This document provides information on the diagnosis, symptoms, signs, screening, and treatment of diabetes mellitus. It defines the main types of diabetes as type 1, type 2, gestational diabetes, and prediabetes conditions. It outlines the diagnostic criteria and recommendations for screening asymptomatic individuals. Signs and symptoms of diabetes as well as potential complications are described. Treatment aims and options including lifestyle modifications, oral hypoglycemic agents, and insulin therapy are summarized. The document also discusses prevention and management of diabetes complications focused on cardiovascular, renal, foot, and eye health.
Perioperative Management of Hypertensionmagdy elmasry
Hypertension is most common medical reason for postponing surgery.How important is peri-operative hypertension?Hypertensive comorbidities associated with adverse perioperative outcomes .New Guidelines for managing patients with high blood pressure before surgery
Consequences of anesthesia on blood pressure regulation.
Perioperative Management of Hypertensionmagdy elmasry
Hypertension is most common medical reason for postponing surgery.How important is peri-operative hypertension?Hypertensive comorbidities associated with adverse perioperative outcomes .New Guidelines for managing patients with high blood pressure before surgery
Consequences of anesthesia on blood pressure regulation.
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
Testicular cancer for public awareness by Dr RubzDr. Rubz
A presentation prepared for Charity Dinner with Fun Charity. All the profits of the event will go to FReHA (a NGO which supports women's and reproductive health.)
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
Testicular cancer for public awareness by Dr RubzDr. Rubz
A presentation prepared for Charity Dinner with Fun Charity. All the profits of the event will go to FReHA (a NGO which supports women's and reproductive health.)
This student "cheat sheet" is designed to provide medical students with basic information regarding the diagnosis and treatment of type 2 DM. It includes Questions to Ask, what to look for on a Physical Exam, Labs to Order, and basic Treatment Plans.
These guides are particularly designed for first and second-year medical students as an introduction to ambulatory care medicine and attempts to tie in the basic pathophysiology that is high-yield for USMLE Step 1.
Any and all feedback is very welcomed.
This student "cheat sheet" is designed to provide medical students with basic information regarding the diagnosis and treatment of type 2 DM. It includes Questions to Ask, what to look for on a Physical Exam, Labs to Order, and basic Treatment Plans.
These guides are particularly designed for first and second-year medical students as an introduction to ambulatory care medicine and attempts to tie in the basic pathophysiology that is high-yield for USMLE Step 1.
Any and all feedback is very welcomed.
HIV discrimination among health providers in Malaysia by Dr RubzDr. Rubz
Although doctors took oath that they will treat everyone the best they can and without judging anyone but discrimination still exist especially in HIV affected people. Due to this issue, Pertubuhan Advokasi Masyarakat Terpinggir Malaysia has taken a step to engage with doctors at government sector and desensitize them and find the line to stand together.
Prostate cancer for public awareness by DR RUBZDr. Rubz
A presentation prepared for Charity Dinner with Fun Charity. All the profits of the event will go to FReHA (a NGO which supports women's and reproductive health.)
Breast Cancer for public awareness by Dr RubzDr. Rubz
A presentation prepared for Charity Dinner with Fun Charity. All the profits of the event will go to FReHA (a NGO which supports women's and reproductive health.)
This is the first phase (qualitative) of the current project we are working on with the supervision of University Malaya and Yale School of Medicine.It will be publish as IBBS 2013 by end of the year. This slide is just a rough picture of what we are doing at the moment. This is copyright protected!
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. Diabetes Mellitus Diagnosis
DM Symptomatic with one of the following
- Casual plasma glucose ≥ 11.1mmol/L
Symptoms: - Fasting plasma glucose ≥ 7.0 mmol/L
Type I Type II
- Post 75g OGTT 2h plasma glucose ≥ 11.1 mmol/L
Thirst Frequently asymptomatic nd
Asymptomatic individuals require a 2 positive reading on a
Polyuria Chronic fatigue separate day
Nocturia Malaise Immediate dx in the presence of DKA or HHNK
Rapid LOW
Impaired Glucose Fasting plasma glucose <7.0mmol/L AND
Uncontrolled diabetes may present with increased susceptibility to infections (boils, genital Tolerance (IGT) Post 75g OGTT 2h plasma glucose 7.8-11.0 mmol/L
candidiasis, pruritus vulvae or balanitis)
Impaired Fasting Fasting plasma glucose 6.1-6.9 mmol/L AND
Glucose (IFG) Post 75g OGTT 2h plasma glucose <7.8 mmol/L
Signs GDM Any degree of glucose intolerance with onset or first recognition
Type I Type II during pregnancy.
