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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

Chapter 10; DM /Diabetes

Mellitus/ (የስኳር በሽታ)
Dr. Mulualem. G

Clinical features and how to write hx of DM patient

History

N.B Type one DM patients usually present with poly symptoms. But type two
DM patients may present with complication or Asymptomatic and
diagnosed accidentally while patients visit a health facility for other
reason.
Poly symptoms (3P)
➢ Poly urea → Write in terms of Day to Night ratio (e.g. poly urea of 8:6
day to night ratio).
☛ The 24-hour urine voided by a healthy adult range from
600 to 2000ml
☛ Polyuria considered when there is consistent elimination of
an abnormally large volume of urine, > 2000ml/24hr
➢ Polydipsia → ask How much litre of water he/she drinks per day
➢ Polyphagia → less common smx than Polydipsia and Poly urea
Weight loss despite increased appetite
Generalized weakness or malaise
DKA smx’s like Vomiting, Abdominal pain and LOC
Recurrent skin infections
Recurrent itching of the vulva (candida infections)
Symptoms related to chronic complications can be present at initial diagnosis in
type II diabetic patients
➢ Numbness or pain over the lower limbs
➢ Visual impairment Or Blurred vision
➢ Foot abnormalities (ulcer, ischemia, deformity)
➢ Body swelling
Hyperglycemia features include → 3P, DKA/HHS, blurring of vision, dry mouth
and other signs of DHN especially in HHS

Risk factors
For Type II DM* For Type I DM*
The ADA recommends screening All Individuals >45 ✓ Genetic (abnormality in HLA region on
years every 3 years and Screening individuals at An Chromosome 6)
Earlier Age if they are Overweight [ BMI >25 kg/m2] and
Have One additional Risk Factor for diabetes
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o The concordance of type 1 DM
in identical twins ranges between

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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

Individuals with any one of the following need screening 40 and 60%, indicating that
for type II diabetes. If the result is normal, repeat additional modifying factors are
screening every 3 years; but if the result is in the likely involved in determining
whether diabetes develops.
prediabetes range repeat the test every year.
o Although the risk of developing
type 1 DM is increased tenfold in
✓ HTN relatives of individuals with the
✓ Dyslipidemia (HDL < 35mg/dl and/or triglyceride level >
disease, the risk is relatively low:
250mg/dl) 3–4% if the Parent has type 1
✓ Family history (First-degree relative with diabetes) diabetes and 5–15% in a Sibling
o Type II DM pts have strong genetic association (depending on which HLA
than type I DM haplotypes are shared). Hence,
o The concordance of type II DM in identical twins most individuals with type 1 DM
is between 70 and 90%. do not have a first-degree
o If both parents have type II DM, the risk relative with this disorder.
approaches 40%. ✓ Autoimmunity→ like Hashimoto’s
✓ Environmental factors thyroiditis
o Overweight or central obesity (BMI >25kg/m2) ✓ Environmental factors
▪ ≥ 80% of type II DM pt’s are Obese o Diet→cow milk during infancy→
o Physical inactivity antibody to cow insulin is similar
o Increased intake of Raw meat, fat and lipid to human insulin known as
containing food antigen mimickeracy
o Smoking
o Toxin → which affect pancreatic
o Alcohol intake B cells
✓ Old age (age ≥ 45) o Mumps, rubella, coxsackie
✓ Ethnicity→ common in African American infection
✓ Individuals with prediabetes should be tested yearly ✓ Young age (age <30)
✓ PCOS (polycystic ovary sxx) in females or acanthosis
nigricans
✓ History of atherosclerotic Cardiovascular disease
✓ Drugs → steroids (prednisolone), Phenytoin, thiazide
✓ Women with history of GDM (gestational DM)
✓ Chronic pancreatitis
✓ Pheochromocytoma
✓ Acromegaly
*no clear-cut boundary for Type I & II DM in RF. One can be RF for the other.

