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Carbohydrate Metabolizing:

The regulation of blood glucose cork is of critical importance and is regulated by the hormone, impair. Several hours after O’Neal, as goose only. Return to baseline, insulting production is decrease concomitantly. The liver new convents from on organ it net guacos uptake to one of net glucose production and supports corolla. Conc. until the next meal. After prolonged fasting, insulin levels decline farther and allow the for muscle breakdown and lipless these provides subtask for glucoses gorses and ketene boy production by over, which can used as an alternative fuel.

CHO multibillion during pregnancy:

During penance, the major chary is the hovel menthe of insulin resistance chatty manifested in skeletal muse where there is appropriate soy. Reduction in insulin sensitivity by the third trimester. This chars is attributed to several humeral factors of material and placate sources 9e.s-haman place. Betoken placental grow hour. Variant a significant sincere in the maternal air cone. of cortical, is observable elevated cons. of estrogen, proteome and prolixity also may affect insulin sensitivity during prig. Other retribution and ten caloric fee body weight and ten caloric intakes. it was propose that the insular resistance of pregnancy serves to shanty nutrients preferential to the growing fetus, while small animosity allowing for the accumulation of calorie storage in maternal adipose fissure. Because of insane resistance, prig. Is characterized by elevation cir. insulin conc. as their maternal pancreas compensates for new peripheral demands compensates for new peripheral demands. There for in the normal situation, maternal glaciate levels during gestation remain normal or near normal if adequate companion does not occur, gestational diets reefs.

In the fasted stag, twp patter important chases occur in maternal intermediary metabolism a several decree in plasma glucose unc. I ten for catabolism. In summary, in the pregnant woman, ctto metabolizing is sometimes of a paradox. After meals, there is a tendency for uncurl and insulin levels of fat stories is promoted. Durians fasters, however, gluon and insulin levels ? and prioress is stimulation. These changes may have developed to cruse adequate nutrient supply to the mother and fetus.

Diabetes Overview:

Definition: DM is a tectonic metabolic condition that is marked by ten circulating conc. Of glucose, is accosting. The development of loons term Vascular complicated. The two freedoms. Forms- type & (II)

Diagnosis of diabetes:

i) Pts complaining of symptoms suggesting diabetic

– Test urine for slucose and ketene.

– Measure random or fasting blood glucose diagnosis confirmed by- fasting plasmas glucose ? 7.0 mmol /L (126 mildly)

2) Indications for oral glucose tolerance test:

– Fasters plasma glucose 6.1 – 7.0 mmol/L (140 – 199 ms/dl)

Oral glucose tolerance test – Who diacignostic criteria:

Glucose Conc.
Venous plasmammol/L (mg/lds) Venous whole blood mmol/L (ons/dl Capilory whele blood mmol/L (msldl)
Diabetes fasting 2hrs. after glucose ? 7 ( ? 126)11.1 ( ? 200) ? 6.1 ( ? 110 )? 10 ( ? 180 ) ? 6.1 ( ? 110 )? 11.1 ( ? 200)
Impaired glucose tolerance fasting ? 7 ( ? 126)7.8 (140 – 199) ? 6.1 ( < 110 )6.7 – 9.9 (120 – 179) < 6.1 ( <110 )7.8 – 11.0 ( 140 – 199 )


Type I DM:

Forlornly rferres to ‘juvenile onset ou’ or IDDM mainty attlicts lean children, teers an yours adults usauy anti-iset cell ab. Deectable Clinically the onset usually is abrupt and sever, with mark taper glycerin that develops over several days to weeks that is assoc. e weight loss, fatigle, polyuria, polydipsia, burring of vision and evidence of volume contraction,

Type of ping:

Adut orset Pm or NIOOM Pts who have T2DM usually are older than 40 years and overweight or oversee. Recently, however, because of the ? ing obesity rates in the young. It is not uncommon for feenagers or even older children to present T20m.

T2om is a dis. Of dual often defects – insulin resistance and relative insulin deficiency.

Because insulin secretion persists to some extent in virtually all patients, ketoocdosis is rare, in pts. Who have T20m, other clinical and biochemicals features often are present, inklings central adiposity, TNo and dispirit demean; there place pts. At an ? we rise of caves disseat The constellate firm often thermo as “metabolic syndrome”, or the ‘insular persistence Sandrine’. In wormer of childbearing age, polycystic over syndrome is a common manifestation of insulin resistance.

