Morning hyperglycemia in Diabetics

There are 2 conditions which can cause this :

1. Somogyi Effect
2. Dawn Phenomenon

1. Somogyi Effect

• Also known as "rebound hyperglycemia"
• Usually due to:
  
  • missed night meals despite taking insulin regularly
  • a person who takes long-acting insulin without supper
  • night/ long-acting insulin dose too high
• Relative Insulin Excess-> Early morning (2-3am) hypoglycemia -> Body's counter-regulatory mechanism activated -> Hormones (cortisol, glucagon, epinephrine) released to counter insulin effect -> Morning Hyperglycemia

2. Dawn Phenomenon

• Can occur in normal person
• Exaggerated response in diabetics
• In a normal human physiology, counter-regulatory hormones (cortisol, glucagon, epinephrine) are released during early morning hours to sustain blood glucose level without food. These hormones also antagonize insulin effect, hence there is a relative higher insulin resistance during the night.
• In patients with Type I diabetics esp, insulin production is low, hence there is an exaggerated Dawn phenomenon --> morning hyperglycemia
• It typically occurs (more often) in Type I diabetic patients during puberty or pregnancy due to marked production of counter-regulatory hormones (cortisol, glucagon, epinephrine, growth hormone), thus also causing exaggerated Dawn phenomenon.

How to differentiate then ?
Check blood sugar levels (Dextrostix) around 2 - 3 a.m. for several nights.

• If the blood sugar level is low at 2 a.m. to 3 a.m., suspect Somogyi effect (Rebound phenomenon).
• If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it's most likely Dawn phenomenon.
  (which is even more likely if the patient is a type I diabetic at early onset of puberty/ pregnancy, although Somogyi effect must be ruled out first)

How to prevent/treat ?

Somogyi effect

• Have regular meals and never skip them.
• Have a light snack (preferably protein) before bedtime.
  
• Go to bed with a glucose level slightly higher than usual.
• Bring your diabetic logbook (with your result of early morning 2am-3am blood glucose) while consulting your physician, in case your insulin dose may require adjustments.

Dawn Phenomenon

• Exercise later in the day. It may have more glucose-lowering effect throughout the night.
• Limit bedtime carbohydrates and try more of a protein/fat type of snack (nuts, peanut butter, cheese, or meat).
• Talk with your doctor of a possible medication adjustment (usually insulin) to control the higher fasting readings (common in DM Type I at onset of puberty).
• Eat breakfast to limit the dawn phenomenon’s effect. By eating, your body will signal the counterregulatory hormones to turn off. -> peliknya...

Why bother ?
Good blood glucose control is essential for diabetic patients. The adjustment of medication (insulin) dose depends on which is the culprit, as one needs to lower the blood glucose prior to bedtime (Dawn phenomenon) or increase the blood glucose level prior to bedtime (Somogyi effect). 

Therefore, if the patient is having persistent morning hyperglycemia despite increased insulin dose, suspect Chronic Somogyi.

Thanks to Dr.Ngiu for asking us weeks ago.

Source : Wikipedia, 2 other internet sources (by Alvis Lee) - July 26th, 2010
Edited by Wong Yee Ming - May 15th, 2011

Read more »

Sepsis & SIRS

Infection:  Inoculation of pathogen into normally sterile tissue

Systemic inflammatory response is triggered by ischaemc, inflammation, trauma, infection to protect the host from the damaging effect of insult. However, the response can be overexaggerated when the damage and insult is too great.

Systemic inflammatory response syndrome (SIRS) criteria---> 2 or more of the following:

• Temp: <36 or >38
• HR: > 90 bpm
• RR: > 20/ min
• WCC: >12 X 10^9/L or <4X10^9/L
• MAP: <65 mmHg (Systolic BP < 90 mmHg/ Diastolic BP < 60mmHg)

Sepsis: SIRS with the presence of infection (documented).