N.B Metabolic SXX

✓ a.k.a syndrome x, insulin resistance sxx, obesity dyslipidaemia sxx
✓ It Includes (Mnemonics → Angeles Have Healthy Life style)
o Abdominal obesity (BMI > 40 kg/m2 for male and >30 kg/m2 for
female or waist circumference >102 cm for male and >88 for
female)
o Hyperglycemia (DM)
o HTN
o Lipid abnormality (Hyperlipidemia, dyslipidemia)

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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

1. Acute complications
▪ DKA
▪ HHS
▪ Hypoglycaemia
▪ Infection
▪ Lactic acidosis
➢ Acute complications may occur at any stage of the disease

Chronic complications

➢ Chronic Complications begin to appear during the Second Decade of

hyperglycemia.
➢ Individuals with previously undetected Type II DM may present with chronic
complications of DM at the time of diagnosis.
➢ Classified as microvascular, macrovascular and avascular complications
❖ Micro vascular
▪ Retinopathy (Non proliferative or proliferative), Macular oedema
Almost everyone with Type I DM will eventually develop
Nonproliferative Retinopathy. But luckily, the retinopathy that
destroys vision, Proliferative Retinopathy, is far less common.
▪ Neuropathy
It can be Mono neuropathy, poly neuropathy, mono neuropathy
multiplex or autonomic neuropathy
Most common (50-75%) cause of non-traumatic foot Amputation
▪ Nephropathy
DM is most common cause of renal insufficiency or renal failure.
ESRD is more common in Type I DM than Type II DM
Diabetic Nephropathy have 5 stages
1) Renomegaly, increased GFR
2) Basement membrane thickening
3) Micro albuminuria (30-300 mg/dl)
4) Macro albuminuria (>300 mg/dl)
5) ESRD (End stage renal disease), Uraemia, HTN
❖ Macro vascular
▪ CAD (coronary artery disease like MI & IHD. N.B DM is the most
common cause of Silent MI (the so called ‘’DM is silent killer’’))
▪ CVA (cerebrovascular Attack like stroke & TIA)
▪ PAD (Peripheral arterial disease)
❖ Avascular
▪ GIT
Gastro paresis → manifest with Diarrhoea, post prandial bloating,
fullness and discomfort, intestinal obstruction
Motility disorders → atony (manifest with constipation) or
hypersonic (manifest with Diabetic Diarrhoea)
▪ GUS → uropathy, sexual dysfunction (like decreased libido, impotence)
▪ Skin → diabetic foot ulcer (cellulitis, gangrene)
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▪ Infections → UTI, pneumonia, periodontal infection, Malignant Otitis

externa (specific to DM), Rhino orbito cerebro mucoro mycosis (extremely
rare but specific to DM)
▪ Cataract, glaucoma
▪ Bone destruction
▪ Others which are specific to DM
Acalculous cholecystitis
Tubular papillary necrosis (ATN)
Volvo vaginal candidiasis, oral candidiasis

Look at Screening and management of Chronic complications of DM below

under management section

Sample history
Chief compliant

polydipsia and polyuria of three weeks duration

HPI

This patient was last relatively healthy 03 weeks back at which time he started to
experience polyuria of 7- 8 times during night and 10-12 times during daytime with
increased feeling of thirst for which he drinks 4 - 6 liters of water per day but no
polyphagia.

Associated with this he also experienced unquantified but significant weight loss to
the extent his trousers become loose despite increased appetite, generalized
weakness to the extent he couldn’t perform his routine daily activities.

For this complaint he visited a private clinic in Gondar town where he was told to
have increased blood sugar level and referred to our hospital for better investigation
and management. From the referral paper, RBS was 350mg/dl and repeated on next
day of first determination and the value was 289 mg/dl, FBS was 194 mg/dl, from
U/A glucose was +2 and ketone free but no treatment given.

