TBL - Jaundice and Hepatitis

jaundice / hepatitis

jaundice

Jaundice is a yellowish colouration of the tissue resulting from the deposition of bilirubin

This only happens in the presence of serum hyperbilirubinemia, and is a sign of either

·         Liver disease

·         Hemolytic disorder (less commonly)

The degree of bilirubin elevation can be estimated by PE.

Sclera icterus = at least 51micromol/L (3mg/dL)

May be even green in colour if long-standing (oxidation of bilirubin to biliverdin)

Differential of yellow skin

·         Caretenoderma

·         Quinacrine

·         Phenol exposure

Increased bilirubin occurs when there is an imbalance between the production and clearance of bilirubin.

It may result from

·         Over-production of bilirubin

·         Impaired…

o    Uptake

o    Conjugation

o    Excretion

·         Regurgitation of unconjugated / conjugated bilirubin from damaged hepatocytes / bile ducts.

Initial steps in jaundice patient evaluation

History taking

Some presentation of jaundice are quite characteristic, and such history presentation should warrant a confirmatory  investigations.

·         Fever + nausea + Anorexia (even cigarettes also does not want)

o    Suggestive of viral hepatitis

§  Comfirmation by HepA IgM, Hep B surface antigen, Hep C IgM etc.

·         Pruritis + dark urine + pale stools

o    Suggestive of cholestasis

§  Check by bilirubin study (urobilinogen,

§  Alkaline phosphatase

§  Ultrasound of bile ducts

·         Fatty food triggers colicy pain

o    Suggestive of bile stone causes

§  Ultrasound

§  ERCP

·         Progressive jaundice + fever + chills + rigors (Charcot’s triad)

o    Stone obstructive cholangitis

§  ERCP

§  Ultrasound

·         Jaundice + fever + Conjuctivitis + muscle aches + passage of small and dark urine

o    Leptospirosis

§  Darkfield microscopy

·         Recurrant mild jaundice which worsen with fasting / fever

o    Gilbert syndrome

·         Hematemesis + easy brising, mental confusion, inverted sleep pattern after severe illness like CHF, Shock etc

o    Liver insufficiency causing hepatic encelopathy

§  Liver function tests

Physical examination

Physical examination is often useful, after a sufficient history has been taken from the patient.

History and physical exam should come hand in hand, to provide a solid Differential Diagnosis for us to proceed onto the investigations.

Investigations

·         Full blood count

o    To rule out hemolytic causes

o    Leucocyte – bac. infection

·         Liver biochemistry

o    To rule out hepatocellular causes

·         Bilirubin study

o    Conjugated hyper bilirubinemia

§  Hepatocellular origin

o    Unconjugated
hyper bilirubinemia

§  Over production,

§  Impared hepatic intake

§  Impared conjugation

·         Viral Markers

o    hepatitis viruses

o    EBV

o    CMV

·         Serum alpha-fetoprotein

o    Hepatocellular carcinoma,

o    Germ cell tumors

o    metastatic cancers of the liver.

·         Serum Albumin:

o    low level indicative of chronic liver disease.

·         Prothrombin Time:

o    sensitive indicator of chronic liver disease. Will be prolonged. Vitamin K deficiency must be excluded.

·         Aspartate Aminotransferase:

o    increased in hepatic necrosis, MI, muscle injury, CCF

·         Alkaline Phosphatase:

o    increased in cholestasis(intra/extrahepatic), metastasis of liver, cirrhosis.

·         Ȣ-Glutamyl Transpeptidase:

o    increases with alcohol consumption and drugs i.e. phenytoin

imaging

·         Ultrasound Imaging

o    Bile duct imaging

o    Gallstones?

o    Hepatic mets?

o    Pancreatic mass?

·         CT Scan

o    Abdominal malignancy?

o    Masses in abdomen?

·         Endoscopy (ERCP)

o    Bile duct opening

o    Bile duct obstruction

algorhythm of jaundiced patient (from Harrison 16th ed)

polyuria / polydipsia

Polyuria

When we talk of polyuria, we must first make sure we know what it means.

·         Polyuria is defined by a urine output of more than 3literes per day (hence 24 hour urine collection is essential)

·         It must be distinguished from frequency of urination which is just more frequent urination and not necessarily the amount of urine output.

Potential mechanisms of polyuria includes;

·         Excretion of nonabsorbable solutes (e.g. glucose) SOLUTE DIURESIS

·         Excretion of water (usually from a defect in ADH production or renal responsiveness) WATER DIURESIS

How do we know whether the patient is having a solute / water dieresis?

·         Urine osmolality measurements

o    Usual person excretes between 600-800 mosmol of solutes per day

§  As urea and electrolytes

o    Urine output is >3litres per day, and urine is dilute (<250mosmol / Litre), then total amount of solutes excreted is normal, and patient is having WATER DIURESIS.

§  Arising from

·         Polydipsia

·         Inadequate secretion of ADH (central DI)

·         Failure of renal tubules to respond to vasopressin (nephrogenic DI)

o    Urine output is >3 litres per day, and urine is >300mosmol/litre, then a SOLUTE DIURESIS is present, and the solute responsible for it must be found out, like;

§  Glucose

§  Mannitol

§  Urea

§  Diuretics

o    Poorly controlled diabetes with glucosuria is the most common cause of solute dieresis, leading to volume depletion and serum hypertonicity.

polydipsia

The primary stimulus for water ingestion is thirst, which is mediated by …

·         Increase in effective osmolality

·         Decrease in ECF volume or blood pressure

The osmoreceptors

·         Located in the anterolateral hypothalamus

·         Stimulated by a rise in tonicity

Urea and glucose does NOT play a role in stimulating thirst.

