UCLH digestive rotation Flashcards

(38 cards)

1
Q

what is odynophagia

A

pain on swallowing

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2
Q

what is dysphagia

A

difficulty in swallowing

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3
Q

what is Charcot’s triad

A

three common signs and symptoms in acute cholangitis: right upper quadrant pain, jaundice, and fever

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4
Q

what is cholangitis

A

bile duct inflammation

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5
Q

what is the WHO safe surgical checklist

A

aiming to decrease errors and adverse events, and increase teamwork and communication in surgery.

19-item checklist has gone on to show significant reduction in both morbidity and mortality

it has 3 checkpoints: before induction of anaesthesia, before skin incision and before the PT leaves the operating theatre

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6
Q

what is the aim of a pre-assessment clinic

A

to pre-optimise the PT so they are as fit as they can be prior to surgery, this considers comorbidities and the risk of postponing surgery vs the potential improvement to risk factors this might give.

reduce on the day surgical cancellations which waste time and money.

blood ordering if necessary - do a group and save.

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7
Q

what does CPex stand for

A

cardiopulmonary exercise test - ECG, lung function tests, find the aerobic/anaerobic threshold. if threshold is above 11 then they are a low risk candidate, is less than 11 then there is an 18% mortality risk in the over 65s.

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8
Q

what is nephrotic syndrome

A

Nephrotic syndrome is a nonspecific kidney disorder characterized by a number of signs of disease: proteinuria, hypoalbuminemia and edema.[1] It is characterized by an increase in permeability of the capillary walls of the glomerulus leading to the presence of high levels of protein passing from the blood into the urine (proteinuria at least 3.5 grams per day per 1.73m2 body surface area);[2] ( > 40 mg per square meter body surface area per hour ) low levels of protein in the blood (hypoproteinemia or hypoalbuminemia), ascites and in some cases, edema; high cholesterol (hyperlipidaemia or hyperlipemia) and a predisposition for coagulation.

The cause is damage to the glomeruli, which can be the cause of the syndrome or caused by it, that alters their capacity to filter the substances transported in the blood. The severity of the damage caused to the kidneys can vary and can lead to complications in other organs and systems. However, patients suffering from the syndrome have a good prognosis under suitable treatment.

Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either limited to the kidney, called primary nephrotic syndrome (primary glomerulonephritis), or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome (e.g. SLE, diabetes, sarcoidosis).

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9
Q

what is nephritic syndrome

A

Nephritic syndrome (or acute nephritic syndrome)[1] is a collection of signs (known as a syndrome) associated with disorders affecting the kidneys, more specifically glomerular disorders.[2] It is characterized by having a thin glomerular basement membrane and small pores in the podocytes of the glomerulus, large enough to permit proteins (proteinuria) and red blood cells (hematuria) to pass into the urine. By contrast, nephrotic syndrome is characterized by only proteins (proteinuria) moving into the urine. Nephritic syndrome, like nephrotic syndrome, may involve hypoalbuminemia due to protein albumin moving from the blood to the urine.

Hematuria can be caused by bleeding anywhere in the urinary tract, but if the RBCs are trapped in urinary casts, it is more likely that the bleeding originated in the nephron, and nephritic syndrome becomes more probable.

It is usually distinguished from nephrotic syndrome, but sometimes the two are described as associated in a minority of cases (occasionally — and confusingly— referred to as “nephritic/nephrotic,” although this is considered a progression of a nephritic syndrome and categorically not a nephrotic syndrome).[3] Some conditions can cause either syndrome, and both syndromes can have a similar appearance upon biopsy. Neither term represents a definitive diagnosis, but both terms can be useful in the early stages of a differential diagnosis.

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10
Q

what is gallop rhythm

A

A gallop rhythm refers to a (usually abnormal) rhythm of the heart on auscultation.[1] It includes three or four sounds, thus resembling the sounds of a gallop.

The normal heart rhythm contains two audible heart sounds called S1 and S2 that give the well-known “lub-dub” rhythm; they are caused by the closing of valves in the heart.

