Pseudohypertension, also known as pseudohypertension in the elderly, noncompressibility artery syndrome, and Osler's sign of pseudohypertension is a falsely elevated blood pressure reading obtained through sphygmomanometry due to calcification of blood vessels which cannot be compressed. There is normal blood pressure when it is measured from within the artery. This condition however is associated with significant cardiovascular disease risk.

Because the stiffened arterial walls of arteriosclerosis do not compress with pressure normally, the blood pressure reading is theoretically higher than the true intra-arterial measurement.

To perform the test, one first inflates the blood pressure cuff above systolic pressure to obliterate the radial pulse. One then attempts to palpate the radial artery, a positive test is if it remains palpable as a firm "tube".

It occurs frequently in the elderly irrespective of them being hypertensive, and has moderate to modest intraobserver and interobserver agreement. It is also known as "Osler's maneuver".

The sign is named for William Osler.

The diagnosis for thrombophlebitis is primarily based on the appearance of the affected area. Frequent checks of the pulse, blood pressure, and temperature may be required. If the cause is not readily identifiable, tests may be performed to determine the cause, including the following:

- Doppler ultrasound

- Extremity arteriography

- Blood coagulation studies (Blood clotting tests)

Prevention consists of walking, drinking fluids and if currently hospitalized, changing of IV lines. Walking is especially suggested after a long period seated, particularly when one travels.

Midline shift measurements and imaging has multiple applications. The severity of brain damage is determined by the magnitude of the change in symmetry. Another use is secondary screening to determine deviations in brain trauma at different times after a traumatic injury as well as initial shifts immediately after. The severity of shift is directly proportional to the likeliness of surgery having to be performed. MLS also has the aptitude to diagnoses the very pathology that caused it. The MLS measurement can be used to successfully distinguish between a variety of intracranial conditions including acute subdural hematoma, malignant middle cerebral artery infarction, epidural hematoma, subarachnoid hemorrhage, chronic subdural hematoma, infarction, intraventrical hemorrhage, a combination of these symptoms, or the absence of pertinent damage altogether.

Doctors detect midline shift using a variety of methods. The most prominent measurement is done by a computed tomography (CT) scan and the CT Gold Standard is the standardized operating procedure for detecting MLS. Since the midline shift is often easily visible with a CT scan, the high precision of Magnetic Resonance Imaging (MRI) is not necessary, but can be used with equally adequate results. Newer methods such as bedside sonography can be used with neurocritical patients who cannot undergo some scans due to their dependence on ventilators or other care apparatuses. Sonography has proven satisfactory in the measurement of MLS, but is not expected to replace CT or MRI. Automated measurement algorithms are used for exact recognition and precision in measurements from an initial CT scan. A major benefit to using the automated recognition tools includes being able to measure even the most deformed brains because the method doesn’t depend on normal brain symmetry. Also, it lessens the chance of human error by detecting MLS from an entire image set compared to selecting the single most important slice, which allows the computer to do the work that was once manually done.

Although normally benign, idiopathic renal hypouricemia may increase the risk of exercise-induced acute renal failure.

In one study, hypouricemia was found in 4.8% of hospitalized women and 6.5% of hospitalized men. (The definition was less than 0.14 mmol l-1 for women and less than 0.20 mmol l-1 in men.)

Chvostek's sign is not a very specific sign of tetany as it may be seen in 10% to 25% of healthy adults. It is therefore not a reliable clinical sign for diagnosing latent tetany. The sensitivity is lower than that in the corresponding Trousseau sign as it is negative in 30% of patients with hypocalcemia. Due to the combination of poor sensitivity and specificity the clinical utility of this sign is reduced.

Hypoparathyroidism can be diagnosed using blood tests, the Chvostek sign, and the Trousseau sign. If comorbid conditions like congenital malformations, impaired growth, and intellectual disability are present, it may be a genetic form of hypoparathyroidism; the affected gene can be determined using a DNA test.

Causes include

- Acute pancreatitis, whereby methemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas.

- Pancreatic hemorrhage

- Retroperitoneal hemorrhage

- Blunt abdominal trauma

- Ruptured / hemorrhagic ectopic pregnancy.

- Spontaneous bleeding secondary to coagulopathy (congenital or acquired)

- Aortic rupture, from ruptured abdominal aortic aneurysm or other causes.

Some malignancies, especially gliomas (25%), as well as adenocarcinomas of the pancreas and lung, are associated with hypercoagulability (the tendency to form blood clots) for reasons that are incompletely understood, but may be related to factors secreted by the tumors, in particular a circulating pool of cell-derived tissue factor-containing microvesicles. Some adenocarcinomas secrete mucin that can interact with selectin found on platelets, thereby causing small clots to form.

In patients with malignancy-associated hypercoagulable states, the blood may spontaneously form clots in the portal vessels, the deep veins of the extremities (such as the leg), or the superficial veins anywhere on the body. These clots present as visibly swollen blood vessels (thrombophlebitis), especially the veins, or as intermittent pain in the affected areas.

Trousseau sign of latent tetany is a medical sign observed in patients with low calcium. From 1 to 4 percent of normal patients will test positive for Trousseau's sign of latent tetany. This sign may be positive before other manifestations of hypocalcemia such as hyperreflexia and tetany, as such it is generally believed to be more sensitive (94%) than the Chvostek sign (29%) for hypocalcemia.

To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for ""hand of the obstetrician"") because it supposedly resembles the position of an obstetrician's hand in delivering a baby.