Other Forms:

In addition to gestational diabetes, other forms include so-called “secondary DM’ – when hyper sly ceria results from a separate dis. Process. These include. Of endocrine pancreas – (pancreatitis, cystic sin. Carnage, Phaeton chronocytoma) prodder will)

Moody – a fascination group & develops early in life with a dominant-inheritance pattern. Although pts of MODY may present severe hyperglycemia, there diabetes is mild.


Acute: Mayor acute complications income hype rejoice & hypoglycemic emergencies.

DKa in Tom and hyperglycemic presumes syndrome in T2an. If notation there conditions can result in severe compilations and require client medical attention inning aggressive dehydration, insuring ordination an cautions mentioning of metabolic and homodynamic starts

Hypoglycemia: Initially hypoglycemia (plasmas Illuc9ose <50-60 ng/dl) Ideas to peregrines/c signs as symptoms – diaphoresis pallor, Tachycardia and tremor. It untreated, naturedly Copernican manifestations may follow including personality change cog five impairment, loss of cons class ness no seizures.


Mayor chronic complications of diabetes are those related to vascular dis. These are distinguished by the size of vessel affected.

Mcroangiopathy: Predominantly affects the kidneys, eyes and heaves

Although still controversial, most of the evidence points to elevated glucose occur through a company series of nitro cellular derangements that are the scapulae of oxidative stress. Duration of diabetes and inadequacy of glucose control are the best predictors of these complications.

Diabetic healthy:

In remained one of the most common causes of neural failure in the world diabetic nephropathy begin with a period of glomerular hoporittration and intraglametules WTN. After years, glomeralar injury develops with eventual loss of filtration rate coexist HTN hastens this decline. Eventually foeman may develop and dialectic therapy is remained.

Arousal albumin excretion is the first sins of glomerular dis and may progress slowly from indri albumin (20-300 mgld) to macro albaminuria (>300 mg/d) to frank nephritic syndrome. Aggressive BP control articulations e ACEL or Banishers (II) receptor blockers, delays this progression.

Diabetic retinopathy:

Background diabetic retinopathy does not result in visual impairment. It is marked by early fandocopic changes there include lipid deposits (hard exudates), microtone-rims and minor haemorrhages. This may progress to prep lifetime retinopathy that is charactering by ores of retinal infarction (cotton- wool spots). The ischemia provides an antigenic stimulus that leads to growth of new and more fragile sledded blood vases. As the dis. progresses forth, proliferate retinopathy direst from these abnormal veils and eventually there is loss of Visigoth.

Diabetic neuropathy: miry which stems form ischemic and metabolic insult-occurs to sensory, motor and atomic nerves, therefore, this condition has various manifests.

Loss of sensation in a “Stocking glove” distribution that may be assoc. Perestholay or painful distension is the most common presentation. Loss of sensation in the lower extremiffes also is a major factor in the development of foot ulcerations that can lee to limb loss. Autonomic neuropathy can print as erectile dysfunction in men and orthostatic hypotension in men and orthostatic and Ortho’s attic hypotension, gastro paresis, diabetic diarrhea, and atomic bleeder. Other than improving glucose, control, there is no direct treatment for diabetic neuropathy.


Atherosclerosz – Major cause of death in Da. predominantly as are sand of coronary artery and CVD that lead to Mi, CHF & stroke.

Peripheral Vascular disease with limb ischemia contributes to foot ulceration, infections and gangrene

In pts. Who have T20ms, the immures is compounded by the assoc. Features of the insulin resist synod. These include HTN. Lyshipid hypercoasul ability and vas Inferno.

Other morbidities: choric hyperglycemia also delays wound healing and impairs normal fancy. of immure sys. So, diabetics are prone to infections and complication that are relent to sonically & honsursicay wounds.

Therapy – Insulin for TIDM

Insulin type Rapid-acting Orient Peak Duration
Insulin lispro 10-15 min 1-2 h 3-5 h.
Rapid action 10-15 min 1-2 h 3-5 h.
Short acting
Regular inns. 0.5- 1 h. 2-4 h. 4.8 h.
NPH Lenten 2.4h 4-12 h. 12-20 h.
Untalented 6-8 h. 16-24 h.
Insulin glaring 2-3 h. 24 h.