▪ No family hx of similar illness (Genetics)

▪ No self or family hx of HTN (RF)
▪ No hx smoking or chronic alcohol intake (RF)
▪ No hx of Drug (prednisolone, thiazide, phenytoin predispose to DM, lithium and diuretics are
DDX for polyuria)
▪ He/she usually eats injera made of ‘‘teff’’ and ‘‘machilla’’ and ‘’wott’’
made of ‘‘atter’’ and ‘‘dagusa’’ 3-4 times per day. Occasionally he
eats meat during holidays (Increased intake of Raw meat, fat and lipid containing food are
RF for DM)
▪ No hx of Anterior neck swelling, heat intolerance, profuse sweating,
sleep disturbance, palpitation, tremor or irritability (autoimmune disease like

▪
Hashimoto’s thyroiditis can occur concomitantly with Type I DM)
No hx of LOC, Abdominal pain or Vomiting (DKA→CXN)
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▪ No hx of blurring of vision, eye pain or discharge (retinopathy →CXN)

▪ No hx of Flank pain, dysuria, hematuria, urgency or frequency
(Nephropathy, UTI →CXN)
▪ No hx of numbness, tingling, burning sensation, or wound over the
body (DM patients don’t sense pain during trauma due to neuropathy which predispose to Diabetic
ulcer →CXN)
▪ No hx of body weakness or sensory loss (CVA like stroke →CXN)
▪ No hx of chest pain, Dyspnea, orthopnea, PND or Palpitation (CAD/MI/
ending up in CHF →CXN)
▪ No hx of cough, fever or fast breathing (pneumonia →CXN)
▪ No hx of intermittent claudication, bluish discoloration of skin, cold
skin or skin Ulcer (PAD →CXN)
▪ No hx Nausea, vomiting, diarrhoea, or constipation (Gastroparesis, motility
disorder →CXN)
▪ No hx of Head injury or Neurosurgery (central Diabetic Insidious→ DDX)

Finally, he was admitted to our hospital walking by himself.

Physical examination (pertinent findings)

In your physical examination assess signs of DKA and Diabetic Foot

ulcer together with these pertinent findings.

1 GA

✓ Obesity
✓ Cushionoid face
Vital signs
✓ OHT→ due to Autonomic neuropathy
✓ HTN → >130/80 is HTN in DM
✓ Resting tachycardia → due to Autonomic neuropathy
✓ Obesity → calculate BMI and measure Waist circumference
HEENT
✓ Hair loss
✓ Periorbital swelling → Mucor mycosis
✓ Active Ear discharge → Malignant otitis externa
✓ Oral thrush → oral candidiasis
✓ Poor dental hygiene (tooth loss)
✓ Xanthelasma → N.B it is common around eye lids and Achilles tendon
✓ Cataract
LGS
✓ Thyroid enlargement → poly glandular autoimmune disorder (PGAID)
✓ Loss of sweating → due to Autonomic neuropathy
RS
✓ Signs of consolidation → pneumonia (common infection in DM) 519
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CVS
✓ Arterial examination especially posterior tibial artery and dorsalis pedis
artery (PAD)
✓ IHD
Abdominal examination
✓ Hepatomegaly → from fatty liver
✓ Abdominal distention → from Gastroparesis or atony
✓ Intestinal obstruction → from autonomic neuropathy
✓ Murphy sign +ve → acalculous cholecystitis
GUS
✓ Supra pubic tenderness or CVAT → UTI, pyelonephritis
✓ Active vaginal discharge or whitish plaque → vaginal candidiasis (common
than oral candidiasis)
✓ Urinary bladder atony → voiding difficulty → due to Autonomic neuropathy
✓ Impotence → due to Autonomic neuropathy
MSS
✓ Diabetic foot ulcer
✓ Deformities → hammer toes, claw toes, prayers hand sign
✓ Duptyrens contracture

Image; prayers sign

IS
✓ Cold/dry skin, crackles, fissures → autonomic neuropathy
✓ Hair loss
✓ Skin atrophy
NS
✓ GCS
o LOC → DKA
✓ Cranial nerve
o Cranial nerve palsy (CN III, IV, VI and VII)
✓ Motor
o Muscle wasting
o Hypotonia
o Decreased power
o Hyporeflexia
o Peripheral neuropathy
▪ Motor neuropathy → foot drop, wrist drop, mono neuropathy

✓ Sensory
multiplex
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oPeripheral neuropathy → distal symmetric polyneuropathy (DSPN)

which is glove and stocking pattern with sensory loss or
paraesthesia. Pain and temperature loss are common.
✓ Autonomic neuropathy
• Urinary bladder atony → voiding difficulty
• Impotence
• Resting tachycardia
• Loss of sweating
• GI neuropathy → Gastroparesis, Diabetic diarrhoea

N.B several Rare Infections are seen almost exclusively in the diabetic population.
Examples include
❖ Rhino-cerebral Mucor-mycosis
❖ Emphysematous Infections of the Gall Bladder and Urinary Tract
❖ "Malignant" or Invasive Otitis Externa.

