1. Dr.Debajyoti Chakraborty
PGT UnitII G.M.

3. 
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Diabetic Glomerulopathy*
(including diabetic tubulopathy)
Renal artery stenosis
Papillary necrosis
Renal tubular acidosis
Urinary tract infections
CIN

4. 
Diabetic nephropathy is the leading cause of
ESRD in the United States and a leading cause
of DM-related morbidity and mortality . Both
microalbuminuria and macroalbuminuria in
individuals with DM are associated with
increased risk of cardiovascular disease.
Individuals with diabetic nephropathy comm
only have diabetic retinopathy .

5. Approximately one third of type 1
diabetic patients will have a GFR
higher than the upper normal range of
age matched healthy nondiabetic
subjects. The degree of hyperfiltration
is less in type 2 diabetic patients and
reported lacking in some studies. The
GFR elevation is particularly
pronounced in newly diagnosed
diabetic patients and during other
intervals with poor metabolic control.
Intensified insulin treatment and nearnormal blood glucose control reduce
GFR toward normal levels after a
period of days to weeks in both type 1
and type 2 diabetic patients

6. 
Assess urine albumin excretion annually (B)
◦ In type 1 diabetic patients with diabetes duration of
≥5 years
◦ In all type 2 diabetic patients at diagnosis

Measure serum creatinine at least annually (E)
◦ In all adults with diabetes regardless of degree of
urine albumin excretion
◦ Serum creatinine should be used to estimate GFR
and stage level of chronic kidney disease, if present

7. .Under most circumstances untimed (‗‗spot‘‘) urine samples should be used to
detect and monitor proteinuria in children and adults.
• It is usually not necessary to obtain a timed urine collection (overnight or 24hour) for these evaluations in either children or adults.
• First morning specimens are preferred but random specimens are acceptable if
first morning specimens are not available.
• In most cases screening with urine dipsticks is acceptable for detecting
proteinuria. Patients with a positive dipstick test should undergo confirmation
of proteinuria by a quantitative measurement (ACR)within 3 months.
• Patients with two or more +ve quantitative tests temporally spaced by1to2
weeks should be diagnosed as having persistent proteinuria and undergo further
evaluation and management for ckd.
• Monitoring proteinuria in patients with chronic kidney disease should be
performed using quantitative measurements.

9. Kimmelstein wilson lesion

10. 
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
Light chain deposition disease
Amyloidosis
Nodules may occur in advanced stages of
subendothelial membranoproliferative or
mesangiocapillary glomerulonephritis, also
called membranoproliferative or mesangiocapillary glomerulonephritis type 1

11. 

a large majority of patients have albuminuria. Lack
of albuminuria may occur in DN rarely but should
prompt for search of alt. cause for altered RFT
the urinary sediment is characteristically
unremarkable—i.e., there are usually no casts, no
white blood cells, and no red blood cells—although
red blood cells (2 to 15 /hpf) may be seen in up to
30% of patients , still active sediments are to be
always suspected as a herald for other diseases
Most common: interstitial
nephritis>PIGN> memb. Neph.>FSGS

12. 

the majority of patients have retinopathy
before the onset of diabetic kidney disease.
Lack of retinopathy in face of progressive
renal injury must draw attention
as previously noted, the duration of the
disease is also important; it is relatively
unusual to diagnose diabetic nephropathy
before 5 years of diabetes.

13. There are some novel markers for estimation of
stage of ckd like cystatin based GFR, urinary
glycoprotein, CYP24A1, MANBA, CUNB(gene
polymorphisms) but recent KDOQI guidelines have
recommended that these are not required at present
to include in monitoring ckd pts.

14. eGFR
Recommendation for monitoring
of eGFR
All patients
Yearly (rule out possibility of
NDRD)
45-60
6 monthly
30-44
3 monthly
<30
Referal to nephrologist
<60
Evaluate for complications of CKD
According to Kdoqi guidelines every pt. s with stage3 & above
should be evaluated for bone disease by routine measurements of
Ca2+ , PO43- , iPTH for evaluation of bone disease .