TBL - Weakness and Stroke

limb weakness  / stroke

In the light of previous TBL, I have realized that thinking about the MECHANISM of specific signs / symptoms helps greatly in thinking about the differential diagnosis and patient evaluation (and perhaps management as well)

what is limb weakness?

For us to discuss a particular topic, we must first define or describe what it is.

Weakness is a word used to describe a loss of power or control of voluntary muscle.

Some difficulty in movement may be interpreted as “loss of dexterity” as well.

It should be distinguished from…

·         Increased fatiguability

o    Inability to sustain the performance of an activity that should be normal for a person of that age, gender, and size

·         Bradykinesia

o    Increased time is needed for full power to be exerted

·         Apraxia

o    Loss / disorder of planning and initiating a skilled or learned movement unrelated to a significant motor/sensory deficit.

·         Loss of proprioception

o    May cause “weakness” due to difficulty in coordination

Mechanism of limb weakness

How does limb weakness occur?

·         3 main causes of limb weakness - derangement of;

o    Upper motor neuron disorder

§  Cerebral cortex

§  Descending tract

§  Internal capsule

§  Brainstem

§  Spinal cord

o    Lower motor neuron disorder

§  Ventral horn of spinal cord

§  Axons in spinal roots

§  Peripheral nerves

§  Neuromuscular junction

§  Skeletal muscle

o    Myopathic origin

§  Muscle fibre loss / disorder

§  Decrease in the number or contractile force of muscle fibres activated within motor units

§  On EMG, size of each motor unit action potential decreased

§  A little different from diseases of the neuromuscular junction (MG)

o    Biochemical origin

§  Hypo / hyper kalemia

§  Hyper calcemia

§  Hypernatremia

§  Hyponatremia

§  Hypophosphatemia

§  hypermagnesemia

important questions to ask in weakness (Hx)

·         WHERE is the weakness?

o    Hemiparesis

o    Paraparesis

o    Quadriparesis

o    Monoparesis

o    Distal

o    Proximal

o    Restricted

·         HOW SEVERE is the weakness?

o    Total paralysis

o    Paresis

·         How long did it take to develop?

o    Instant

o    Insidious

o    Episodic

·         Any associated symptoms?

o    Language deficit

o    Sensory disturbances

o    Cognitive abnormalities

o    seizures

more questions to ask in specific weakness (HX)

Hemiparesis

Hemiparesis results from an UMN lesion above the midcervical spinal cord

Most such lesions above the foramen magnum

·         Presence of other neurological symptoms? -

o    language, sensory, cognitive abnormalities and seizures all point to cortical lesion.

o    If no associated symptoms, only PURE motor deficit, it may point towards a small discrete lesion in the posterior limb of the internal capsule cerebral peduncle or upper pons.

·         Combination with cranial nerve signs

o    Is no cranial nerve signs -

§  may be due to lesion in the high cervical spinal cord

o    Ipsilateal cranial signs and contralateral hemiparesis

§  Brainstem lesion

·         Combination with mixture of neuro signs

o    Ipsilateral loss of proprioception and contralateral loss of pain and temp. sense

§  Brown-sequard $ - (hemi-block of spine)

·          Acute / Chronic / episodic?

o    Acute / episodic onset

§  Usually from ischemic / hemorrhagic stroke

§  May also relate to hemorrhage from a SOM

§  Trauma

§  Inflammatory process as in

·         MS,

·         Abscess,

·         Sarcoidosis

o    Subacute onset (over days / weeks)

§  Extensive DD

·         Subdural hematoma

o    Elderly and anticoagulated more common

·         Infectious causes

o    Cerebral abscess

o    Fungal granuloma

o    Meningitis

o    Parasitic infection

o    Toxoplasmosis

§  Esp. in AIDS

·         Neoplasms

·         Inflammatory

o    MS

o    Sarcoidosis

o    Chronic

§  Usually neoplasms or vascular malformation

§  Chronic subdural hematoma

§  Degenerative disease

physical examination of weakness

In PE, we usually try to find out whether it is a

·         UMN /LMN

·         Involving cranial nerve or not

·         Purely motor, or mixed

Sign	UMN	LMN	Myopathic
Atrophy	None	severe	Mild
Fasciculations	None	common	None
tone	Spastic	decreased	Normal / decreased
Distribution of weakness	Pyramidal / regional	Distal / segmental	Proximal
Tendon reflexes	Hyperactive	hypoactive	Normal / hypo
Babinski’s sign	present	none	None

·         Is the patient alert and conscious!?

Glasocow Coma Scale (GCS)

·         Comprises of 3 components

o    Best verbal response (max 5)

§  1

·         No speech at all

§  2

·         Incomprehensive vocalization (ohhh ahhh)

§  3

·         Inappropriate words (random words, no conversation)

§  4

·         Conversing but disoriented and confused

§  5

·         Conversing and oriented.

o    Eye opening (max 4)

§  1

·         No eye opening at all

§  2

·         Open in response to painful stimulus

§  3

·         Open to any verbal stimulus only (don’t touch)

§  4

·         Spontaneously open

o    Best Motor response (max 6)

§  1

·         No response at all

§  2

·         Abnormal extension to pain (decerebrate posture)

§  3

·         Abnormal flexion to pain (decorticate posture)

§  4

·         Withdrawal to pain (pull hand away from pain)

§  5

·         Purposeful movement, Localizing to pain (pushes source of pain away)

§  6

·         Obeying commands

o