DDX

For Patient presenting with polyuria and/or polydipsia

1. DM
2. Diabetic insipidus (DI)
DI is a disorder resulting from abnormalities of Antidiuretic hormone (ADH)
production from the hypothalamus or ADH action in the kidney. Final common
pathway → no response to ADH
Characterized by polyuria and polydipsia → the passage of copious amounts of
dilute urine (low specific gravity, usually < 1.010).
There are 4 Types of DI, the 1st two are common forms
Nephrogenic DI → a.k.a peripheral DI. Due to increased resistance of ADH
receptors in kidney to ADH
✓ Nephrogenic causes
• Congenital
• Acquired
o CRF
o Lithium
o Hypokalemia
o Hypercalcemia
Neuropathic DI → a.k.a central, hypothalamic, pituitary or neurohypophyseal DI.
Caused by decreased secretion or lack of secretion of ADH from posterior
pituitary. Head injury or neurosurgery are risk factors for central DI.
▪ Central/Cranial causes
➢ Congenital
➢ Acquired
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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

 Post traumatic
 Iatrogenic (post-surgical)
 Tumours
 Infection
 Idiopathic
Gestational DI → Caused by a deficiency of the antidiuretic hormone, vasopressin,
that occurs only during pregnancy
Dipsogenic DI → a form of primary polydipsia. Caused by Abnormal thirst and
Excessive intake of water or other liquids

3. Drugs → lithium, diuretics (Furosemide, thiazide), Alcohol

4. Pheochromocytoma
5. AKI/CKD
6. Psychogenic polydipsia → patient drinks as he/she assume of being dry
mouth, common in mental disorders
7. Hypercalcemia/hypokalaemia
8. Addison’s disease
9. ? Cushing sxx

IX

1. Blood sugar → look at table below under discussion part for ADA diagnostic
criteria of DM
✓ RBS
N.B FBS and HbA1c are
✓ FBS
✓ OGTT reliable for screening
✓ HbA1c → tells about the past 3 months sugar level. Normal value is 4 -
5.6% of body Haemoglobin.
2. U/A → what do you expect from U/A
✓ Glucosuria (glucose +2, +3…)
✓ Ketonuria from DKA (ketone +2, +3…)
✓ Albuminuria from DM nephropathy
✓ WBC casts → suggest infection like UTI, pneumonia, sepsis
3. CBC → what do you expect from CBC
✓ Leukocytosis
✓ Anemia
✓ Ketone bodies
4. Serum electrolyte → hyperkalaemia despite decreased K+ level in cells because
acidosis impairs H+/ K+ pump (i.e. impair K+ absorption from blood stream). K+
Increase in blood during analysis but hypokalaemia in cells.
5. RFT
6. Lipid profile → increased LDL, Triglyceride, and cholesterol but decreased HDL
7. PICT
8. ECG & CXR → if indicated
9. Serum insulin level and C-peptide → C-peptide < 0.6 ng/dl in Type I DM
and > 1 ng/dl in >1-2 years for type II DM (Serum insulin or C-peptide
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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

measurements do not always distinguish type 1 from type 2 DM, but a low C-
peptide level confirms a patient's need for insulin.
10. Islet cell auto antibody → Anti - GAD (Glutamic acid decarboxylase) & Anti -
insulin antibody
11. Blood and urine culture
12. Serum PH and ketone
13. ABG (Arterial blood gas) analysis
✓ PH → acidosis
✓ Serum bicarbonate → low which shows metabolic acidosis
✓ Anion gap = 2Na+ - (CI- + HCO3-) or (Na+ + K+) - (CI- + HCO3-)
✓ O2 & CO2 → low CO2 due to respiratory compensation.