Usually no physical signs - LOW Overweight / obesity
DKA – HPT
- Ketoacidosis: Kussmaul’s breathing, Hyperlipidaemia ± xanthelasma / Screening of Asymptomatic Individuals
ketotic breath xanthomata Frequency
- Salt & water depletion: tachycardia, Necrobiosis lipoidica diabeticorum (usually - High risk individuals w N glucose tolerance: 3 yearly screening
hypotension, loss of skin turgor, furred on pre-tibial surface of LL) - Individuals w IFG or IGT: annual screening
tongue, cracked lips, reduced Cx of diabetes - Criteria for high risk individual. Screen from 30YO onwards
intraocular pressure - Peripheral neuropathy Obesity (BMI>27)
- Altered mental state - Glove & stocking paraesthesia HPT
- Foot ulcer st
1 degree relative with DM
- Cataracts / retinopathy Previous GDM
- Peripheral vascular disease Coronary artery disease
- Dermopathy - All other individuals to be screened from 40YO onwards.
Method: rapid capillary blood glucose by glucometer. Do a formal venous blood glucose
Lack of insulin test if:
- Fasting CBG >6.0 mmol/L
- Casual CBG ≥ 7.8 mmol/L
↓ anabolism ↑ secretion of: ↑ catabolism
Glucagon
Cortisol
Fatigue Hyperglycaemia GH Glycogenolysis ↑
catecholamines Gluconeogenesis ↑ Wasting
Lipolysis ↑ LOW
Vulvitis Glycosuria
Balanitis
Hyperketonaemia
Polyuria Osmotic diuresis
Polydipsia Hyperventilation
Tachycardia Salt & water Acidosis Peripheral
↓BP depletion vasodilatation
DKA
Hypotension
Death Hypothermia
2. Treatment (MOH CPG on DM 1999) Initial therapy
Significant hyperglycaemia Sulphonylurea or Metformin
Aim: Overweight PTs Metformin (causes weight loss)
to maintain general health so as to allow the person to live a normal and active live. *α-glucosidase inhibitors: add to diet or other OHGA therapy to improve glucose control, or
avoidance of acute hyper/hypoglycaemic complications and chronic vascular complications. as a monotherapy
A) Lifestyle modification – first line Rx for type 2 diabetics. Attempt for 2-4 mths C) Insulin Therapy
Medical Nutrition Therapy Low saturated fat & cholesterol Indications
Low sodium for individuals with HPT Type 1 diabetics
Physical Activity & Exercise Recommendation: 3-5X / wk, 60-85% max heart rate, 20- Failure of lifestyle modification and OHGA in glycaemic control in type 2 diabetics
60min each time. Aerobic exercise recommended. During acute illness or stress for glycaemic control in type 2 diabetics
Precautions
- Proper footwear Regimen (short acting = Actrapid, long-acting = Insulatard)
- Adequate hydration Multiple daily injections (regular insulin before each meal + intermediate or long acting
- Avoid heavy resistance & isometric exercise insulin as basal insulin)
- Avoid exercise when severly hyperglycaemic or 2 injections per day (mixture of regular & intermediate-acting insulin before breakfast and
hypoglycaemic for Type 1 diabetics dinner – 2/3 of total daily dose in the morning in ratio of 1:2 of short:intermediate acting
Prevention of hypoglycaemia insulin; 1/3 of total daily dose in the evening)
- Reduce medication prior to exercise Single injection of intermediate acting insulin at bedtime + OHGA during the day (for Type
- Consume some CHO 30-60 min before exercise and 2 diabetics only)
after 30 mins of exercise Alternatives: Rapid-acting insulin analogues (eg lispro) – not recommended as for now.