Severe sepsis : SIRS with organ dysfunction (SOFA criteria)

Septic shock : Sepsis-induced hypotension despite fluid resuscitation

Sepsis Organ Failure Assessment (SOFA) criteria

Goal in treating sepsis :

1. MAP > 65 mmHg (To maintain BP > 90/60 mmHg)

2. ScvO2 > 70%

3. CVP: 8-12mmHg

4. Urine output > 0.5ml/kg/h

Recap MAP calculation:

MAP : (systolic - diastolic)1/3 + diastolic

A114954

Edited by: Wong Yee Ming

Read more »

Stroke and TIA

Rule Out Stroke In Emergency Room (ROSIER scale)

The aim of this assessment tool is to enable medical and nursing staff to differentiate patients with stroke and stroke mimics.

* Stroke is likely if total scores are > 0. Scores of completely excluded.

The ROSIER scale is not suitable for patients with suspected TIA with no neurological signs when seen. Please use the ABCD2 assessment for patients with suspected TIA. This assessment assists in the identification of patients with a high or low risk of early disabling stroke.

High risk TIA patients (scoring 5 or more on ABCD2 score) should be:-

�� Seen within 24 hours of the event at the TIA clinic (patients referred to the TIA clinic at the RVI need a TIA clinic referral form completed)

or

�� Out of hours (e.g. at weekends), contact the on-call Stroke Consultant and admit for review,

urgent investigation and initiation of secondary prevention.

Any patient with more than one episode in the last week is at a greater than 30% risk of stroke within a week and should be admitted to EAU for investigation and review by a Consultant Stroke Physician.

This ABCD2 scale is not a substitute for a full medical assessment.

The modified Rankin Scale (mRS) is widely used to assess global outcome after stroke.

A114954

Read more »

Unilateral Pleural Effusion of Adults

Please download more details BTS guideline info HERE.

Thanks to Dr Ngiu for teaching us on British Thoracic Society (BTS) guidelines for investigation of unilateral pleural effusion.

A115262

Read more »

Ascitic fluid analysis and its differential

~emmzesyra~

Read more »

2 scales/scores for stroke patient : Modified Ranking & NIHSS

1st one is Modified Ranking Score, to assess the functional status of a stroke patient (refer to previous post)

2nd one is NIHSS (National Institute of Heatlh Stroke Scale)

- a 15-item neurologic examination stroke scale used to evaluate the effect of acute cerebral infarction
- valid for predicting lesion size and can serve as a measure of stroke severity.
- to be a predictor of both short and long term outcome of stroke patients.
- serves as a data collection tool for planning patient care and provides a common language for information exchanges among healthcare providers. (comment author : Ya meh, tak dengar pun...)

Summary of what's in this complicated form of NIHSS
- Level of consciousness
- Best Gaze
- Visual
- Facial Palsy
- Motor Arm
- Motor Leg
- Limb Ataxia
- Sensory
- Best language
- Dysarthria
- Extinction and inattention (neglect)

For those who's interested, here's the link to the form
http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf

Thanks to Dr. Ngiu for asking us this.

Read more »

Infranuclear opthalmoplegia

CASE :

Young male teenager presented with 1 week history of progressively worsening vision of his left eye. He claims that he cannot see well with that eye. He has fever and headache as well. He has severe facial acne.
Cranial nerve examination noted left sided external and internal opthalmoplegia,and loss of sensation over the left forehead. Other neurological examination is normal. What can be your diagnosis?

DISCUSSION :

All the 3rd, 4th and 6th cranial nerves, together with opthalmic branch (V1) and maxillary branch (V2) run forward in the lateral wall of cavernous sinus.

V2 (maxillary branch of trigeminal nerve) leaves the mid-portion of cavernous sinus to exit the skull through foramen rotundum.

V3 （mandibular branch) langsung not in the lateral wall of cavernous sinus at all. Exits the skull through foramen ovale as soon as it leaves the trigeminal ganglion.

