Monday, June 28, 2010

Kerley's Line (Septal Line)

Kerley’s A line
An essentially straight linear opacity 2–6 cm long and 1–3 mm wide, usually situated in an upper lung zone, that points to the hilum centrally and is directed toward but does not extend to the pleural surface.
These are longer (at least 2cm) unbranching lines coursing diagonally from the periphery toward the hila in the inner half of the lungs. They are caused by distension of anastomotic channels between peripheral and central lymphatics of the lungs. Kerley A lines are less commonly seen than Kerley B lines. Kerley A lines are never seen without Kerley B or C lines also present.

Kerley’s B line

An essentially straight linear opacity 1.5–2 cm long and 1–2 mm wide, usually situated in the lung base and oriented at right angles to the pleural surface with which it is usually in contact peripherally.
These are short parallel lines at the lung periphery. These lines represent interlobular septa, which are usually less than 1 cm in length and parallel to one another at right angles to the pleura. They are located peripherally in contact with the pleura, but are generally absent along fissural surfaces. They may be seen in any zone but are most frequently observed at the lung bases at the costophrenic angles on the PA radiograph, and in the substernal region on lateral radiographs. Kerley B lines are seen in Congestive Heart Failure (CHF) and Interstitial Lung Diseases (ILD).

Kerley’s C line
A group of branching, linear opacities producing the appearance of a fine net, situated at the lung base and representing Kerley’s B lines seen en face.
These are the least commonly seen of the Kerley lines. They are short, fine lines throughout the lungs, with a reticular appearance. They may represent thickening of anastomotic lymphatics or superimposition of many Kerley B lines.


A115262
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Chest X-Ray in Left Ventricular Failure

MNEMONIC
A - Alveolar Edema (Bat's Wing)
B - Kerley B lines (Interstitial Edema)
C - Cardiomegaly
D - Dilated prominent upper lobe vessels
E - Pleural Effusion





Thanks to Dr Shahul for asking this question during ward round.

A115262


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Sunday, June 27, 2010

Some brainstem lesions & its manifestation

Lateral Medullary Syndrome is covered already.

Medial Medullary Syndrome/ Dejerine Syndrome

Causes :
Stroke of
-Anterior spinal artery
-Basilar Artery
-Vertebral Artery

Clinical features:
-Contralateral
Pyramidal Tract -> hemiparesis
Medial lemniscus (dorsal column) -> LO concious propioception, LO discriminative touch, LO vibration

-Ipsilateral
Hypogossal nerve -> deviation of tongue to the AFFECTED SIDE (weakness side)

Need help with this, very confusing. If the tongue deviates to the right, meaning the stroke is on right medial medullary ?

Extra : Locked-In Syndrome

Causes :
Stroke in Basilar Artery

Presentations:
-quadriplegia
-cannot speak (vocal cord is not paralysed, but voice and breathing is not coordinated well, hence reduced ability to speak)
-Retain full consciousness & cognitive function
-Eye movement & blinking is still retained -> can be used to communicate

Some call this as "pseudocoma"

by alvis

Thanks to Dr. Ngiu for asking us Wallenburg and thanks to Fadhli for posting that info and stimulate me to find the other brainsteam lesion

Source :
- Netter Neuroanatomy
- Oxford
- Year 2 lecture note
- http://www.strokecenter.org/prof/syndromes/index.htm
(If you guys are intesrested on stroke syndromes, can visit this site)
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Saturday, June 26, 2010

Some random things about Chronic Liver Disease


Q1 : What to look for in chronic liver disease during PE ?


Signs of hepatic failure
- Jaundice ( skin + sclera + mucous membrane, conjugated + unconjugated bilirubin ) + scratch marks
- Hepatomegaly ( due to extramedullary haemopoiesis)
- Anaemia
- Purpura (coagulopathy - factor II, VII, IX & X)
- hypoalbuminaemia -> Ankle edema, +\- ascites, nail changes (Leukonychia, Muehrcke's Line), oedema
- Finger clubbing

Signs of hyperestrinism (Hyper-estrogen-ism) - because liver cannot breakdown estrogen and cannot synthesize estrogen binding protein
- Spider Naevi
- Pectoral alopecia
- Female : Breast atrophy (dun ask me, tak tahu kenapa. xD)
- Male : Gynecomastia, Altered Pubic hair distribution, testicular atrophy
- Loss of axillary hair
- Palmar Erythema

Signs of decompensated liver disease (Portal Hypertension)
- Hypersplenism -> splenomegaly, Pancytopenia -> Pallor conjunctiva
- Caput medusae (blood flow towards the legs, must differentiate from visible veins due to IVC/SVC obstruction)
- Ascites
- Venous Hum
- Esophageal varices -> Pallor conjunctiva

Causes of Chronic Liver disease
- Hepatitis -> tattoo, IVDU needle injection scar, tender liver
- Alcoholism -> Dupuytren's contracture, parotid swelling
- Haemochromatosis -> Hyperpigmentation of the skin
- Thalassemia -> Desferrioxamine infusion pump, thalassemia facies, laparotomy scar, slate-gray hyperpigmentation of skin, stunted growth (Chronic liver failure is a sign of iron overload in Thalassemia)
- Wilson's disease -> Kayser-Fleischer Ring
- Hepatocellular Carcinoma -> Liver bruit/rub, firm and irregular liver on palpation

Complications of chronic liver disease
- Hepatic encephalopathy -> drowsiness, confusion, asterixis, constructional apraxia (Ask patient to draw a 5 point star, see picture)
- Spontaneous Bacterial Peritonitis -> reduced bowel sound

Q2 : Why anemia happens in Chronic Liver disease ?
- Hypersplenism
- Anemia of chronic liver disease
- Poor nutrition due to chronic illness
- Oesophageal Varices

Q3 : Why Spironolactone is the diuretic of choice in decompensated chronic liver disease with portal hypertension & ascites ?