- Gradual progression of exercise intensity
- Avoid late night exercise Type 1 Diabetics: Multiple daily injection or Continuous subcutaneous insulin infusion (CSII)
Smoking cessation Type 2 Diabetics: stepwise therapy with multiple pharmacological therapies needed over
Alcohol Alcohol consumption discouraged time to maintain target glucose control. 2 or more OHGA, or insulin Rx ± OHGA may be
required
Side effects:
B) Pharmacotherapy – when diet & exercise fail to control glycaemia in type 2 diabetics Hypoglycaemia
Weight gain
Peripheral oedema (cause salt and water retention initially when started)
Drugs available
Insulin antibody
Sulphonylurea Stimulate pancreatic insulin release Higher risk of
Local allergy
Tolbutamide: short T1/2, gd for elderly hypoglycaemia c.f. other
Lipodystrophy at injection site
Chlorpropamide: long T1/2, may cause drugs
prolonged hypoglycaemia. Other SE:
cholestatic jaundice, rash, bld dyscrasia, Monitoring of Blood Glucose Control
SIADH Self-Monitoring of Blood Glucose (SMBG)
Glibenclamide: risk of severe - Indications
hypoglycaemia. Avoid in the elderly - All insulin treated PTs (1-2 days per week)
Biguanide Decrease hepatic gluconeogenesis GI side effects - Pregnant women with GDM or pregestational DM
(Metformin) Enhance peripheral glucose uptake CI in hepatic & renal - Non insulin treated PT with risk of developing hypoglycaemia
Delay glucose absorption insufficiency due to risk - All PTs who fail to achieve glycaemic goals
of lactic acidosis - PT education: to interpret results of SMBG and modify Rx accordingly if possible for
optimal benefit.
α-glucosidase Slow absorption of starch and sucrose in GI side effects:
inhibitors the gut by inhibiting disaccharidases. flatulence, bloating,
diarrhoea Self-monitoring of Urine Glucose
(Acarbose)
- Inaccurate as raised renal threshold for glucose might mask persistent
Thiazolidinediones Insulin sensitizers hepatotoxic
hyperglycaemia. Only for PTs unable or unwilling to perform SMBG
(Rosiglitazone) CI: hepatic impairment
- target control for SMBG:
Repaglinide Prandial glucose regulator(take b4 meals) Hypoglycemia
3. premeal h/c postmeal h/c
ideal (non-DM) 4.0-6.0 5.0-7.0
optimal 6.1-8.0 7.1-10.0
suboptimal 8.1-10.0 10.1-13.0
unacceptable >10.0 >13.0
Self-monitoring of Urine Ketones Prevention of CVS complications
- For type 1 DM, GDM and pregestational diabetes in pregnant women Main complications: CAD, CVA, PVD
- Indications Main risk factors to control: HPT, dyslipidaemia, smoking
- Acute illness or stress Investigations & examination:
- Persistent elevated blood glucose >14 mmol/L - Annual screen for dyslipidaemia
- Symptoms of ketoacidosis (N/V, abdo pain, acetone breath) - Annual ECG, BP, BMI
- Examination for PVD, femoral bruit (↑ risk of cardiovas dz) & carotid bruit (↑ risk of
HbA1c CVA)
- Measure of average glycaemia over previous 2-3 months
- Frequency: 3-4mthly in unstable glycaemic control, change in thearpy or failure to Management:
meet target. 6mthly in stable glycaemic control 1) Hypertension
Aim: < 130/80 mmHg
Rx: Choice of drug depends on additional benefits eg renal & cardioprotective effects
Targets of Glycaemic Control
Intensive blood glucose control reduce risk of microvascular disease in PTs with type 1 2) Dyslipidaemia
or 2 diabetes (Diabetes Control & Complications Trial (DCCT) & UK Prospective ↑ LDL HMG-CoA reductase inhibitor (statin)
Diabetes Study (UKPDS)) SE: ↑ liver transaminases (check CK and LFT 2-3 mths after starting Rx, stop if
However, intensive treatment increases the risk of hypoglycaemic events ALT/AST >3X N or CK >10X N), myopathy, rhabdomyolysis
Therefore, targets must be individualized to the patient Target: 2.5 mmol/L
↑ TG Moderate ↑TG: fibrates.
