart muscle. The anterior wall will not hypertrophy as it is formed by the right atrium and ventricle and both of these hypertrophy after the left ventricle.

A median nerve block is a simple, safe, and effective method of obtaining anaesthesia to the palmar aspect of the thumb, index finger, middle finger, radial portion of the palm and ring finger. The median nerve lies deep to the flexor retinaculum and about one centimetre under the skin of the volar wrist.
The palmaris longus tendon lies superficial to the retinaculum and is absent in up to 20% of patients.
The median nerve is located slightly lateral (radial) to the palmaris longus tendon and medial (ulnar) to the flexor carpi radialis tendon.

The procedure is as follows:
– Check sensation and motor function of the median nerve. Wear gloves and use appropriate barrier precautions.
– Locate the flexor carpi radialis and palmaris longus tendons, which become prominent when the patient flexes the wrist against resistance. The palmaris longus tendon is usually the more prominent of the two tendons.
– Needle-entry site: The needle will be inserted adjacent to the radial (lateral) border of the palmaris longus tendon just proximal to the proximal wrist crease. If the palmaris longus tendon is absent, the needle-entry site is about 1 cm ulnar to the flexor carpi radialis tendon.
– Cleanse the site with antiseptic solution. Place a skin wheal of anaesthetic, if one is being used, at the needle-entry site.
– Insert the needle perpendicularly through the skin and advance it slowly until a slight pop is felt as the needle penetrates the flexor retinaculum. When paraesthesia in the distribution of the median nerve confirms proper needle placement, withdraw the needle 1 to 2 mm.
– Aspirate to exclude intravascular placement and then slowly (i.e., over 30 to 60 seconds) inject about 3 mL of anaesthetic. If the patient does not feel paraesthesia, redirect the needle in an ulnar direction, under the palmaris longus tendon. If paraesthesia is still not felt, slowly inject 3 to 5 mL of anaesthetic in the proximity of the nerve 1 cm deep to the tendon.
– Allow about 5 to 10 minutes for the anaesthetic to take effect.

Etomidate causes the least cardiovascular depression of the intravenous induction agents, with only a small reduction in the cardiac output and blood pressure. In the past, etomidate was widely used to induce anaesthesia in the shocked, elderly or cardiovascularly unstable patient. However, more recently it has become less popular as a single induction dose blocks the normal stress-induced increase in adrenal cortisol production for 4 – 8 hours, and up to 24 hours in elderly and debilitated patients. Although no increase in mortality has been identified following a single dose during induction of anaesthesia, the use of etomidate has declined due to a perceived potential morbidity.

Capillaries are designed with a small diffusion distance for nutrition and gaseous exchange with the tissues they serve. Because oxygen and carbon dioxide are both highly soluble in lipids (lipophilic), they can easily diffuse along a concentration gradient across the endothelial lipid bilayer membrane. In contrast, glucose, electrolytes, and other polar, charged molecules are lipid-insoluble (hydrophilic). These chemicals are unable to pass through the lipid bilayer membrane directly and must instead travel through gaps between endothelial cells.
Capillaries are divided into three types: continuous, fenestrated, and sinusoidal. Each of these capillary types contains different sized gaps between the endothelial cells that operate as a filter, limiting which molecules and structures can pass through.

The permeability of capillaries is affected by the wall continuity, which varies depending on the capillary type.
Skeletal muscle, myocardium, skin, lungs, and connective tissue all have continuous capillaries. These capillaries are the least permeable. They have a basement membrane and a continuous layer of endothelium. The presence of intercellular spaces allows water and hydrophilic molecules to pass across. Tight connections between the cells and the glycocalyx inhibit passage via these gaps, making diffusion 1000-10,000 times slower than for lipophilic compounds. The diffusion of molecules larger than 10,000 Da, such as plasma proteins, is likewise prevented by this narrow pore system. These big substances can pass through the capillary wall, but only very slowly, because endothelial cells have enormous holes.

The kidneys, gut, and exocrine and endocrine glands all have fenestrated capillaries. These are specialized capillaries that allow fluid to be filtered quickly. Water, nutrients, and hormones can pass via windows or fenestrae in their endothelium, which are connected by a thin porous membrane. They are ten times more permeable than continuous capillaries due to the presence of these fenestrae. Fenestrated capillaries have a healthy basement membrane.
The spleen, liver, and bone marrow all have sinusoidal capillaries, also known as discontinuous capillaries. Their endothelium has huge gaps of >100 nm, and their basement membrane is inadequate. They are highly permeable as a result, allowing red blood cells to travel freely.