- Because spironolactone has aldosterone antagonist activity
- In chronic liver disease, liver cannot metabolize aldosterone -> Hyperaldosteronism
- Might further precipitate oedema & ascite -> very bahaya

Q4 : Which electrolytes imbalance can cause confusion ?

- ONLY Sodium, Urea & calcium !!!

Q5 : How to quantify alcohol intake per week ?
- Male should consume less than 21 unit
- Female less than 14 unit
- 1 can of beer = 1 unit
- 1 shot of whiskey = 1 unit
- 1 serving of wine (half glass) = 1 unit

Q6 : List out clinical signs of alcoholism
- Peripheral neuropathy
- Proximal myopathy
- Beri-beri heart (CCF) - due to thiamine deficiency
- Cerebellar signs (ataxia)
- Wernicke's encephalopathy -> CNVI palsy (lateral rectus)
- Korsarkoff's psychosis -> Amnesia, confabulation

Q7 : Patient has G6PD, how can you see from investigations/signs that patient is having haemolysis of RBC right now ?
- Serum haptoglobulin decrease
- LDH high
- Reticulocyte high
- Normocytic initially, might be macrocytic later (MCV high)
- Dark Urine

Sources :
-Ward rounds and teaching with Dr. Paras. Thank you Dr Paras, we love you and we will miss you. >.<
- Prof Izham's Short case & you
- Oxford Handbook
- Burton Aids
- Netter's clinical anatomy

by Alvis
Please correct me if I am wrong, or if there are any uncertainties, thanks.
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Wallenberg's Lateral Medullary Syndrome



CAUSE
Posterior Inferior Cerebellar Artery (PICA) occlusion
(lead to brainstem infarction)


FEATURES
dysphagia, dysarthria (IX and X nuclei)
vertigo, nausea, vomiting, nystagmus (vestibular nucleus)
ipsilateral ataxia (inferior cerebellar peduncle)
ipsilateral Horner's syndrome (descending symphathetic fibers)
loss of pain & temperature sensation on ipsilateral face (V nucleus)
loss of pain & temperature sensation on contralateral limbs (spinothalamic tract)
NO limb weakness (pyramidal tracts are unaffected)

Thanks to Dr Ngiu for showing us patient with Wallenberg's Lateral Medullary Syndrome.

A115262
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Pleural Rub

An elderly chinese gentlemen with a background hx of parkinson disease come to the A&E with dyspnea, fever and reduce counciousness since 2 days ago.

On examination he was dyspnoeic with RR of 28 + use of accessory muscle + course crepts + bronchial breath sound + pleural rub over the left upper zone.

What is your differential for pleural rub? - one MO ask...
  • pleurisy - secondary to pneumonia or pulmonary infarction
  • rare - pleural malignancy, spontaneous pneumothorax, pnemodynia
Describe the pt's tone (UL exam)
  • cogwheel / plastic / leadpipe rigidity - ↑ tone with interrupted nature → muscle give way → jerks
  • due to exagerated stretch reflex interrupted by tremor
Assess the pt's GCS score
  • eye - 4
  • motor - 1
  • verbal - 1
  • = 6
A114141
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C-peptide?

A 42-year-old woman is brought to the emergency room by ambulance for altered mental status. The glucose level by fingerstick monitoring was below the measurement capabilities of the monitor (<40 mg/dL). After 2 ampules of 50% dextrose, the patient’s fingerstick glucose remains at 42 mg/dL. She remains unconscious and had a 1-min seizure while in transport. She has no history of diabetes mellitus. Her family denies that she has been recently ill, but recently she has been depressed. She works as a registered nurse on a medical floor of the hospital.

Which of the following tests would confirm an overdose of exogenous insulin?
A. Plasma glucose <55>18 pmol/L, and plasma C-peptide levels undetectable
B. Plasma glucose <55>18 pmol/L, and plasma C-peptide levels >0.6 ng/mL
C. Plasma glucose <55 mg/dL, plasma insulin <18 pmol/L, and plasma glucagon <12 pmol/L
D. Plasma glucose <55 mg/dL, plasma insulin <18 pmol/L, and C-peptide levels undetectable

The answer is A.
When an individual presents with profound hypoglycemia and no history of diabetes mellitus, one must determine the cause expediently and treat accordingly. Immediate treatment of this patient should include ongoing glucose administration while attempting to determine the cause. The initial step for diagnosing this patient is to determine the plasma glucose, insulin, and C-peptide levels. When the plasma glucose level is <55 mg/dL, the plasma insulin levels should be low. If the insulin levels are inappropriately high (≥18 pmol/L or ≥3 μU/mL), the C-peptide level should be assessed simultaneously. C-peptide is the protein fragment that remains after proinsulin is cleaved to insulin. C-peptide would be high (≥0.6 ng/mL) in individuals with an endogenous source of hyperinsulinemia such as insulinoma. However, C-peptide levels are low or undetectable when the source of insulin is exogenous, such as in surreptitious insulin intake or insulin overdose. One exception to consider in this individual is surreptitious intake or overdose of a sulfonylurea, an insulin secretagogue. In this case, insulin and C-peptide levels would both be elevated, and a sulfonylurea screen is also appropriate in this patient.

A114141
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