Ideal 4.5-6.4% Not attainable by most diabetic patients SE: cholesterol gallstone dz, myopathy, ↑CK (rhabdomyolysis), ↑ liver enzymes
Desired target for pregnant women with GDM or
Severe ↑TG: combination fibrate with omega-3 polyunsat. fatty acid
pregestational diabetes
Target: 1.7 mmol/L
Optimal 6.5-7.0% Desired target for diabetic PTs
Mixed Drug of choice depend on predominant lipid abN
Increased risk of hypoglycaemia
Suboptimal 7.1-8.0% Attainable for most diabetic PTs Statin + fibrate combination usually used
Unacceptable >8.0% Risk of acute metabolic decompensation &/or Cxs of ↓ HDL Fibric acid defivatives.
hyperglycaemia Target: 1.0 mmol/L
Requires reassessment & readjustment of therapy. 3) Cardiovascular events
+ macrovascular dz Low dose aspirin (100-300 mg/day)
Most diabetics should aim for ‘Optimal’ control. No macrovascular dz Antiplatelet agents. Check for CI (allergy, blding tendencies, recent
Indications for ‘Suboptimal’ target levels (generally PTs at risk of permanent injury from GI bld, active hepatic dz)
hypoglycaemia):
- Older PTs with significant atherosclerosis
- PTs with severe DM Cx or comorbidities (severe CAD, CVA, renal failure,
proliferative retinopathy, advanced autonomic neuropathy)
- Preadolescent children: unpredictable food intake and activity level, poor
compliance to treatment
4. Prevention of Renal Complications Diabetic Foot Complications
Main risks: ulcers & LL amputations
Diabetic nephropathy (DN) accounts for 40% of PTs starting renal dialysis in S’pore Major cause of disability & mortality
Type 1 DM usually presents with Microalbuminuria 5-15 yrs after onset Screening: at dx & annually.
Type 2 DM usually presents already with overt proteinuria Wagner’s Classification:
Rate of decline in GFR = 2-20ml/min/year. a. At risk for lower extremity amputation
Screening for Microalbuminuria b. Not at risk for lower extremity amputation
Dipstix test Risk factors for lower limb amputation
Type 1: annually after 5YO Previous Hx of prev. ulceration
Type 2: at dx Ulceration
PVD pedal pulses absent absence of gradual temp.
intermittent claudication / gradient
rest pain absence of hair
Dipstix + Dipstix – Peripheral negative Semmes- negative turning fork
st
24h UTP Random daytime / 1 void neuropathy Weinstein 5.07 (128kHz) sensation
Creatinine clearance urine for alb: creatinine ratio monofilament sensation paraesthesia or
negative pin prick anaesthesia
sensation
Diabetic callus interdigital maceration
Positive Negative dermopathy ingrown / mycotic toenails fissuring esp at heels
Repeat 2X over 3mths. Microalb. Repeat test annually neglect / poor foot skin &/or tinea pedis
dxed if 2 of 3 samples are positive hygiene infection
Foot deformity gross foot deformity Charcot changes
bunions (rockerbottom foot)
* Dipstix only detects > 200mg/L albumin, flat feet Claw, hammer, mallet,
Intervention to limit progression to not microalbuminuria high arched feet retracted toes
overt nephropathy Abnormal gait
Monitor UTP or microalb every 6-12 Poor footwear Slippers, flip-flops, thongs Abnormal wear patterns
mths Tight or ill fitting shoes
Management:
DM neph: Optimal glycaemic control
Stage I: glomeular hyperfiltration Smoking cessation
Stage II: microalbuminemia (>30 mg/d)
Stage III: preoteinuria (>300mg/d)—irreversible from here onwards Not at risk Primary med practitioner & Screening of foot
Stage IV: renal impairment (Cr >200) diabetic foot care nurse DM footcare education
Stage V: ESRF (Cr >900)—start preparing for dialysis when Cr ~>500 At risk Specialist footcare team Wound debridement
Pressure analysis
Management: Orthoses / insoles for pressure distribution
Glycaemic control Aim for HbA1c <7% Footwear adaptations
BP control Aim for <130/80mmHg DM footcare education
For those with over nephropathy w proteinuria >1g/day, aim for
<125/75mmHg
st
ACE-I is preferred 1 line drug as it reduces proteinuria and slows
rate of decline of GFR. Check electrolytes 7days after introduction,
and monitor for ↑K+ or ↓ing GFR
Low Protein diet Delay progression of CRF in type 1 diabetics with overt nephropathy
Lipid control Reduce proteinuria and rate of decline in GFR in DN
Smoking Risk factor in devt of DN
5. Diabetic Retinopathy Management:
- Yearly follow-up if no retinopathy, shorter interval depending on severity if
Leading cause of blindness in adults in S’pore retinopathy present
DRP likely in the presence of albuminuria and neuropathy (microvascular Cxs) - Optimal glycaemic control