Legionella pneumophilais a Gram negative bacterium that is found in natural water supplies and in the soil, transmitted predominantly via inhalation of aerosols generated from contaminated water (direct person-to-person spread of infected patients does not occur). It is the cause of Legionnaires’ disease. Outbreaks of Legionnaires’ disease have been linked to poorly maintained air conditioning systems, whirlpool spas and hot tubs.

The clinical features of the pneumonic form of Legionnaires’ disease include:
Mild flu-like prodrome for 1-3 days
Cough (usually non-productive and occurs in approximately 90%)
Pleuritic chest pain
Haemoptysis
Headache
Nausea, vomiting and diarrhoea
Anorexia
Legionella pneumophilainfections can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used.
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur with Legionnaires’ disease and will result in hyponatraemia as is seen in this case.
Legionella pneumophilainfections are resistant to amoxicillin but can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used. The majority of cases of Legionnaires’ disease are caused by Legionella pneumophila, however many other species of Legionella have been identified.
Legionella longbeachae is another less commonly encountered species that has also been implicated in outbreaks. It is predominantly found in soil and potting compost, and has caused outbreaks of Pontiac fever, the non-respiratory and less severe variant of Legionnaires’ disease.

Clostridium perfringens is an obligate anaerobe and has exotoxin mediated effects. It is the most common cause of gas gangrene. C. perfringens is also implicated in food poisoning, cellulitis, enteritis necrotican (life-threatening infection involving ischaemic necrosis of the jejunum), and rarely, CNS infections such as meningitis and encephalitis.

M. tuberculosis is the causative agent of pulmonary tuberculosis (TB). The most commonly used diagnostic test for the diagnosis of pulmonary TB is the direct sputum smear microscopy (DSSM) wherein the presence of acid-fast bacilli (AFB) is tested.

The most common method is the hot method or also known as Ziehl-Neelsen method. This is a staining method special for Mycobacteria species because they are known to be acid-fast which means that they are not easily decolorized by acid alcohol. Once the DSSM tests positive for acid-fast bacilli, this indicates possible infection with tuberculosis. The gold standard for diagnosis is still culture but Mycobacteria species are slow-growers that is why DSSM is considered the best diagnostic method. A positive AFB smear and correlation with symptoms is usually used by physicians to create a final diagnosis of pulmonary tuberculosis.

Megaloblastic anemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage to the mitosis stage. This leads to continuing cell growth without division, which presents as macrocytosis, with an increase in mean corpuscular volume (MCV). The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically vitamin B12 deficiency or folate deficiency.
Folate is an essential vitamin found in most foods, especially liver, green vegetables and yeast. The normal daily diet contains 200 – 250 μg, of which about 50% is absorbed. Daily adult requirements are about 100 μg. Absorption of folate is principally from the duodenum and jejunum. Stores of folate are normally only adequate for 4 months and so features of deficiency may be apparent after this time.

Angiotensinogen is an alpha-2-globulin generated predominantly by the liver and released into the blood. Renin, which cleaves the peptide link between the leucine and valine residues on angiotensinogen, converts it to angiotensin I.

Angiotensinogen levels in the blood are raised by:
Corticosteroid levels have risen.
Thyroid hormone levels have risen.
Oestrogen levels have risen.
Angiotensin II levels have risen.

About 20% of patients that suffer an anaphylactic reaction suffer a biphasic response 4-6 hours after the initial response (sometimes up to 72 hours after).

Dobutamine is a synthetic isoprenaline derivative that is used to provide inotropic support to patients with low cardiac output caused by septic shock, myocardial infarction, or other cardiac conditions.

Dobutamine is a sympathomimetic drug that stimulates beta-1 adrenergic receptors in the heart to produce its primary effect. As a result, it has inotropic properties that increase cardiac contractility and output. It also has a small amount of alpha1- and beta-2-adrenergic activity.

A summary of the mechanism and effects of different inotropic agents is shown below:
Inotrope
Mechanism
Effects
Adrenaline (epinephrine)
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Noradrenaline (norepinephrine)
Mainly alpha-agonist;
Beta-1 and -2 agonist at increasing doses
Vasoconstriction;
Some increased cardiac output
Dopamine
Dopamine agonist at low doses;
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Dobutamine
Mainly beta-1 agonist
Increased cardiac output