15. Microalbuminuria(30299mg/d)

17. 
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Lowering A1C to below or around 7% has been shown to
reduce microvascular complications and, if implemented
soon after the diagnosis of diabetes, is associated with
long-term reduction in macrovascular disease (B)
Therefore, a reasonable A1C goal for many nonpregnant
adults is <7% (B)
Providers might reasonably suggest more stringent A1C
goals (such as <6.5%) for selected individual patients, if
this can be achieved without significant hypoglycemia or
other adverse effects of treatment (C)
Appropriate patients might include those with short
duration of diabetes, long life expectancy, and no
significant CVD (C)

18. Less stringent A1C goals (such as <8%) may
be appropriate for patients with (B)
History of severe hypoglycemia, limited life
expectancy, advanced microvascular or
macrovascular complications, extensive comorbid
conditions
• Consider aspirin therapy (75–162 mg/day) (C)
As a primary prevention strategy in those with type
1 or type 2 diabetes at increased cardiovascular
risk (10-year risk >10%)
Includes most men >50 years of age or women
>60 years of age who have at least one additional
major risk factor
Family history of CVD
Hypertension
Smoking
Dyslipidemia

19. 
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Use aspirin therapy (75–162 mg/day)
◦ Secondary prevention strategy in those with
diabetes with a history of CVD (A)
For patients with CVD and documented aspirin
allergy
◦ Clopidogrel (75 mg/day) should be used (B)
Combination therapy with aspirin (75–162 mg/day)
and clopidogrel (75 mg/day)
◦ Reasonable for up to a year after an acute
coronary syndrome (B)
Nonpregnant patient with modestly elevated (30299 mg/day) (C) or higher levels (≥300 mg/day)
(A) of urinary albumin excretion
◦ Use either ACE inhibitors or ARBs

20. 
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Reduction of protein intake may improve measures
of renal function (urine albumin excretion rate,
GFR) (B)
1. To 0.8–1.0 g/kg body wt per day in those
with diabetes, earlier stages of CKD
2.To 0.8 g/kg body wt per day in later stages
of CKD
When ACE inhibitors, ARBs, or diuretics are used,
monitor serum creatinine and potassium levels for
the development of increased creatinine or changes
in potassium (E)dm comp1.docx
Reasonable to continue monitoring urine albumin
excretion to assess both response to therapy and
disease progression (E)
When estimated GFR is <60 mL/min/1.73 m2,
evaluate and manage potential complications of
CKD (E)

21. 
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People with diabetes and hypertension should be
treated to a systolic blood pressure goal of <140 mmHg
(B)
Lower systolic targets, such as <130 mmHg, may be
appropriate for certain individuals, such as younger
patients, if it can be achieved without undue treatment
burden (C)
Patients with diabetes should be treated to a diastolic
blood pressure <80 mmHg (B)
For BP>120/80 lifestyle & dietary changes, if
BP>140/80 drugs have to be introduced along with
lifestyle changes & if ne essary multiple drugs have to
be used to reach BP goal
In pregnant patients with diabetes and chronic
hypertension, blood pressure target goals of 110–
129/65–79 mmHg are suggested in interest of longIn the UKPDS, a fetal
term maternal health and minimizing impaired reduction in BP
from 154 to during
growth; ACE inhibitors, ARBs, contraindicated144 mm Hg was
associated with a 30% reduction
pregnancy (E)
in microalbuminuria

24. A pure or predominant motor
polyneuropathy with few or no sensory
symptoms or signs is rarely due to
diabetes and should trigger a search for
alternative causes of weakness, such as
motor neuron disease, primary muscle
disease, spinal cord disease, or other
potentially treatable causes of peripheral
neuropathy, such as chronic inflammatory
demyelinating polyneuropathy

25. Diabetic Neuropathy
Symmetric
1.Distal symmetric sensorimotor
polyneuropathy
2. Autonomic neuropathy
3. Acute painful neuropathy
4. Hyperglycemic neuropathy
5. Treatment-induced neuropathy
6. Symmetric proximal lower extremity
neuropathy
7. CIDP
Asymmetric
Focal and multifocal
neuropathy
1. Cranial
neuropathy
2.Thoraco abdominal
neuropathy
3. Focal limb
neuropathy
4. Diabetic
amyotrophy

26. RISK FACTORS
1.Hyperglycemia is now well established as a
risk factor in both patients with type 1
diabetes and patients with type 2 diabetes.
2.Age
3.Duration of diabetes,
4. quality of metabolic control,
5. height,
6. diabetic retinopathy,
7. cigarette smoking,
8.high-density lipoprotein cholesterol, and
9.the presence of cardiovascular disease .