So,
Retrocavernous sinus -> 3 branches of CNV, CNIII, CNIV & CNVI
Posterior portion of cavernous sinus -> CNV1, CNV2, CNIII, CNIV & CNVI
Anterior portion of cavernous sinus -> CNV1, CNIII, CNIV & CNVI

Questions :
1. What is the most likely diagnosis ?

Lesions at the left anterior portion of cavernous sinus, which is most probably due to left cavernous sinus thrombosis secondary to facial acne.

2. What is internal and external opthalmoplegia ?

Internal -> paralysis affecting only the sphincter muscle of the pupil and the ciliary muscle

External -> paralysis affecting one or more of the extrinsic eye muscles

Total opthalmoplegia -> Internal + External

3. Differential diagnosis ?

- Pituitary Tumour (Pituitary gland is situated between the left and right cavernous sinus)
- Intracavernous carotid artery aneurysm
- Cavernous-carotid arteriovenous fistula
- Metastases (eg, nasopharyngeal carcinoma extension)
- Meningioma
- Sphenoidal sinusitis

4. What other condition can present with similar conditions ?

Lesions at superior orbital fissure -> Trauma, Tolosa-Hunt Syndrome (idiopathic granulomatous disease)

Reason : After cavernous sinus, CN3,4,6 and V1 bersama-sama enter superior orbital fissure. That's all.

5. Why facial acne cause Cavernous sinus thrombosis ?

Facial acne -> Acne pecah -> Kebetulan acne burst at the place of danger area of the face -> bacteria enters Facial Vein -> ophthalmic vein connects facial vein and cavernous sinus, and because these connections are valveless, retrograde infections can spread from facial vein to cavernous sinus -> Thrombophlebitis of the cavernous sinus -> haha !

6. Other signs/symptoms of cavernous sinus thrombosis ?
- Swollen eyelids, chemosis and proptosis
- Papilloedema
- Usually involves both eye

7. Name 1 condition very similar to cavernous sinus thrombosis ? State the difference.

Orbital cellulitis. Jawapan dekat Dhingra pg 191.

Summary : Cavernous sinus thrombosis is more acute, involve both eyes.

8. How to confirm cavernous sinus thrombosis ?
CT scan

9. Other source of cavernous sinus thrombosis ?
Dhingra pg 191.

Please correct me if I am wrong, some of these questions is I sendiri fikir punya. Thanks.

Source : Red book of neuro examination, Dhingra, Oxford

Thanks to Dr. Yeoh for asking us this interesting case through facebook. It's very rare but it happens in Teluk Intan.

Read more »

MODIFIED RANKIN SCORE (FUNCTIONAL ASSESSMENT OF STROKE)

Thanks Dr Ngiu for asking us this question.

A115262

Read more »

Colour Coding for Antenatal (KIA)

RED (admit hospital)	YELLOW (FM specialist or OnG speacialist)
*Eclampsia *PE- ↑BP with urine alb 1+/symptomatic/ BP> 160/110mmHg *heart problem with symptoms(palpitation n dyspnea *dyspnea on light activities *uncontrolled GDM or urine ketone≥ 1+ *pervaginal bleed *AbN fetal HR ^FHR≤110bpm after 26w ^FHR≥160bpm after 34w *symptomatic anemia *premature contraction *PROM *severe asthmatic attack	*HIV +ve *Hep B +ve *BP 140-160/90-110 mmHg with –ve urine alb *GDM *post date >7days
GREEN (MO)	WHITE
*rhesus –ve *mother wt <45kg *current medical prob (psy or OKU) *past gynae surgery *on drugs abuse, alcoholism, or smoker *recurrent miscarriage ≥3x *past obs hx: ^LSCS or instrumental delivery ^Hx of PIH,PE,E,GDM ^Baby birth wt <2.5 or >4.0 kg ^retained placenta or PPH ^stillbirth *twin pregnancy *urine alb 1+ *wt >80kg or increase wt >2kg/week *AbN lie at ≥36w *head not engaged at ≥38w for primid	White I (hospital) *primid *age <18 and > 40 year old *grandmultipara *gap between birth <2 years or > 5years *mother prob (ht <145cm, ibu tunggal) White II(home/alternative birth centre) *gravid 2-5 *no past obs hx, no medical prob, no cx after delivery. *ht >145cm *mother age >18, < 40 year old *married mother with good family support *POA >37 w and < 41w *estimated birth wt >2.5-3.5kg

source: buku merah (buku f/up antenatal)