A gallop rhythm contains another sound, called S3 or S4, dependent upon where in the cycle this added sound comes.

It can also contain both of these sounds forming a quadruple gallop, and in situations of very fast heart rate can produce a summation gallop where S3 and S4 occur so close as to be indistinguishable.

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11
Q

what is a normal LVEF

A

about 2/3. retain 1/3 to reduce initial wall tension (think blowing up a baloon).

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12
Q

what is batwing consolidation

A

Batwing
A bilateral perihilar distribution of consolidation is also called a Batwing distribution.
The sparing of the periphery of the lung is attributed to a better lymphatic drainage in this area.
It is most typical of pulmonary edema, both cardiogenic and non-cardiogenic.
Sometimes it is seen in pneumonias.

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13
Q

steps to scrubbing in

A

1 - scrubs, hat, face mask, set up sterile field.
2 - wash and rinse forearm with iodine and scrubbing brush and nail pick. always rinse from hand to elbow, never let the flow reverse so elevate hands before drying.
3 - 2nd wash with iodine for nails
4 - 3rd wash with iodine for hands.
5 - pat dry with paper towels from sterile field, one for each hand.
6 - put on gown, one hand into each wing and then slip on in one motion. keep hands within white cuffs until gloves are on. get assistant to tie internal ties.
7 - pick up gloves, lay on hand in reverse direction, thumb over thumb. manipulate through gown.
8 - final tie - give card sheet to assistant but only touch the cord after this. tie up.

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14
Q

what are bence jones proteins

A

A Bence Jones protein is a monoclonal globulin protein or immunoglobulin light chain found in the urine, with a molecular weight of 22-24 kDa.[1] Detection of Bence Jones protein may be suggestive of multiple myeloma or Waldenström’s macroglobulinemia.

Bence Jones proteins are particularly diagnostic of multiple myeloma in the context of end-organ manifestations such as renal failure, lytic (or “punched out”) bone lesions, anemia, or large numbers of plasma cells in the bone marrow of patients. Bence Jones proteins are present in 2/3 of multiple myeloma cases.[2]

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15
Q

what is toxic megacolon

A

Toxic megacolon (megacolon toxicum) is an acute form of colonic distension.[1] It is characterized by a very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes fever, abdominal pain, or shock.

Toxic megacolon is usually a complication of inflammatory bowel disease, such as ulcerative colitis and, more rarely, Crohn’s disease, and of some infections of the colon, including Clostridium difficile infections, which have led to pseudomembranous colitis. Other forms of megacolon exist and can be congenital (present since birth, such as Hirschsprung’s disease). Also, it can be caused by Entamoeba histolytica and Shigella.

Abdominal pain
Abdominal bloating
Abdominal tenderness
Fever
Tachycardia (rapid heart rate)
Dehydration
There may be signs of septic shock. A physical examination reveals abdominal tenderness and possible loss of bowel sounds. An abdominal radiography shows colonic dilation. White blood cell count is usually elevated. Severe sepsis may present with hypothermia or leukopenia.

If the condition does not improve, the risk of death is significant. In case of poor response to conservative therapy, a colectomy is usually required. This may involve all or part of the colon being removed, with the resulting option of anastomosis or ileostomy.

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16
Q

Causes of pancreatitis (mnemonic)

A

A catchy mnemonic for recalling the some of the causes of pancreatitis is:

I GET SMASHED
Mnemonic

I: idiopathic
G: gallstones
E: ethanol (alcohol)
T: trauma
S: steroids
M: mumps (and other infections) / malignancy
A: autoimmune
S: scorpion stings/spider bites
H: hyperlipidaemia/hypercalcaemia (metabolic disorders)
E: ERCP
D: drugs
The first four letters also represent the most common causes of pancreatitis.
17
Q

Pancreatitis Scoring (Modified Glasgow Score)

A

A score >= 3 indicates Acute Severe Pancreatitis
A score < 3 indicates Acute Mild Pancreatitiss

Assessing the severity of acute pancreatitis
Glasgow prognostic score: (NOTE PANCREAS ACRONYM)
PaO2 < 8kPa (60mmhg)
Age > 55 years
Neutrophils: (WBC >15 x109/l
Calcium < 2mmol/l
Renal function: (Urea > 16mmol/l)
Enzymes: (AST/ALT > 200 iu/L or LDH > 600 iu/L)
Albumin < 32g/l
Sugar: (Glucose >10mmol/L)

Any 3 factors means acute severe pancreatitis

Also consider the Ranson’s Score and APACHE score for these patients with acute pancreatitis.