27. 
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Most common type of Neuropathy in Dm pt.s as a whole is
Distal symmetric sensorymotor neuropathy
Symmetric involvement in a length dependent manner giving
rise to ―glove & stocking‖ pattern, though an asymmetric
pattern due to involvement of root or nerve m/b superimposed
Once developed this symm. Neuropathy is irreversible but may
have intercurrent exacerbations with infections, depression
This variety is often associated with autonomic involvement
In more severe cases, distal portions of thoracic intercostal
nerves are affected, producing an asymptomatic midline
sensory loss in a teardrop distribution over the anterior thorax
and abdomen that gradually spreads laterally . This thoracic
and abdominal sensory loss differs from focal thoracic truncal
radiculopathy in that it manifests as a painless, bilateral,
symmetrical, and persistent form of neuropathy

28. 
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SFN involvement
pattern
Burning or lancinating pain
Hyperesthesia, Paresthesia
Loss of pain and
temperature sensation
Dysautonomia
Foot ulceration
Loss of visceral pain
Early in onset with
no/minimal Ncv
abnormality
This pattern of isolated
small fiber symptoms when
involves U.limbs is known
as ―pseudosyringomyelia‖
pattern
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LFN involvement pattern
Areflexia
NCV test abnormal
Loss of vibration & joint
position sense
patients with
disproportionate large-fiber
involvement may manifest
muscle weakness, atrophy of
the intrinsic foot muscles,
and weakness of the
extensors and flexors of the
toes and ankles with foot
drop. When these deficits
are combined with
proprioceptive deficit in the
toes and feet, a
―pseudotabetic‖ gait ataxia
may result

29. Other symmetrical
polyneuropathies
Features
Acute painful neuropathy
•Diabetic neuropathic cachexia
• Correlates poorly with severity of diabetes or
presence of other diabetic microangiopathic
complications.
• Prognosis may be good in some patients, with
gradual recovery over a period of months
Treatment induced
neuropathy
•Starts with onset of t/t with insulin or OHA
•Gradually improves over months, m/b reversible
Hyperglycemia induced
neuropathy
•May occur in states of DKA/HONK
•rapidly improve with control of hyperglycemia.
•diffuse rather than distal distribution of
paresthesias
Chronic inflammatory
demyelinating neuropathy
• symmetric weakness with demyelination and
conduction block on electromyography and
demyelination on nerve biopsy.
•The clinical progression is characteristically more
rapid than that of diabetic polyneuropathy,
weakness may be more prominent

30. 
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This neuropathy typically occurs with a peak incidence in
the fifth or sixth decade in patients with type 2 diabetes
The clinical picture is one of acute or subacute pain,
weakness, and atrophy of the pelvic girdle and thigh
musculature
Symptoms begin unilaterally but extend to the opposite
extremity within weeks or months. Most patients have
weight loss, and some appear cachectic.
subtle sensory symptoms and signs are commonly present.
The knee jerk is nearly always reduced or absent on the
affected side, whereas ankle jerks may be preserved unless
compromised by a coexistent distal polyneuropathy.
The prognosis is usually good, with most patients showing
resolution of pain followed later by gradual return of
strength over a period of 6 to 18 months.

31. 
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The finding of slow nerve-conduction velocities in femoral
and distal nerves and of features of demyelination in nerve
biopsy specimens in these patients indicates that ―diabetic
amyotrophy‖ is a form of diabetic neuropathy
Electromyography of patients with diabetic amyotrophy
characteristically displays abundant fibrillations in the
affected limb muscles and the paraspinal muscles. Nerveconduction studies are unable to differentiate patients
with diabetic amyotrophy from those with a generalized
polyneuropathy.
Patients with unilateral and relatively focal pain and
weakness seem to improve more rapidly and completely
than patients with more widespread involvement.