In newly diagnosed patients

➢ Diagnostic tests: Fasting or random blood glucose, glycated hemoglobin
(HbA1c)
➢ Urine ketones
➢ Urine albumin
➢ BUN and creatinine
➢ Fasting lipid profile
➢ ECG (adults)
In diagnosed patients, follow up investigations
➢ Glycemic control: HbA1c, FBS together with post prandial plasma glucose
(i.e. RBS 2hr after breakfast, 2hr after lunch, and 2hr after dinner)
➢ Screening for complications: Urine albumin/protein, retinal screening by
ophthalmologist, serum creatinine and urea.
➢ Other cardiovascular risk screening: Lipid profile (if not already on statin).

Discussion

Diabetes Mellitus (DM) was derived from two words; Diabetes = “siphon” or
“running through” meaning Large urine volume and Mellitus = sweet to indicate
Glucose in urine.
DM refers to a heterogenous group of common metabolic disorders that share
the phenotype of hyperglycemia.
Several distinct types of DM are caused by a complex interaction of genetics
and environmental factors.
Depending on the etiology of the DM, factors contributing to hyperglycemia
include Reduced Insulin Secretion, Decreased Glucose Utilization, and
Increased Glucose Production.
Diabetes is the leading cause of cardiovascular disease, CKD (ESRD), visual
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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

Etiologic classification of diabetes mellitus

The classification of diabetes includes four clinical classes

A. Type I diabetes → results from beta cell destruction, leading to absolute insulin
deficiency (complete or near-total insulin deficiency).
1. Immune-mediated
2. Idiopathic
B. Type II diabetes
➢ It is a heterogeneous group of disorders characterized by variable degrees
of insulin resistance, impaired insulin secretion, and increased glucose
production.
➢ May range from predominantly insulin resistance with relative insulin
deficiency to a predominantly insulin secretary defect with insulin resistance
C. Gestational diabetes mellitus (GDM) → diabetes diagnosed during pregnancy in
previously non-diabetic woman
D. Other specific types of diabetes
➢ Chromosomal abnormalities (from MODY 1 to MODY 6, MODY = Maturity
onset diabetes of the young /in youth/)
 MODY is a subtype of DM characterized by autosomal dominant
inheritance, early onset of hyperglycemia (Usually <25 years), and
impairment in insulin secretion
➢ Genetic defects in insulin action
➢ Diseases of the exocrine pancreas (Pancreatitis, Trauma/pancreatectomy,
Neoplasia, Cystic fibrosis, Hemochromatosis….)
➢ Endocrinopathies (Hyperthyroidism, Acromegaly, Cushing's
syndrome,Glucagonoma, Somatostatinoma, Pheochromocytoma,
Aldosteronoma…)
➢ Drug or chemical induced (Glucocorticoids, Thyroid hormone, Thiazides,
Pentamidine, Nicotinic acid, Beta-adrenergic agonists, Alpha interferon…)
➢ Infections (Congenital rubella, CMV…)
➢ Other genetic syndromes sometimes associated with diabetes (Down
syndrome, Klinefelter syndrome, Turner syndrome, Porphyria, Friederich's
ataxia….)
➢ MRDM (Malnutrition related DM)
➢ Others

The clinical course and treatment of the different types of diabetes are
different; hence, classification of the type of diabetes is very important to
determine therapy.
The traditional thinking that type II diabetes as the disease of adults and type
I diabetes as the disease of children is not accurate as both diseases can
occur in both age groups. So, age is not a criterion in the classification
system.
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The terms insulin-dependent diabetes mellitus (IDDM) and non-insulin-

dependent diabetes mellitus (NIDDM) from previous classifications are obsolete
nowadays.
Since many individuals with type II DM eventually require insulin treatment for
control of glycemia, the use of the term NIDDM generated considerable
confusion.