18
Q

what is Ranson’s Criteria

A

Ranson’s criteria are used as a tool to calculate the severity of acute pancreatitis.

Yes = 1 point. No = 0 points.

On admission
Age > 55 yrs
WCC > 16,000
LDH > 600 U/I
AST > 120 U/I
Glucose > 10 mmol/l
Within 48 hours
Haematocrit fall > 10%
Urea rise > 0.9 mmol/l
Calcium < 2 mmol/l
pO2 < 60mmHg
Base deficit > 4
Fluid sequestration > 6 l
The predicted mortality
< 3  =  1%
3-4  =  15%
5-6  =  40%
> 6  =  100%
19
Q

key features of osteoarthritis on xray

A

Osteoarthritis (OA), or degenerative joint disease (DJD), is the most common of the arthritides.

Pathology

It is believed to be caused by trauma, either overt or as an accumulation of microtrauma over years, although there is also a hereditary form called primary osteoarthritis that occurs primarily in middle-aged women.

Radiographic features

General imaging features

The hallmarks of DJD are joint space narrowing, sclerosis, and osteophytosis. If all three of these findings are not present on a radiograph, another diagnosis should be considered. Joint space narrowing is the least specific finding of the three, yet it is virtually always present in DJD. Unfortunately, it is also seen in almost every other joint abnormality.

Joint space narrowing: characteristically in osteoarthritis is asymmetric whereas the joint space narrowing in inflammatory conditions is symmetric eg. In the hip the narrowing occurs superiorly or sometimes axially in osteoarthritis.

Sclerosis: should be present in varying amounts in all cases of DJD unless severe osteoporosis is present. Osteoporosis will cause the sclerosis to be diminished. For instance, in long-standing rheumatoid arthritis in which the cartilage has been destroyed, DJD often occurs with very little sclerosis.

Osteophytosis: will also be diminished in the setting of osteoporosis. Otherwise, sclerosis and osteophytosis should be prominent in DJD.

Some osteophytes carry eponymous names such as at the proximal interphalageal joint (Bouchard nodes).

Primary osteoarthritis is a familial arthritis that affects middle-aged women almost exclusively and is seen only in the hands. It affects the distal interphalangeal joints (Heberden nodes), the proximal interphalangeal joints, and the base of the thumb in a bilaterally symmetric fashion. If it is not bilaterally symmetric, the diagnosis of primary osteoarthritis should be questioned.

There are a few exceptions to the classic triad of findings seen in DJD (sclerosis, joint space narrowing, and osteophytes). Several joints also exhibit erosions as a manifestation of DJD: the temporomandibular joint, the acromioclavicular joint, the sacroiliac joints, and the symphysis pubis. When erosions are seen in one of these joints, DJD must be considered, or inappropriate treatment may be instituted.

Subchondral cyst or geode: often found in joints affected with DJD. Geodes are cystic formations that occur around joints in a variety of disorders (including, in addition to DJD, rheumatoid arthritis, calcium pyrophosphate dihydrate crystal deposition disease (CPPD) and avascular necrosis). Presumably, one method of geode formation takes place when synovial fluid is forced into the subchondral bone, causing a cystic collection of joint fluid. Another etiology is following a bone contusion, in which the contused bone forms a cyst. They rarely cause problems by themselves but are often misdiagnosed as something more sinister.