Type 1 DM: 25% at 5yrs, 97.5% after 15 yrs of DM - HPT control
Type 2 DM: 28.8% at 5 yrs, 77.8% at 15 yrs of DM - Lipid control
- Smoking cessation
Classification of DRP - Sight-threatening DRP: laser photocoagulation, occasionally vitretomy
Non-Proliferative Mild/moderate NPDR Microaneurysms only
Retinopathy (Background diabetic Mild degree of venous loops, retinal No macular edema None
(NPDR) retinopathy) hemorrhages, hard exudates, Macular edema threatening or involving macular centre Focal / grid macular laser
Microaneurysms cotton wool spots NPDR Mild/moderate None
Hard exudates Severe NPDR (Pre- One of the following: Severe/ very severe Consider scatter laser
Cotton wool spots proliferative diabetic Retinal hemorrhages or PDR Non high-risk & high-risk Scatter laser w/o delay
Retinal h’age retinopathy) microaneurysms in 4 quadrants
Advanced Scatter laser w/o delay
Venous beading Venous beading in 2 quadrants
Non-resorbing vitreous opacities, traction retinal Vitreous surgery
Intraretinal microvascular
detachment threatening or involving the macula,
abnormalities in 1 quadrant
combined rhegmatogenous & traction retinal
Very severe NPDR 2 or more signs of severe
detachment or progressive fibro-proliferative DRP
(Severe pre-proliferative retinopathy
diabetic retinopathy
Proliferative Non high-risk PDR 1-2 of the following:
Retinopathy new vessels
(PDR) new vessels at or near the optic
neovascularization disk
vitreous h’age moderate or severe new vessels
(>1/4 disk area)
vitreous hemorrhage
High-risk PDR 3 or more of the features above
Advanced PDR extensive neovascularisation,
vitreous hemorrhage or fibro-
vascular proliferation with or w/o
retinal detachment
Clinically any of the following
Significant Macular thickening of the retina at or w/in 500 microns of the centre of the
Edema (CSME) macula
retinal thickening hard exudates at or w/in 500microns of the centre of the macula,
hard exudates if associated with thickening of the adjacent retina
areas of retinal thickening 1 disk area or larger, any part of which
is w/in 1 disc diameter of the centre of the macula
Eye examination schedule (fundal photography, indirect ophthalmoscopy with slit-lamp
or direct ophthalmoscopy through dilated pupils)
st
1 examination Routine minimum F/U
Type 1 DM w/in 3-5 yrs of dx Yearly
Type 2 DM At diagnosis Yearly
st
Pregestational DM Prior to conception & during Depends on 1 trimester
st
1 trimester screening
6. Hypoglycaemia
Venous blood glucose <3.0 mmol/L a/w typical S&S relieved upon correction of bld Morbidity of severe hypoglycaemia
glucose CNS Coma Brain damage
Usually in diabetic pts treated with insulin or sulphonylureas Convulsions Impaired cognitive function
TIA/Stroke Intellectual decline
Causes Heart Arrhythmias MI
Missed / delayed / inadequate meals Alcohol / salicylates / β-blockers Eye Vitreous hemorrhage Worsening of DRP
Gastroparesis Other endocrine disorders – GH & Others Hypothermia Accidents
Unexpected / unusual exercise cortisol insufficiency
Deficient glucose counter-regulation Sepsis & shock
Impaired awareness of hypoglycaemia Infection
Poorly designed insulin regimen Liver failure / congenital metabolism
Factitious disorders
Errors in OHGA / insulin dose / schedule Cardiac failure
Renal failure
Symptoms
Autonomic activation Sweating Pallor
Trembling Hunger
Tachycardia Anxiety
Neuroglycopenia Confusion Inability to concentrate
Drowsiness Incoordination
Speech difficulty Seizures
Focal neuro deficits
Non-specific Nausea Headache
Tiredness
Management
1. Monitoring: ECG, pulse oximetry, vital signs
2. Supplemental low-flow O2
3. Check capillary blood glucose stat
4. Hx & examination: medication hx, recent change in drug / doses, recent & chronic
illnesses
5. Investigations: venous blood glucose, U/E/Cr, LFT, FBC
6. Treatment
Conscious PT Oral carbohydrate rich drink
Unconscious PT IV access available: IV dextrose 50% 40-50ml
No IV access: IM/SC glucagon 1mg (not for hypoglycaemia
due to sulphonylurea or liver failure)
Chronic alcoholism IV thiamine 100mg
Adrenal insufficiency IV hydrocortisone 100-200mg
Associated injuries Tetanus prophylaxis
7. Continued glucose monitoring: capillary blood glucose every 30 mins for first 2 hrs, Digitally signed by DR WANA HLA SHWE
hourly thereafter. DN: cn=DR WANA HLA SHWE, c=MY, o=UCSI
University, School of Medicine, KT-Campus, Terengganu,
8. Persistent altered mental state despite resolution of hypoglycaemia: CT head to exclude ou=Internal Medicine Group, email=wunna.