Suggestive clues to Differentiate Type I DM from Type II DM*

Type I DM Type II DM
Common in young age (usually < 30) Common in middle aged and elderly
Normal BMI or lean body mass > 80 % of pts are obese, but elderly may
Usually No immediate family hx be lean
Short duration of symptoms (days to weeks) Usually have +ve family hx
and present with poly symptoms Asymptomatic or present with complication
Can present with DKA (skin infections, pruritis, vulvovaginitis,
Management is based on Insulin only vascular and avascular cxn) and Symptoms
GDM is rare in Type I DM may persist for months or years (i.e. chronic
Associated with other auto immune disease cxn are cmn)
(like hashimoto’s thyroiditis, autoimmune Can present with HHS
hemolytic anemia, pernicious anemia, coeliac Oral hypoglycemic drugs are mainstay of
disease, vitiligo) treatment (unless insulin indicated)
destruction of the pancreatic beta cells and GDM is common in Type II DM
insulin deficiency. Associated with metabolic syndrome (DM,
HTN, Dyslipidemia, Abdominal obesity)
Impaired Insulin Secretion and Insulin
Resistance are central to the development of
Type II DM.
*no clear-cut boundary for Type I & II DM clinically.

Table. Current ADA diagnostic criteria for diabetes mellitus

Diagnostic test Normal Pre-diabetes Diabetes Remarks
Fasting blood 75 to < 100 100-125mg/dl >126 At least 2 tests needed*
glucose (FBS)  mg/dL mg/dl
Hemoglobin A1C 4.0 – 5.6% 5.7-6.4% > 6.5% At least 2 tests needed*
(HbA1C) #

02-hour plasma < 140 mg/dl 140-199mg/dl >200mg/dl At least 2 tests needed
glucose tolerance
test (OGTT)
Random blood 65 to < 140 ? 140-199mg/dl >200mg/dl DM diagnosed Only if RBS
glucose (RBS) mg/dL
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>200mg/dl is accompanied
by Classic Symptoms of DM
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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

(Polyuria, Polydipsia, Weight

Loss)
1 mmol/l = 18 mg/dl (e.g >126 mg/dl means > 7.0 mmol/l)
* If both fasting blood sugar and hemoglobin A1C are done initially and both are in the diabetic
range, repeat test is not necessary for the diagnosis.
#
If there is significant discrepancy between HbA1C and blood glucose measurements, use the
blood glucose level.

Fasting is defined as no caloric intake for at least 8 hours

OGTT test should be performed (as described by the WHO), using a glucose load containing the
equivalent of 75-gram anhydrous glucose dissolved in water. Then measure glucose level after 2
hrs of taking 75-gram glucose (in our set up we use 9 vials of D40, since 1vial of D40 is 8gram,
which means 8 x 9 = 72gram)

Some use the term "increased risk for diabetes" (ADA) or "intermediate hyperglycemia" (WHO)
rather than "prediabetes."

Prediabetes patients are at Greater Risk of progressing to Type II Diabetes and have an
increased risk of Cardiovascular Disease.

Insulin secretion and action

Glucose is the key regulator of insulin secretion by the pancreatic beta cell,
although amino acids, ketones, various nutrients, gastrointestinal peptides, and
neurotransmitters also influence insulin secretion.
Insulin is the most important regulator of this Metabolic Equilibrium, but neural
input, metabolic signals, and other hormones (e.g., glucagon) result in
integrated control of glucose supply and utilization

In the Fasting State

low insulin levels Increase Glucose Production by Promoting Hepatic
Gluconeogenesis and Glycogenolysis and Reduce Glucose Uptake In Insulin-
Sensitive Tissues (Skeletal Muscle and Fat), Thereby promoting mobilization of
Stored Precursors such as Amino Acids and Free Fatty Acids (Lipolysis).
Glucagon, secreted by Pancreatic Alpha Cells when blood glucose or insulin
levels are low, Stimulates Glycogenolysis and Gluconeogenesis by the Liver
and Renal Medulla.