20
Q

what is Boutonniere deformity

A

Boutonniere deformity is a deformed position of the fingers or toes, in which the joint nearest the knuckle (PIP) is permanently bent toward the palm while the farthest joint (DIP) is bent back away (PIP flexion with DIP hyperextension). It is commonly caused by injury[1] or by an inflammatory condition like rheumatoid arthritis, or genetic conditions like Ehlers Danlos Syndrome.

This flexion deformity of the proximal interphalangeal joint is due to interruption of the central slip of the extensor tendon such that the lateral slips separate and the head of the proximal phalanx pops through the gap like a finger through a button hole (thus the name, from French boutonnière “button hole”). The distal joint is subsequently drawn into hyperextension because the two peripheral slips of the extensor tendon are stretched by the head of the proximal phalanx (note that the two peripheral slips are inserted into the distal phalanx, while the proximal slip is inserted into the middle phalanx). This deformity makes it difficult or impossible to extend the proximal interphalangeal joint.

21
Q

what is Swan neck deformity

A

Swan neck deformity is a deformed position of the finger, in which the joint closest to the fingertip is permanently bent toward the palm while the nearest joint to the palm is bent away from it (DIP hyperflexion with PIP hyperextension). It is commonly caused by injury or inflammatory conditions like rheumatoid arthritis or sometimes familial (congenital, like Ehlers-Danlos syndrome[1]).

Swan neck deformity has many possible causes arising from the DIP, PIP, or even the MCP joints. In all cases, there is a stretching of the volar plate at the PIP joint to allow hyperextension, plus some damage to the attachment of the extensor tendon to the base of the distal phalanx that produces a hyperflexed mallet finger. Duck bill deformity is a similar condition affecting the thumb (which cannot have true swan neck deformity because it does not have enough joints).

22
Q

muscles of the rotator cuff inc origin and insertion

A

1 - infraspinatus - infraspinous fossa - greater tuberosity of the humerus
2 - supraspinatus - supraspinous fossa - greater tuberosity of the humerus
3 - teres minor - inferior border of the scapula - greater tuberosity of the humerus
4 - subscapularis - subscapular fossa - lesser tuberosity of the humerus

23
Q

direction of muscle and blood supply to different segments of the oesophagus

A

upper third - circular m - inferior thyroid artery
middle third - circular and long m - aorta
lower third - long m - left gastric artery

24
Q

at what level does the oesophagus penetrate the diaphragm

A

T10 The esophageal hiatus is situated in the posterior part of the diaphragm, located slightly left of the central tendon through the muscular sling of the right crus of the diaphragm.
It contains the esophagus, and anterior and posterior vagal trunks.[3]