Although most pts who have TIDN can prevent ketocieidosis coith one ing- of intermediate or long-acting insulin per day. Dosing at best twice daily is required for any reassemble decree of three to for daily in. That involve combination of long & short- acing insulin’s, with calibrated basal rates and measured ‘blouses’ before means. Any comprehensive management program also must include adequate sot management education, a well proportioned meal plan an radar physical exercise

Typically puts who lone T2Dm are fretted initially a close restricts olet, weight loss (if necessary) and exercise. Oral thposlycemics are not proud for use during prig.

Therapy is started e a single agent: if control is not achieved. Dares from defense classes are added in combination. Along the more common combinations include motorman e a secretagogue proportion of pts develop enough insulin deficiency of require. Exogenous insulin in.

Table- 2 – page – 914

Glucose control:

The most reliable assassinate of overall glisten status its periodic meanvrement of the HBAIc. With they single fest. The practitioner can determine the average degree of lamia DVER the previous 2 to 3 months.

Current ADA guidelines are to midtown, HBA, C at less then 7th. (Normal range 4%-6%) plasma glycols should be kept betwen 90 mgldi and in 120 mg/dl before meal & less than 180 mldl 2lmy after meal.

Pre-existing diabetes in prig. (Pre gestational pn)

Generally, Ilycemic control during the preconption period and in the early phoses of gestation determines the risk of fetal eons. Malformations. In contrast, maternal. In cotrast, maternal outeomes and the risk of fetal macro-sonia (and related abs. scapulae) are predicted best by glucose control during the second third trimesters.

Because of two societal pioneering Marlene is it foist prge. And Indy rates of obesity, (with resulting insulting resistance) pre-existing T2DM is being a me foremast phenomena class.

Of diabetes in pregnancy:

A) Pre gestation diabetes:

i) Type diabets

A) Uncomplicated (no Hun, retinopathies, nephropathy. or cardiovascular dis.)

b) omplicated (presence of at least are of the above)

b) Gestational DM:

a) i) fasting plasma glucose less the 105

b) ii) fasting plasma glucose greeter then 105 mg/ld

Impact or mother:

When advance micro vascular complication is present in a woman who has presentational diabetes, primacy may exacter body the condition.

Retinopathy: Generally, background retinopathy doesn’t progress to proliferate retinopathy during prig. IN contrast, however, established privative retinopathy may advance during gestation, particulate if severe, as demonstrate in the diabetes in early prig study predictors of retinopathy deterioration include the quality ct glycolic control as well as the coexisted of HTN. It was recommended to women Coho have reiterative are follow-up be an opthalmols is recommended in preened women wh. have how diabetes for at less 5 years In women who have established proliferate retinopathy, evaluation by an ophthalmologist lest each trimester – is mandatory.


Generally, background retinopathy does not progress to proliferate, retinopathy during prig. In contrst, however, established proliferative retinopathy may advance during gestation, parallel sly it severe, as demonstrate it severe, as demonstrate in the diabetes in early prig. Study Predictors of retinopathy deterioration include the quality ct glycolic coagulation therapy be administered to women coho have proliferate retinal changes before conception. Evaluation are follow-up by an ophthalmols its in recommended in pronto women who have how diabetes for at less 5 years. Retinopathy, evaluation by an opthalonagit at least each trimester is mandatory.


Uncomplicated oregano in a diabetic woman who has Norman renal funk. Doesn’t ­es her subsellent nephropathy. In a woman who has mild pre-existing nephropchy the expected progression of her nenal fore. Shouldn’t age attired; however, glomeralar filtration rate nay decline more rapidly in those who have established ecru. Renal failure or advance proteinuria-tenderfoots close follow-up of blood profuse, s.e reactive I Uring albumin excretion rate ageing. During the diabetes Prg. Also, the fruity used ACEL raw Abs show be discommode after prig. Is conformal because of possible teratogenik effects.


There is little evidence that neuropathy workers prig. Althea women who have pre-existing carol fennel sin. Are at rigor are at rigor for worsening symptoms during gestation. And pregnancy is potty federated in women who have severe autonomic dyes function.

Cordially, d.s: Active Cromarty ortery dis. is women who have diabetes.

Obstetric complication:

Diabetic pregnancies are at ­Ed risk for obstetric & medical complications, such as HTN, preterm later, unitary tract & other inf. periodontal dis, c/s, and obis, trauma.

