Diabetes Mellitus Flashcards
Definition, classification, diagnostic criteria, risk factors, etiology
DM is a metabolic disease characterized by hyperglycemia
resulting from defects of insulin secretion, action or both.
Classification
Type 1 (IDDM)- Autoimmune B cell destruction of cells leading to complete or absolute insulin deficiency.
Type 2(NIDDM)- Insulin resistance or secretory defects due to abnormal structure of insulin or change in insulin receptors or relative insulin deficiency.
Gestational DM placenta produces hormones that makes cells less sensitive to insulin.
Main target of insulin: muscles, liver and adipocytes.
Diagnostic criteria
According to anamnesis-polydipsia,polyphagia and polyuria
b)random glucose test- if it is > 11.1 mmol/l it confirms it but you have to do it multiple times
c)fasting glucose test- if it is >7 mmol/l it confirms it but we have to do it multiple times
d)glucose tolerance test >11.1 mmol/l
-we give patient glucose within the first 30 mins there will be increase of glucose level
-in 1 hour time the glucose level will start reducing
-after 2 hours it will reduce to normal glucose level ,if it is greater than 11.1 mmol/l the person is diabetic.
Glycated hemoglobin level >39mmol/l >6.5
Obese patients
Physical inactivity
Testing age 45years
Prediabetes
FGT-5.6-6.9mmol/l
Glucose tolerance test- 7.8-10.9mmol/l
Glycated hemoglobin- 39 and above or to 47mmol/l or 5.7-6.4
Risk factors
Obesity, genetics, physical inactivity,hypertension,autoimmune disease, atherosclerosis
Type 1 DM
Etiological factors
Genetic predisposition, environmental triggers, immune mechanism gone wrong( autoimmune) with destruction of beta cells
Progressive destruction of 50% of beta cells
Manifestations of DM
Total destruction of cells.
Clinical features
Labile duration, polyuria,polydipsia, dehydration, glucosuria, hyperglycemia
Investigation
Lab findings
FBG, OGTT, Glycated hemoglobin, strip test, serological markers of autoimmune process
Treatment
Fast-acting (begin to work within 5-15 min and are active for 3-4 hrs)
– Aspart
– Lispro
– Glulisine
Short-acting (begin working within 30 min and is active about 5-8 hrs) – Regular insulin
– Actrapid
– Humulin R
Intermediate-acting (begin working in 1-3 hrs and is active 16-24 hrs) – Protaphane
– Monotard
Long-acting (begin working within 1-2 hrs and continue to be active, without major peaks or dips, for about 24 hrs)
– Glargine
Ultra-long acting (begin working within 30–90 min and continues to be ac-
tive for greater than 24 hrs) – Degludec
-Combination insulin products (begin to work with the shorter acting insulin
and remain active for 16-24 hrs)
– Novolog Mix 70/30 – Novomix 30
– Humalog Mix
Aspart+ nph in ratio 1:2 before meals, morning and evening.
Type 2 DM
Etiology
Receptor abnormalities( number, shape, blocking antibodies),
pre-receptor: abnormal insulin
Post receptor: mutation and defective signal transduction
Symptoms; normally asymptomatic
Insulin may be normal
How to differentiate between type 1 and type 2
Immunological assay: antibodies to insulin,islet cells present in type 1 and absent in type 2
Treatment
dietary treatment
Avoid eating sugary foods
Eat healthy
Exercise
Avoid sedentary lifestyle
Drugs
Biguanides- metformin which increases insulin sensitivity and decrease liver production of glucose.
a- glucosidase inhibitors- acarbose- delays intestinal absorption of glucose
Sulfonylurea- glibenclamide- stimulates insulin release, inhibits lipolysis
Thiazolinidiones- rosiglitazone- improves insulin sensitivity in muscles and reduce glucose production in liver.