25
where is the aortic hiatus through the diaphragm
T12 The aortic hiatus is in the posterior part of the diaphragm, between the left and right crus. It contains the aorta, the azygos vein, the hemiazygos vein, and the thoracic duct.
26
at what level does the IVC pass through the diaphragm
T8 The caval opening passes through the central tendon of the diaphragm. It contains the inferior vena cava,[3] and some branches of the right phrenic nerve
27
innervation of the diaphragm
The diaphragm is primarily innervated by the phrenic nerve which is formed from the cervical nerves C3, C4 and C5.[3] While the central portion of the diaphragm sends sensory afferents via the phrenic nerve, the peripheral portions of the diaphragm send sensory afferents via the intercostal (T5-T11) and subcostal nerves (T12).
28
what is neurofibromatosis
Neurofibromatosis (NF) refers to a number of inherited conditions that are clinically and genetically distinct and carry a high risk of tumor formation, particularly in the brain.[1] Neurofibromatosis is an autosomal dominant disorder, which means only one copy of the affected gene is needed for the disorder to develop. Therefore, if only one parent has neurofibromatosis, his or her children have a 50% chance of developing the condition as well (it is rarely the case that one person has the mutated gene twice, which would imply a 100% chance of their children developing NF). The severity in affected individuals can vary; this may be due to variable expressivity. Approximately half of cases are due to de novo mutations and no other affected family members are seen. It affects males and females equally. In addition, some individuals may have mosaic NF, in which some but not all cells of the body carry the mutation. The neurofibromatoses are as follows: Neurofibromatosis type I, in which the nerve tissue grows tumors (neurofibromas) that may be benign and may cause serious damage by compressing nerves and other tissues. Neurofibromatosis type II, in which bilateral acoustic neuromas (tumors of the vestibulocochlear nerve or cranial nerve 8 (CN VIII) also known as schwannoma) develop, often leading to hearing loss. Schwannomatosis, in which painful schwannomas develop on cranial, spinal and peripheral nerves.
29
what is an Ileostomy
Ileostomy can refer to a stoma (surgical opening) constructed by bringing the end or loop of small intestine (the ileum) out onto the surface of the skin and to the surgical procedure which creates this opening. Intestinal waste passes out of the ileostomy and is collected in an artificial external pouching system which is adhered to the skin. Ileostomies are usually sited above the groin on the right hand side of the abdomen.
30
what is Diverticulitis
Diverticulitis is a common digestive disease which involves the formation of pouches (diverticula) within the bowel wall. This process is known as diverticulosis, and typically occurs within the large intestine, or colon, although it can occasionally occur in the small intestine as well. Diverticulitis results when one of these diverticula becomes inflamed. People often have left lower quadrant abdominal pain and tenderness, fever, and an increase white blood cell count. They may also complain of nausea or diarrhea; others may be constipated. The severity of symptoms depends on the extent of the infection and complications. Less commonly, an individual with diverticulitis may have right-sided abdominal pain. This may be due to the less common right-sided diverticula or a highly redundant sigmoid colon. Some patients report bleeding from the rectum.
31
what is PND
Paroxysmal nocturnal dyspnea (or PND) refers to attacks of severe shortness of breath and coughing that generally occur at night.[1] It usually awakens the person from sleep, and may be quite frightening.[2] Though simple orthopnea may be relieved by sitting upright at the side of the bed with legs dependent (legs dangling),[3] in a patient with paroxysmal nocturnal dyspnea, coughing and wheezing often persist even in this position.
32
what is Orthopnea
Orthopnea or orthopnoea (Greek from ortho, straight + pnoia, breath) is shortness of breath (dyspnea) which occurs when lying flat,[1] causing the person to have to sleep propped up in bed or sitting in a chair. It is the opposite of platypnea. It is commonly seen as a late manifestation of heart failure, resulting from fluid redistribution into the central circulation, causing an increase in pulmonary capillary pressure. It is also seen in cases of abdominal obesity or pulmonary disease.[2]
33
what is Sleep apnea
Sleep apnea (or sleep apnoea in British English; /æpˈniːə/) is a type of sleep disorder characterized by pauses in breathing or instances of shallow or infrequent breathing during sleep. Each pause in breathing, called an apnea, can last for several seconds to several minutes, and may occur 5 to 30 times or more in an hour.[1] Similarly, each abnormally shallow breathing event is called a hypopnea. Sleep apnea is classified as a dyssomnia, meaning abnormal behavior or psychological events occur during sleep.[2] When breathing is paused, carbon dioxide builds up in the bloodstream. Chemoreceptors in the blood stream note the high carbon dioxide levels. The brain is signaled to wake the person sleeping and breathe in air. Breathing normally will restore oxygen levels and the person will fall asleep again.[3] Sleep apnea is often diagnosed with an overnight sleep test called a polysomnogram, or "sleep study".
34