114289

Read more »

ECG changes in MI

General ECG Changes suggestive of acute MI

1. New left ventricular strain pattern

2. New Left Bundle Branch Block

3. Q Waves (.04 sec and 1/3 height of R Wave)

Unless isolated in Lead III

4. T Wave inversion

Unless isolated to Lead III or Lead V1

5. ST-T elevation (more than 1mm in limb or precordial leads)

6. ST depression in Lead V1, Lead V2 (Posterior MI)

7. Hyperacute T Waves (over 50% of preceding R)

Read more »

Brain in the CT scan

sorry because the picture not clear..

emmzesyra.blogspot.com

Read more »

Cerebellum: Knowing their functions then knowing their dysfunctions

Functions of cerebellum

3 parts:

1) vestibulocerebellum

-maintain balance

-controls eye movement

2) spinocerebellum

- enhance muscle tone

-coordinate skilled voluntary movement

3) cerebrocerebellum

-plan and initiate voluntary activity

-provide input cortical motor area

Cerebellar dysfunction

· Ataxia (unsteady widebased, limp on side of lesion, cannot walk in straight line)

· Scanning speech (dysarthria- cannot coordinate skilled voluntary movement)

· Dysmetria/ past pointing (unable to plan and initiate voluntary activity. Usually had problem to past his/her finger initially but still can reach at the end of process)

· Intentional tremor

· Unable to stop movement promptly- rebound phenomenon

· Dysdiadochokinesia

· Ipsilateral hypotonia

· Cerebellar nystagmus

· Pendular jerk

· Romberg’s test usually negative, positive when lesion at dorsal column tract

Function of basal nuclei:

5 components:

1. Caudate nuclei

2. Putamen

3. Globus pallidus

4. Subthalamic nucleus

5. Substantia nigra

Roles:

1. Inhibit muscle tone throughout body

2. Select and maintain purposeful motor activity

3. Suppress useless/unwanted pattern of movement

4. Coordinate slow, sustained movement

Dysfunction causes:

1. Hyperkinesia

· Chorea- rapid involuntary movement

· Athetosis- continous slow writhing movement(dance-like)

· Ballism/hemiballism- involuntary movement that are flailing, intense, violent

2. Hypokinesia

· Akinesia - difficult initiate movement

- Reduce spontaneous movement

· Bradykinesia - slowness of movement

Disease due to basal ganglia dysfunction:

1. Huntington’s disease

· Hyperkinetic due to loss of GABAergic pathway

· Autosomal dominat (chr 4)

· Early: jerk trajectory of hand when reaching to touch spot

· Later: hyperkinetic choreiform

· Slurred speech

· Progressive dementia

· Death 10-25 years after onset

2. Parkinson disease

· Both hyperkinetic (rigidity and tremor) and hypokinetic (akinesia and bradykinesia)

· Sporadic idiopathic/ familial

· Loss of dopaminergic neuron and dopamine receptors in basal ganglia

source: lecture note second year by Prof Ruszymah

*alert: this info can be ask during short or long cases (in case dpt parkinson and cerebellar disorder)

~emmzesyra~

Read more »

diabetic nephropathy staging

source: CPG

JH

Read more »

Chronic Kidney Disease VS Diabetic Nephropathy

STAGES OF CHRONIC KIDNEY DISEASE

STAGES OF DIABETIC NEPHROPATHY

please refer to other way to stage diabetic nephropathy
based on clinical practice guideline.

Learning Issue : How to calculate GFR?