The evidence of pre-eclipse is reported 10% to 20% compared e 5% to 8% in mon-diabetics. The ate of preeclampsla Tec e the severity of dickens of protenurin at the onset of pregnancy. The reasons for the ­ed rah of spontaneous preterm (premature) labor are uncles but may be related to poor glycemi, l control, pdchydramnios or infect one study found a 37% ­ed risk for preterm delivery e each 1% ­es in HaAiC befor delivery Impact or peg. And the neonate:

Numerous sturdily have linked the ­Ed rates of miscarriages and fetal anomalies full poor lexemic control. HBAiC value thee are gated than 8% are malformations that is there to six times greater than this cut. off point. Overnice the risk of malformations is up to eight times greeted in no diabetics.

The feats in diabetic nether remains at ­ed risk of prenatal asphyxia. Prenatal asphyxia correlated new-onset nephropathy during the prig, maternal hyperglycemia before delivery and prematurely.

Regarding fetal macrodome, a tighter relationship between maternal post radial glucose and fetal macaroni has been observed, as company e fasting glycols. Those babies are at ­Ed risk for hypoglycemia. Type bilirubinemia and acidosis. Ultrasound has not proven to be sure to clinical exam in pertinacity microbial. However, USG. Measurements man allows the clinician to circumference over bad. Circumflex. Ratio Diabetic vasculopathy of excess only tight control have been link to 10 GR.

Porhyarmnios is seen often in diabetic pregnancies. Babies of diabetic mothers are at had risk of insulin or stincubtory effete of contuse on healthier synthesis. Then our of feral lures maturity has reduced the ark of neonatal death from EOS. The presence of phosphatiadyl geol. in the amniotic fluid is the best predictor of lures maturity in diabetic prig.

Neuron developmental outcomes babbles of diabetic mothers can be expected to be normal good glycolic control. Children of diabetic parents are a risk of developed the same type of dialog. However, the risk fore developing TIOM is higher it the father is the parent who has TIDN.

Type & diabetes in pres: These pregnant same to be at least at the same risk as. These of women who have TIDN. Women who have T2Dn tend to be older, more obese, and have higher riles of enplaned pregnancies in compassion those have TIDN. Studies shooed ­Ed rates of

Hypoglycemia has not been linked with embryopthy although profoundly loci blood glucose levels place the mothers at increase risk of incisory. There fox, care should be taken to improve glycolic control progressed and e close monitoring of any retrial dis. pts. Should be instructed to use a reliable the disarm goal of glycolic control.

Because diabetes are in a high risk category for nural fube defects, folic acid supplement should be placed on a high daily dacage (14-5 mg) during the preconception period and through tat first trimester. Regarding hypertension, antihypertensive medication should be stopped if the pt’s blood pressure is less than 130/80 mg the and restored as needed with the goal of maintaining blood pressure at lace 140% 90 man its.

The metabolic goal dung pregnancy is of maintain blood glucose as to the normal forge as possible, while avoiding severe hypoglycemic.

Must authorities recommend that fasting plane glucose levels be maintained at 70 mg/dl to 105 mg/dl (whole blood, 60-95 mg/dl) before meals and no higher than 130 mg/dl whole blood < 120 mgldi at 2 should be measured ever 4 to 6 weeks, with the goal being a nor value (<6%) foods of lower glycolic index, for example, seam to be suited best for women who have diabetes during prig. in general, the diet should consist of 30 kcal / kg/d to 35 kcal/ kg/d in the form of there main meals and one to two séances- three main meals and one to two sncks-that consists of 50% to 60% carbohydrates, less then 30% for and abdicate dietary fiber.

There are numerous insulin options for women who have diabetes during pregnancy. It the preconception regional is working well in those who have presentational TIDN, this should be contemned. Commonly however, the pt. requires intensification of her regimen to achieve the stricter targets. The actual type of insulin that is used in an actual type of insulin that is used in an individual pt. is not as important as the quality of glycemic control that is achieved. Actions creative regimens may need to be devised for individual pts. Depending on their meal preferences and work schedules. The best treatment regime’s typically combine “basal” insulin in the form to intermediate of lint acting formulation like NPH, lento, Ultralerte that are administered once or fiancé deity and mealtime short acting insulin analogs (insulin lisper, insulin apart).