other causes hlashwe@gmail.com
Reason: This document is for UCSI University, School of
9. Disposition: depends on aetiology, severity, response and comorbidities. Admit all cases Medicine students.
Date: 2009.03.05 09:01:51 +08'00'
due to sulphonylureas due to long half-live of the agent.
7. Diabetic Ketoacidosis 4) Urinary catheter – monitor urine output
Absolute or relative decrease in insulin level in the presence of excess glucagon. 5) IV volume replacement
Usually in type 1 DM First hr NS 15-20 ml/kg/h (~1-1.5L)
Common presentation: PT devt infection causing LOW and PT stop insulin Rx. Nxt 2-4 hr 0.45% NS 10-20ml/kg/h (~1 pint q1-4 hrly)
Causes When S. glucose < 14mmol/L Change to Paeds D/S (D5W/0.45% NS)
o Infections Monitor urine output hourly
o Infarction – MI, CVA, GIT, peripheral vasculature Check U/E/Cr/Glu, beta-hydroxybutyrate & venous pH q2-4 hrs
o Insufficient insulin Correct fluid deficit (4-6L) w/in first 24 hrs, but serum osmolality should not
o Intercurrent illness drop by > 3 mOsm/kg/hr to prevent cerebral edema
Diagnostic criteria 6) Early Potassium replacement
+ +
1) Hyperglycaemia Blood glucose ≥14mmol/L S. K < 3.3 mmol/L Give 20-40 mmol K per hr until K+ >3.3mmol/L
2) Hyperketonaemia Ketonaemia or ketonuria (can be given as 2/3 KCl & 1/3 KHPO4 when S. PO4 is
3) Metab acidosis Arterial pH <7.3, bicarbonate <15mmol/L <0.3mmol/L)
+ +
S. K 3.3-4.9 mmol/L Give 10-15 mmol K per hr
+ + + +
Dehydration: usually about 4-6 L, due to osmotic diuresis. a/w loss of Na & K S. K > 5.0 mmol/L Check S. K every 2 hrs, hold off K+ infusion
+ + +
o K loss due to displacement of intracellular K by H
o Fluid deficit initially from intracellular compartment. Later, depletion of 7) Restore acid-base balance
extracellular fluid result in haemoconcentration, hypovolaemia, & hypotension ± Give NaHCO3 only if severe hyperkalaemia or arterial pH <7.0 (hydration and
renal ischaemia & oliguria insulin will help correct less severe metabolic acidosis)
Potassium depletion: IV 8.4% NaHCO3 50-100ml in 200-400ml sterile water over 1-2 hrs (=50-
o Plasma concentration a poor indicator of total deficit. 100mmol). Repeat in 2 hrs if necessary.
+
o Drop in K will occur after starting insulin Rx due to dilution by IV fluids, 8) Insulin administration
+ +
movt of K into ICF and continued renal K loss. Bolus IV SI 0.15 units/kg
Low dose continuous 0.1 units/kg/hr (5unit/hr in 50kg PT), adjust to obtain
Clinical features infusion rate of drop in S. glucose by 3-4 mmol/L/hr.