normal left ventricular ejection fraction
about 2/3, retain 1/3 to reduce initial wall stress that needs to be overcome (like blowing up a balloon). in decreased LVEF more blood is retained, increasing pressure so you get a loud P2 due to increased pulmonary circulatory pressure = slamming a door.
35
primary cause of oncotic pressure
albumin, so a decrease causes oedema as the fluid extravasates.
36
what are Bence Jones proteins
A Bence Jones protein is a monoclonal globulin protein or immunoglobulin light chain found in the urine, with a molecular weight of 22-24 kDa.[1] Detection of Bence Jones protein may be suggestive of multiple myeloma or Waldenström's macroglobulinemia. Bence Jones proteins are particularly diagnostic of multiple myeloma in the context of end-organ manifestations such as renal failure, lytic (or "punched out") bone lesions, anemia, or large numbers of plasma cells in the bone marrow of patients. Bence Jones proteins are present in 2/3 of multiple myeloma cases.[2] The proteins are immunoglobulin light chains (paraproteins) and are produced by neoplastic plasma cells. They can be kappa (most of the time) or lambda.[2] The light chains can be immunoglobulin fragments or single homogeneous immunoglobulins. They are found in urine due to the kidneys' decreased filtration capabilities due to renal failure, sometimes induced by hypercalcemia from the calcium released as the bones are destroyed or from the light chains themselves.[citation needed] The light chains have historically been detected by heating and now by electrophoresis of concentrated urine. More recently serum free light chain assays have been utilised in a number of published studies which have indicated superiority over the urine tests, particularly for patients producing low levels of monoclonal free light chains, as seen in nonsecretory multiple myeloma[3][4][5] and AL amyloidosis.[5][6][7][8] This is primarily because of the re-absorption of free light chains in the kidneys, creating a "threshold" of light chain production which must be exceeded before measurable quantities overflow into the urine. As such, urinalysis is a fickle witness to changing free light chain production. History[edit] The Bence Jones protein was described by the English physician Henry Bence Jones in 1847 and published in 1848.[9] The protein was later sequenced by Frank W. Putnam Sr. at the laboratory of Fred Sanger in Cambridge, who was the first to report the entire sequence.
37
what is citalopram
Citalopram is an antidepressant drug of the selective serotonin reuptake inhibitor (SSRI) class.
38
subacute sclerosing panencephalitis
Subacute sclerosing pan encephalitis (SSPE) also known as Dawson Disease, Dawson encephalitis, and measles encephalitis is a rare and chronic form of progressive brain inflammation caused by a persistent infection with measles virus (which can be a result of a mutation of the virus itself). The condition primarily affects children and young adults. It has been estimated that about 1 in 10,000 people infected with measles will eventually develop SSPE.[1] No cure for SSPE exists and the condition is often fatal. However, SSPE can be managed by medication if treatment is started at an early stage. Much of the work on SSPE has been performed by the National Institute of Neurological Disorders and Stroke (NINDS). SSPE should not be confused with acute disseminated encephalomyelitis which has a similar etiology but very different timing and course.[2] Characterized by a history of primary measles infection usually before the age of 2 years, followed by several asymptomatic years (6–15 on average), and then gradual, progressive psychoneurological deterioration, consisting of personality change, seizures, myoclonus, ataxia, photosensitivity, ocular abnormalities, spasticity, and coma. The progression of symptoms begins with stage 1—in this stage the individual's behaviour becomes more abnormal and erratic: they can be irritable and personality alterations can occur. This is often accompanied by memory loss and mental deterioration characterised by intellectual difficulty. As the nervous system begins to lose control of movement, the person develops myoclonic spasms/jerks (these being involuntary motions and spasms in extremities). As the disease progresses towards stage 2, the intensity of the spasms and the mental deterioration increases. The spasms can grow to such an extent that loss of the ability to walk can be a common sign. Also, the person will suffer speech impairment and increasingly deteriorated comprehension coupled with difficulty swallowing. The final, advanced stages of SSPE include the steady decline in body function with increased intensity of the stage 2 symptoms/signs and also blindness. At the end of the final stages the person is likely to be mute and/or comatose Characteristic periodic activity (Rademecker complex) is seen on electroencephalogram (EEG) showing widespread cortical dysfunction; pathologically, the white matter of both the hemispheres and brainstem are affected, as well as the cerebral cortex, and eosinophilic inclusion bodies are present in the nuclei of neurons (gray matter) and oligodendrocytes (white matter).[4] The diagnosis of SSPE is based on signs and symptoms (Changes in personality, a gradual onset of mental deterioration and myoclonia) and on test results, such as typical changes observed in EEGs, an elevated anti-measles antibody (IgG) in the serum and cerebrospinal fluid, and typical histologic findings in brain biopsy tissue.