Incretin system drugs
Incretin hormones are secreted by entero- endocrine cells. They control glycemia
DPP4 inhibitors - sitangliptin-incretin mimetic which increases insulin secretion and release only in hyperglycemia
GLP-1 receptor agonist- liraglutide-promotes weight loss
Amylin agonist- decreases postprandial glucose by inhibiting glucagon
SGLT2 inhibitors- dapaglifluzin- decreased hyperglycemia and causes glucosuria by reducing glucose reabsorbtion and increases its excretion
Indications for insulin for type 2
Pregnancy, Post MI, Hig dose corticosteroids therapy
Newly diagnosed, after operation
Criteria
Mild, moderate and severe
Compensated, subcompensated and decompensation
Labile and stabile
Complications of DM
Acute- DKA, lactic acidosis, hypoglycemia,HHS
Chronic- micro vascular and macro vascular
Micro- eyes, nerves, kidney
Macro, heart, brain, blood vessels
DKA
DKA
Definition-It is an acute, major, life-threatening complications of diabetes that occurs mainly in type 1 diabetes patient. It is occurs when your body produces high level of blood acids called ketones.
Symptoms of acidosis
Headache, sleepiness, confusion, loss of consciousness, coma
shortness of breath, coughing ,arrhythmia, increased heart rate, seizures, weakness, nausea, vomiting, diarrhea, ketoacidosis <7.3 pH, ketonuria 2+, kaussmaul breathing, dehydration
Classification of diabetic ketoacidosis.
Mild- plasma glucose is >250, arterial ph is <7.3serum bicarbonate is <15 urine ketone is +, serum ketone is +, effective serum osmolality is variable, anion gap is > 10, mental status is alert
Moderate-plasma glucose is >250mg/dl, arterial ph is <7.2, serum bicarbonate is<10urine ketone is +, serum ketone is +,effective serum osmolality is variable, anion gap is >12, mental status-alert/drowsy
Severe-plasma glucose is 250 mg/dl, arterial ph <7.1, serum bicarbonate is <5 urine ketone is +, serum ketone is +, effective serum osmolality is variable, anion gap is >12, mental status is stupor/coma.
Clinical types
Abdominal, vascular collapse, cerebral, renal, mixed
Treatment
Dehydration
Correct electrolyte imbalance
Decrease hyperglycemia
Hypoglycemia, lactic acidosis
Hypoglycemia <3.9 for DM patients
Etiology is the overdose of insulin
In non-DM patients- exogenous insulin.
Low C-peptide will be low in exogenous insulin but not in endogenous insulin.
Symptoms; sweating, tremor, tachycardia, tachypnea, hunger, lack of concentration, headache, dizziness, seizures, abnormal behavior
Treatment
50%dextrose and then 5/10% dextrose
Check RBS every half hour till patient is conscious, then give food, treat underlying course
OR
Inject IM 1mg glucagon and somatostatin analog
Lactic acidosis
This is caused by metformin.
Increases hepatic production of glucose, nausea, vomiting
Treat with IV sodium bicarbonate
DM retinopathy, nephropathy, neuropathy
Retinopathy is divided into
Background- micro-aneurism, hard exudates and hemorrhages
Pre-proliferative- stage before end stage characterized by cotton wool spots and hemorrhages
Proliferative- new vasculization, maculopathy
Cataracts, glaucoma, rubeosis iridis ( new vascularization)
Nephropathy
Morgensen stages
I- hyper functional kidney
II-stage of initial changes in structure
III- initial nephropathy- microalbuminuria with high or normal GFR
IV- Proteinuria, macroalbuminuria, decreased GFR
V- Chronic renal failure
Nerves( neuropathy)
1. Symmetric sensory polyneuropathy- gloves and socks phenomena- numbness, pin and needles
Monofilament testing
Treat with amitryptilline, paracetamol, gabaoentin
2. mononeuritis complex- cranial nerve palsies(6 and 3)
3. Amyotrophy- painful wasting of quadriceps muscle.
4. Autonomic neuropathy
Macro vascular and dermatological complications
Heart- coronary heart disease
Brain- stroke
Blood vessels- peripheral artery disease
Dermatology
Bacterial infection, fungal infections, chronic puritis, acanthosis nigricans, necrobiosis lipoidica diabeticorum