The sign is named after French physician Armand Trousseau who described the phenomenon in 1861. It is distinct from the Trousseau sign of malignancy.

The occurrence (incidence) on abdominal or chest X-rays is around 0.1% but it can be up to 1% in series of older adults. It has also been reported in children.

Grey Turner's sign refers to bruising of the s, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration, and is a sign of retroperitoneal hemorrhage, or bleeding behind the peritoneum, which is a lining of the abdominal cavity. Grey Turner's sign takes 24–48 hours to develop, and can predict a severe attack of acute pancreatitis.

Grey Turner's sign may be accompanied by Cullen's sign. Both signs may be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding. Grey Turner's sign is named after British surgeon George Grey Turner.

For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.

A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.

Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes

- stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.

- stage 2 -- normalization of ST and PR deviations

- stage 3 -- diffuse T wave inversions (may not be present in all patients)

- stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.

Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick’s sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick’s sign is often a giveaway to the diagnosis.

Rarely, electrical alternans may be seen, depending on the size of the effusion.

A chest x-ray is usually normal in acute pericarditis, but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.

An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.

The term pseudopseudohypoparathyroidism is used to describe a condition where the individual has the phenotypic appearance of pseudohypoparathyroidism type 1a, but is biochemically normal.

The Trousseau sign of malignancy or Trousseau's syndrome is a medical sign involving episodes of vessel inflammation due to blood clot (thrombophlebitis) which are recurrent or appearing in different locations over time (thrombophlebitis migrans or migratory thrombophlebitis). The location of the clot is tender and the clot can be felt as a nodule under the skin. Trousseau's syndrome is a rare variant of venous thromboembolism (VTE) that is characterized by recurrent, migratory thrombosis in superficial veins and in uncommon sites, such as the chest wall and arms. This syndrome is particularly associated with pancreatic, gastric and lung cancer and Trousseau's syndrome can be an early sign of cancer

, sometimes appearing months to years before the tumor would be otherwise detected. Heparin therapy is recommended to prevent future clots. The Trousseau sign of malignancy should not be confused with the Trousseau sign of latent tetany caused by hypocalcemia.

The exact cause is not always known, but it may occur in patients with a long and mobile colon (dolichocolon), chronic lung disease such as emphysema, or liver problems such as cirrhosis and ascites. Chilaiditi's sign is generally not associated with symptoms, and is most commonly an incidental finding in normal individuals.

Absence or laxity of the ligament suspending the transverse colon or of the falciform ligament are also thought to contribute to the condition. It can also be associated with relative atrophy of the medial segment of the left lobe of the liver. In this case, the gallbladder position is often anomalous as well – it is often located anterior to the liver, rather than posterior.

X-linked recessive hypoparathyroidism is treated like other forms of the disease, using calcium and vitamin D supplementation. Supplementation with parathyroid hormone is another treatment option.

Pseudohypoparathyroidism is a condition associated primarily with resistance to the parathyroid hormone. Those with the condition have a low serum calcium and high phosphate, but the parathyroid hormone level (PTH) is appropriately high (due to the low level of calcium in the blood). Its pathogenesis has been linked to dysfunctional G Proteins (in particular, Gs alpha subunit). The condition is extremely rare, with an estimated overall prevalence of 7.2/1,000,000 or approximately 1/140000.

Causes include:

- acute pancreatitis, where methemalbumin formed from digested blood tracks around the abdomen from the inflamed pancreas

- bleeding from blunt abdominal trauma

- bleeding from aortic rupture

- bleeding from ruptured ectopic pregnancy

Importance of the sign is on a decline since better diagnostic modalities are now available.

If nasopharyngeal angiofibroma is suspected based on physical examination (a smooth vascular submucosal mass in the posterior nasal cavity of an adolescent male), imaging studies such as CT or MRI should be performed. Biopsy should be avoided as to avoid extensive bleeding since the tumor is composed of blood vessels without a muscular coat.

Antral sign or Holman-Miller sign (forward bowing of posterior wall of maxilla) is pathognomic of angiofibroma.

DSA (digital subtraction angiography) of carotid artery to see the extension of tumors and feeding vessels

Cullen's sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.

It is named for gynecologist Thomas Stephen Cullen (1869–1953), who first described the sign in ruptured ectopic pregnancy in 1916.

This sign takes 24–48 hours to appear and can predict acute pancreatitis, with mortality rising from 8–10% to 40%. It may be accompanied by Grey Turner's sign (bruising of the flank), which may then be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

Hutchinson's pupil is a clinical sign in which the pupil on the side of an intracranial mass lesion is dilated and unreactive to light, due to compression of the oculomotor nerve on that side. The sign is named after Sir Jonathan Hutchinson.

These can be due to concussion injury to the brain and is associated with subdural haemorrhage and unconsciousness.

The parasympathetic fibers to the pupil are responsible for pupillary constriction. The fibers pass through the periphery of the oculomotor nerve, and hence are the first to be affected in case of compression of the nerve. In Stage 1, the parasympathetic fibers on the side of injury are irritated, leading to constriction of pupil on that side. In stage 2, the parasympathetic fibers on the side of injury are paralysed, leading to dilatation of pupil. The fibers on the opposite oculomotor nerve are irritated, leading to constriction on opposite side. In stage 3, the parasympathetic fibers on both sides are paralysed - leading to bilateral pupillary dilatation. Pupils become fixed. This could typically indicates a very serious underlying condition.