In early pregnancy unit of insulting for every 15g of carvtoydrates consumed may suffice. As insulin resistance wormed moray suffices. As insulin attic may decrease at to 10:1 or less. To compensate for pre pyramidal hyperglycemia an additional “correction bolds” of insulin (1-2 units for every 25-50 mg/dl more than 120 mg/dl) should be considered. All insulin types , except to insulars glaring are approved for use desiring pregnancy. In the women who has pre gestational T20M it is recommended that any oral agent regime 6l converted to insulin during the preconception phase.

Elevated tasting blood glucose should lead to a test of approximately 10% in the drag of the lures or intermediate-aching insulin that is injected at right. Sub optional control before dinner is addressed by increasing the Lang or intermediate actor’s insulin dosage that is given in the morning. It post pyramidal hyperglycemia is noted, the pre-prandial rapid action insular dosage should be dusted similarly. Not be made more treauertly than every 2 to 3 days and should by intumesced by glycolic trends not individual glucose readings.

Because of enhanced biolysis during pregnancy, in TIDM. Maternal detoacido may accrue more treaucntly and at decreased plasma glucose concentrations, there are known deleteriolls fetal effects of ketacidosis this hyperglycemic decompensate should be avoided at all costs.

Glycolic management during labor:

Typically insulin requirements decrease during labor partly as realty o finery uses and partly as a result of the mothers fasting status. None the less, it is savable to give all women who have insulin ideated pre-gestation diabetes an insulin infusion during labor and delivery, especially those who have TIDM. This allows for tight regulation of plasma slipcase in physiologic rinse of to mildly to 100 ogled. An initial dosage of i to 2 omits per thou will suffice in most women. Amine individualized regimen could be estimated from the woman’s total daily insulin intake. Using this method, 50% of the total daily dosage is divided by 24 hours to calculate an initial hourly rate. Concurrently, a doctor’s infusion should be provided to prevent catabolism. Blood glucose must be checked hourly during intravenous insulin intrusion.

Post patron care and lactation:

The insulin resistance of pregnancy resolves an hour’s abler delivery. As a result, the insulin requirements of a woman who has presentational diabetes one decreases dramatically. Insulin dazing during the trust 24 to 48 hours postpartum will need to be reassessed carefully to avoid hypoglycemia. Pts who TIDU will remain insulin dependent. Those who have T 20M mat be able to se switch batch to oral agents soon although insulin shale be continued if sreeastfeodins is planned.

The prevalence of postpartum shady in women who have TIDM is hash. Therefore, signs & symptoms of thyratacicollg or hyoo thyroidal, should be evaluate Ed promptly.

Gestational diabetes mellitus:

GDM indicates carbohydrate intourance that is diatgnosed during preqrancy.

Women who have GDM have soy. Likelihood of developing overt diabetes iin a decade after delivery. Fasting hyperglycemia during pregnancy and the red tar gestation, are assoc. strongly & postpartum persistence of dibbles. Women who house other CVS nick facts lice obesity. Ted triglycerides, hotly are at greater raw for persistence of diabetes postpartum.

GDM has been linked i an red risk for feral macroscmia & its relate maternal perinarl comical children of women who have GDM are at tad fisk for obesity, gulcole intolerance and diabetes as abuts.

Diagnostic criteria for gestational diabetes C by o Sullivan and mahan, us moaificed by carpenter and costar At least two abnormal values venous plasma on hour OTHTT will 100 g. glucose lord .

Fastens 95 mgl/dl or 5.9 mmol/L

1 hour 180 mgl/dl 10.0 mmlo/L

2 hour155 mgl/dl 7.6 mmol/L

3 hour 140 mgl/dl 7.8 mmol/L

Current management of gestational diabetes struts & nutritional wunrselurg.

Insulin is added when diet alone is insullicient to maintain glycerin at the toll owing levels: fasting plasma glucose up to 105 mg/dl or i hour after meals up to 155 mg/ dl or 2 hours after meal up to 130 mg/dl

Postpartum care:

It is now recommended that all women who have a h/o GKM undergo formal re-evaluation & OGTT at 6to 8 woks postpartum or after brstfecdirg has discontinued. In addition, long term monitoring for the development of disables is advisable at least annually & fasten blood glucose and perhaps HBAIC determinations.