Postprandially

the glucose load elicits a rise in insulin and fall in glucagon, leading to a
reversal of these processes.
Insulin, An Anabolic Hormone, Promotes the Storage of Carbohydrate and Fat
and Protein Synthesis.
The major portion of Postprandial Glucose is utilized by Skeletal Muscle, an
effect of insulin-stimulated glucose uptake.
Other tissues, most notably the Brain, utilize glucose in an insulin-independent
fashion.
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Chapter 10; DM /Diabetes Mellitus/ (የስኳር በሽታ)

Pathophysiology

Type I DM
Type 1 DM is the result of interactions of Genetic, Environmental, and
Immunologic Factors that ultimately lead to the destruction of the pancreatic
beta cells and insulin deficiency.
Type 1 DM results from Autoimmune Beta Cell Destruction, and most, but not
all, individuals have evidence of Islet-directed Autoimmunity.
Individuals with a Genetic Susceptibility have normal beta cell mass at birth but
begin to lose beta cells secondary to autoimmune destruction that occurs over
months to years.
This autoimmune process is thought to be triggered by an Infectious or
Environmental Stimulus and to be sustained by a Beta Cell–specific Molecule.
Features of diabetes do not become evident until a majority of beta cells are
destroyed (70 - 80%).
After the initial clinical presentation of type 1 DM, a "honeymoon" phase may
ensue in the first 1 or 2 years after the onset of diabetes.
During which time Glycemic control is achieved with Modest Doses of Insulin
or, rarely, Insulin is Not Needed.
However, this fleeting phase of endogenous insulin production from residual
beta cells disappears as the autoimmune process destroys remaining beta
cells, and the individual becomes insulin deficient.
Some individuals with long-standing type 1 diabetes produce a small amount of
insulin (As reflected by C-peptide production)
And some individuals have insulin-positive cells in the pancreas at autopsy.
Islet Cell Autoantibodies (ICAs) are present in the majority of individuals
(>85%) diagnosed with New-onset type 1 DM.

Type II DM
Type 2 DM is characterized by Impaired Insulin Secretion, Insulin Resistance,
Excessive Hepatic Glucose Production, and Abnormal Fat Metabolism. Insulin
Resistance and Abnormal Insulin Secretion are central to the development of
Type II DM.
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Although the primary defect is controversial, most studies support the view that
Insulin Resistance precedes an Insulin Secretory Defect but that diabetes
develops only when insulin secretion becomes inadequate.
In the early stages of the disorder, glucose tolerance remains near-normal,
despite insulin resistance, because the pancreatic beta cells compensate by
increasing insulin output
In Asian, African, and Latin American), DM that is Ketosis Prone (Often
Obese) or Ketosis-Resistant (Often Lean) is commonly seen.
The disease is polygenic and multifactorial, since in addition to Genetic
Susceptibility, Environmental Factors (Such as Obesity, Nutrition, and Physical
Activity) modulate the phenotype.
Even though, HLA gene Abnormality is speculated in type I DM, the genes
that predispose to type 2 DM are incompletely identified. Genetic
Polymorphisms associated with type 2 diabetes have also been found

Management of DM

Principle of management

Medical Nutrition Therapy (MNT)

Pharmacologic treatment with insulin or oral hypoglycemic drugs
Diabetics education about
 Diet
▪ When they feel hypoglycemia, they have to take table sugar or candy
(they should have candy in their pocket)
▪ Avoid alcohol; which expose to comorbidities like HTN and patient
may miss his/her drug because of alcohol intoxication
▪ Take mixed food; variation between breakfast and dinner if possible
▪ Take vegetable
▪ Avoid refined food since they have high sugar content
▪ Avoid raw meat and fat intake
 DM natural history
 Type and Route of administration of Insulin.
▪ In our setup, patients differentiate regular insulin and NPH based on
color. (regular insulin = ውሃው፣ ውሃ የሚመስለው and NPH = ወተቱ ፣
ወተት መልኩ)

Administration
▪ Morning → periumbilical
▪ Evening → extremities
• This variation is because of exercise increase insulin absorption
(extremities involved in daytime activity)
 storage of insulin
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Nitsbin (ንጽቢን) Bedside oriented Internal medicine 1st edition