Symptoms Signs Monitor blood glucose hrly
Polyuria N/V Dehydration Acetone breath When blood glucose Halve IV SI infusion rate to 0.05-0.1 units/kg/hr & add
Polydipsia Cramps Hypotension Hypothermia <14mmol/L dextrose in IV fluid
LOW Blurred vision Tachycardia Confusion / Aim for bld glucose level of 8-12 mmol/L
Weakness Abdo pain Kussmaul breathing drowsiness / coma Maintain SI infusion until acidosis clears
*raised amylase w/o pancreatitis & leukocytosis due to stress reaction common
9) Treat precipitating factor
Complications 10) Admit
Cerebral oedema: treat with Thromboembolism 11) Admit MICU if hypotensive/oliguric & refractory to initial rehydration, mental
mannitol & oxygen DIVC obtundation/coma or total serum osmolarity >340mOsm/kg
ARDS Acute circulatory failure 12) Monitoring
Cardiac failure H/C Aim for rate of When H/C <14mmol/L
q1hr decrease of 3- Halve IV SI infusion rate to 0.05-0.1 units/kg/hr
Management 4mmol/L/hr Change IV fluid to D5W/0.45%NS 1pint q1-4hr
1) Supplemental high-flow O2 Then aim to maintain H/C of 8-12 mmol/L
+
2) Monitoring: ECG, pulse oximetry, vital signs q15min, blood glucose, ketones, K & acid- Labs U/E/Cr/Glu, beta- Monitor K+, ketonaemia and metab acidosis
base balance q1-2hrs q2- hydroxybutyrate & When acidosis clear (pH >7.3 & HCO3 >15)
3) Lab – assess DKA & look for cause 4hrs venous pH start SCSI q4hr
U/E/Cr/Ca/Mg/PO4/Glucose FBC stop SI infusion after overlap of SCSI of 1 hr
Urinalysis for ketones & leucocytes DIC screen if septic
Urine dipstick Blood culture
Serum Ketones (beta- CXR
hydroxybutyrate) Cardiac enzymes
ABG ECG
8. Hyperosmolar Hyperglycaemic Non-Ketotic state (HHNK)
C.f DKA: clinical course runs into days rather than hours, and there is greater fluid (6-
+
10L) and K loss. PTs are usually more sensitive to insulin, thus less insulin is required
Diagnostic criteria
1 Hyperglycaemia Blood glucose ≥33mmol/L
2 Hyperosmolality S. total osmolality >330mOsm/kg H2O or
effective S. osmolality >320 mOsm/kg H2O*
3 Metab acidosis Arterial pH >7.3, bicarbonate >15mmol/L
4 No ketonaemia or ketouria
+
*Effective S. osmolality = 2XNa + glucose level + urea
** exclude other causes of obtundation if s. osmolality is not high enough
Thromboembolic Cxs common: prophylactic SC heparin may be required
Management
Similar to DKA with certain exceptions
1) Supplemental High-flow O2
+
2) Monitoring: ECG, pulse oximetry, vital signs q15min, blood glucose & K q1-2hrs
3) Labs
FBC
U/E/Cr/Ca/Mg/PO4
Serum osmolality
ABG
Urinalysis
4) Look for cause – ECG, CXR
5) Urine catheter – monitor urine output
6) IV Volume replacement
Significant tissue NS rapid bolus until perfusion improves & BP stabilizes
st
hypoxia 1L NS w/in 1 hr, another 1L over nxt 2 hrs
Then 1 L 0.45% NS over nxt 4 hr
Hypertensive or sig. 0.45% NS
+
hyperNa (>155mmol/L) when S. glucose reaches 16mmol/L, switch to IV D5W
+
7) K replacement – same as DKA
8) Monitoring
9) Insulin administration
Insulin infusion 0.1 units/kg/hr
Adjust to maintain bld glucose at 14-16 mmol/L until S. osmolality ≤315 mOsm/L &
PT is mentally alert Digitally signed by DR WANA
10) Monitoring HLA SHWE
H/C (& venous Aim for rate of When H/C <16mmol/L DN: cn=DR WANA HLA
SHWE, c=MY, o=UCSI
bld glucose if decrease of 3- Halve IV SI infusion rate to 0.05-0.1 units/kg/hr University, School of Medicine,
H/C reads 4mmol/L/hr Change IV fluid to D5W 1pint q1-4hr KT-Campus, Terengganu,
ou=Internal Medicine Group,
“HHH”) Then aim to maintain H/C of 14-16 mmol/L until email=wunna.hlashwe@gmail.
q1 hr plasma osmolarity ≤315mOsm/kg & PT is alert com
Reason: This document is for
Labs U/E/Cr/Glu & Monitor K+, ketonaemia and metab acidosis UCSI year 4 students.
q2-4hrs beta- Date: 2009.02.19 09:28:42
+08'00'
hydroxybutyrate