32. Fda
apprvd.
Management of painful
neuropathy

33. 
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Intensive glycemic control
Stop smoking & alcohol addiction
Management of dyslipidemia
α tocopherol can be used as antioxidant
Aldose reductase inhibitors
Supplementation with methylcobalamin

34. Autonomic
neuropathy
Cardiovascular
involvement
Sudomotor
g.i.
involvemennt
Orthostatic
hypotension
Fludroco
rt &
Midodrin
e,
Genitourinary
involvement
Diabetic
gastroparesis
Erectile
dysfunction
Erythro
mycin &
domperi
done
PDE5
inh.
hyperhydrosis
Topical
anticholi
nergic &
botulinu

36. Rheumatological manifestations of DM
Rheumatic syndromes
uniquely or commonly
associated with
diabetes mellitus
Adhesive capsulitis
Common rheumatological
diseases associated with
diabetes
Osteoarthritis
Dupuytren's disease
Gout and hyperuricemia
Calcium pyrophosphate
deposition arthropathy
Osteopenia
Neuroarthropathy
Osteolysis of forefoot
Shoulder-hand syndrome
Diabetic hand syndrome
Migratory osteolysis of

37. 
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The usual presentation is that of a patient with longstanding diabetes with complications present with an
unilateral painless Jt. Swelling.
The foot is most commonly involved, followed in frequency
by the ankle and knee. Rarely, upper extremity joints are
involved.
Warmth and erythema may be present. When they are
present, the differential diagnosis includes gout,
pseudogout, osteomyelitis, or septic arthritis.
Typically, there are few systemic symptoms and no
documented fever and leukocytosis.
―claw toe‖ arises as chronic motor neuropathy affects the
small intrinsic muscles of the feet. When the larger
muscles of the anterior tibial compartment are unopposed,
subluxation of the proximal interphalangeal metatarsal
joints may result, leading to a claw-toe appearance. This
may lead to excessive pressure on the metatarsal heads
and thus the tendency to form skin ulcers.

38. phase
manifestations
acute
edema,
localized warmth,
erythema, and
joint crepitus with range-of-motion examination
Radiographs are normal but MRI may suggest NA
coalescence
skin temp. begins to equilibrate and jt. Crepitus
diminishes.
Plain radiographs will show resorption of osseous
fragments and the laying down of new bone
Reconstruction This can eventually lead to a stable foot devoid of
/ remodelling
significant motion. Unfortunately, in many cases, the
foot can be severely deformed, with obvious bony
prominences susceptible to ulceration (e.g., the
rocker-bottom foot)

39. Claw toe

41. 


Diagnostic criteria typically require the new bone
formation to bridge four contiguous vertebral
bodies in the absence of degenerative disc disease
and the absence of inflammatory sacroiliac or facet
joint changes
The condition is characterized by widespread new
bone formation ,specifically the presence of new
bone growth into the entheseal regions
Osseous changes are found around the acetabulum
where fluffy new bone is formed, but similar
changes around the knees and wrists have been
documented.

43. Lateral view CXR
DISH changes are most characteristic in the
thoracic spine, where uninterrupted new
bone may ―flow‖ from one vertebra to
another more prominent on the right side
of the thoracic vertebra, thought to be a
consequence of the pressure effect of the
left-sided aorta. The presence of the
anterior longitudinal ligament over the
anterior two thirds of the vertebral bodies
dictates the distribution of the new bone
formation

46. Patients with diabetes mellitus commonly suffer from a wide variety of
cutaneous maladies. Estimates of the frequency of skin disease in people
with diabetes range from 30% overall to 71% of patients with type 1
diabetes mellitus . While several skin conditions are specific to diabetes,
most of them also occur in individuals without diabetes. The clinical
manifestations and complications of skin disease are frequently more
severe in the setting of diabetes
medicineJoslin's Diabetes 14e.chm

47. ACANTHOSIS NIGRICANS:
Eruptive xanthoma: present as 1-4 mm
papules on buttock and extensor surface
of extremities, indicates severe
hypertriglyceridemia associated with
uncontrolled diabetes . Does‘nt correlate
with microvascular complications

48. CHEIROPAT
HY:
•Starts with
DIP of 5th
finger gen.
•Correlated
with
HbA1c% &
prevalence
of
nephropath
y
•Inversely
correlated
with insulin
therapy