Cockcroft-Gault Equation

A commonly used surrogate marker for estimate of creatinine clearance is the Cockcroft-Gault formula, which in turn estimates GFR:It is named after the scientists who first published the formula, and it employs serum creatinine measurements and a patient's weight to predict the creatinine clearance. The formula, as originally published, is:

When serum creatinine is measured in µmol/L:


Where Constant is 1.23 for men and 1.04 for women.

One interesting feature of the Cockcroft and Gault equation is that it shows how dependent the estimation of CCr is based on age. The age term is (140 - age). This means that a 20-year-old person (140-20 = 120) will have twice the creatinine clearance as an 80-year old (140-80 = 60) for the same level of serum creatinine (120 is twice as great as 60). The C-G equation also shows that a woman will have a 15% lower creatinine clearance than a man at the same level of serum creatinine

Thanks to Dr Ngiu for asking us to compare between CKD and diabetic nephropathy.

A115262

Read more »

GOLD Staging System for COPD Severity

GOLD = Global Initiative for Chronic Obstructive Lung Disease;
COPD = chronic obstructive pulmonary disease;
FEV1 = forced expiratory volume in one second;
FVC = forced vital capacity.

A115262

Read more »

indication for dialysis (the mnemonic)

sorry to say that this mnemonic sounds bad, but it aids the memory. :p

Fluid overload (not respond to diuretics)

Uraemia (with encephalopathy)

periCarditis

hyperKalaemia (which not controlled by conservative measures)

MEtabolic acidosis (which is severe)

credit to Dr Yeoh

JH

Read more »

random teaching...

bad things about B-blocker

1)masking effect of hypoglycemia
2) slowing recovery of hypoglycemia
3) aggravate symptoms of peripheral vascular disease (cold extremities)
4) cause dyslipidemia
5) increase incidence of new onset DM
6) erectile dysfunction
7) night mares

B-blocker is contraindicated:

1) obstructive airway disease
2) severe peripheral vascular disease
3) 2nd and 3rd heart block

complications of alcohol

1) alcohol dementia
2) wernicke encephalopathy
3) korsakoff psychosis
4) hepatic encaphalopathy
5) alcohol dilated cardiomyopathy
6) fatty liver
7) liver cirrhosis
8)hepatocelullar carcinoma
9) thiamine deficiency
10) macrocytic anemia
11) coagulopathy
12)portal hypertension
13) subacute combine peripheral neuropathy
14) pancreatitis, pancreas carcinoma
15) decompernsated heart failure

types of dementia

1) Vascular dementia
2) Alzheimer dementia
3) lewy body dementia
4) Alcohol dementia
5) idiopathic

~emmzesyra~

Read more »

Asthma : Severity and Control

IS IT ASTHMA?

LEVELS OF ASTHMA CONTROL

ASTHMA SEVERITY

ASTHMA EXARCEBATION

A115262

Read more »

Hypertension in Young Adult

60 years old Malay female who was diagnosed to have hypertension and diabetis mellitus for 30 years presented to casualty with shortness of breath.

Look at her age and time of diagnosis for DM and HPT. You should realize that this is a known case of young hypertension. She was diagnosed to have hypertension at age of 30.
Remember to ask about :

1) How she was diagnosed at that time?
2) What was her symptoms at that time?
3) Exclude secondary causes - what investigation?
4) Where she was diagnosed? Some small clinic may not investigate for secondary hypertension which means that they did not treat the underlying cause of hypertension. Private hospital or teaching hospital usually would not miss this secondary causes
5) Complication of hypertension
...and so on...

CPG Management of Hypertension, 3rd Edition, Ministry of Health, Malaysia

Of course dont forget about diabetes as well. She was diagnosed to have DM at age of 30 (<40 years old). So what should you ask? Anyway, my post here just want to make sure that you guys would not be tricked with this type of scenario and you should not miss to ask about secondary hypertension. Thanks to Prof Shahrir for this information. This info may not be sufficient to you guys. So please read on secondary hypertension. Oh ya, i'm not going to touch on SOB parts. Please include the complications of HPT and DM to your differential diagnosis to SOB as well (e.g. renal failure). =)
A115262

Read more »