49. Scleredema: Abrupt onset non
pitting induration of skin. Skin
appears as smooth and waxy with
dense dermal infiltration with
prominent follicular ostia , ―peau –
de- orange‖ appearance
Nephrogenic
fibrosing
dermatopathy
Perforating dermatoses: umbillicated
papules with keratinized plaques,
koebnerisation+ve

50. Fibrosing:
Sclerosing:
Scleroderm
a
Fibroblast disorders
Peyronies
disease
Fibrosc
lerosis:
Dupuytrens
contr.
Juvenile
hyaline
fibromatos
es
Morphea
Eosinophilli
c fascitis
lipodermat
osclerosis
Gingival
fibromatos
Scleromucinosi es
s
scleredema
Mucinosis:
Fibromucinosis:
Scleromyxedema
Nefrogenic
fibrosing
dermatopathy
Toxic oil
syndrome
Eosinophillia
myalgia
syndrome
Pretibial myx.
Gen. myx.
CTD
Degos disease

51. Necrobiosis lipoidica

52. Granuloma annulare (GA) is characterized by an annular configuration of
flesh colored or pale red papule and plaques that occur in a localized or
generalized (disseminated) pattern The lesions of GA may vary in size upto
5 cm . Localized GA is most characteristically located on the dorsa of the
hands and feet. A single lesion is present in one half of patients with GA .
The papules develop and enlarge slowly in a centrifugal fashion over a
period of months to years. Generalized GA is characterized by a symmetrical
eruption of hundreds of tiny papules, which can occur all over the body
surface. Localized GA eventually undergoes spontaneous resolution usually
within 2 years. Lesions often recur at the same site.

53. Diabetic dermopathy: small
atrophied pink to brown skin
lesions over lower limbs which
disappear on own
Bullous diabeticorum : painless, non pruritic
bullae over lower limbs arising in normal
skin abruptly and heal spontaneously gen.
without scarring

56. DIARRHOEA in
DIABETES

57. 
Delayed emptying of solid or nutrient meals is found in up to
50% of patients with type 1 diabetes and in 30% of patients
with type 2 diabetes . However, the degree of delay for
various constituents of food, i.e., liquids, digestible solids,
and indigestible solids, is not the same. Simultaneous
assessment of gastric emptying of liquids and digestible
solids using dual markers (99Tc-labeled solid phase and 111Inlabeled liquid phase) showed that indigestible solids are
particularly delayed in persons with diabetes.

58. 
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Patients have symptoms of anorexia, early satiety, and
postprandial abdominal fullness and discomfort that
resemble simple dyspepsia.
Vomiting of old food, however, is indicative of
gastroparesis. Nausea and vomiting are common when
gastric distention is associated with obstruction and
vigorous gastric contractions.
In some patients, atonic dilation of the stomach, even
when massive, may not be associated with nausea or
vomiting.
Nausea and reflex vomiting may be elicited by the
stimulation of the gastric afferents carried via vagal
and sympathetic nerves to the vomiting center in the
brainstem.
If gastric stasis and distention are primary causes of
nausea and vomiting in diabetic gastroparesis, these
symptoms should respond to gastric decompression by
either vomiting or by insertion of a nasogastric tube.

60. Symptomatic
diabetic
gastropathy
Delayed
emptying
Excitatory motor
neuropathy
Prokin
etics
Avoid
antiAch
Normal gastric
emptying
Inhibitory motor
neuropathy
AntiAch
Fast gastric
emptying
Sensory
hyperalgesia
Fundal inhibitory
motor
neuropathy
Antie
metics
clonidi
ne
AntiAch

61. 


Erythromycin at a dose of 3 mg/kg bw i.v. every
8 hours can accelerate gastric emptying . When
oral intake is resumed, treatment with oral 250
mg erythromycin t.i.d. for 2 weeks is worthwhile.
Thereafter, the prokinetic effects of erythromycin
are limited by Tachyphylaxis. Anecdotal findings
suggest that erythromycin may be effective if
courses are separated by a drug - free period
(e.g. lasting 2 weeks).
Decompression of stomach using endoscopy with
dislodging of bezoar if any.
Insulin theapy reqd.

62. Others include:
PTB test +ve
Traumatic foot wound
Ulceration>30 days
Previous lower limb amputation

63. 
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PEDIS:
Perfusion,
Extent (size),
Depth (tissue loss),
Infection,
Sensation (neuropathy)