defect of insulin secretion and/or insulin action

→ chronic hypergylcemia w/ disturbances in fat, carbohy, prot metabolism

→ microvascular → retinopathy, nephropathy, neuropathy

→ macrovascular → CV, cerebrovascular, PAD

<110 mg/dl

<140 mg/dl

Basal: > 126 mg/dl

2h OGTT > 200 mg/dl

Random > 200 mg/dl

Fasing plasma gluc < 126 mg/dl

AND

OGTT between 140 - 200 mg/dl

📷

Fasting plasma gluc 110-125 mg/dl

OGTT <140 mg/dl

>6,5% → diabetes

6-6,5% → prediabetes - increased risk,prevention important!

• DM yes/no
• What Type
• Micro and macrovascular complications
• comorbidities
• CV risk

• 4-P→ Polydypsia, Polyuria, Polyphagia, poundloss
• weight loss
• weakness
• irritability
• ketoacidosis → nausea+vomiting

• dehydration
• fruity breath - Kussmaul
• nausea, vomiting, abdominal pain
• altered neurological state, coma

explanation later

• C-peptide
• Auto-ABs
• plasma glucose levels (fasting, postprandial, noctural)
• HbA1c

Additionally:

• Crea + Albuminuria/ Proteinuria
• Lipidprofile
• Full blood count
• thyroid hormones
• other autoimmune disease marker!

inflammatory! (adipokines)

• C Reactive Protein
• Fibrinogen level
• Liver enzymes: aminotransferases, gamma-GT
• Uric acid

• prior meal + snack
• prior to exercise
• when low Gluc is suspected + after treating low Gluc
• prior to critical task (driving etc.)

⇒ 📷

Type 1:

After initial presentation, honeymoon period often occurs where glycemic control can be achieved with little or no insulin treatment (residual cells still able to produce insulin). Once these cells destroyed→ complete insulin deficiency

Type 2:

Early on, glucose tolerance remains normal despite insulin resistance (B cells compensate with increased insulin production) with time: Insulin resistance and compensatory hyperinsulinism continue ⇒ cells are unable to maintain the hyperinsulinemic state which results in glucose intolerance and DM

Type 1:

Insulin

Type 2:

• Lifestyle modification
• Non-insulin anti-hyperglycemic agents → metformin should be the initial antihyperglycemic agent of choice. Additional agents to be selected on the basis of clinically relevant issues, such as glucose lowering effectiveness, risk of hypoglycemia, and effect on body weight
• Insulin therapy

Type 1: DKA if severe

Type 2: HHS, DKA if severe

• increased risk for spontaneous abortion and congenital malformations
• Macrosomia (big boiii 👶🏼)

• overweight/obese
• mother >35y
• multiparity (also prior signs of GD → macrosomia, fetal mortality)
• history of IFG or IGT
• excessive weight gain (during first 6month of pregnancy)
• PCOS

high risk before week 24 → negative → repeat week 24-28

moderate risk → week 24-28

• DM in pregnancy
• Gestational DM

Random Gluc >200 → check FPG or A1C → if FPG>126 or A1C>6.5% = diabetes mellitus in pregnancy

ONE of:

fasting >92

1h plasma gluc > 180

2h plasma gluc > 153

during pregnancy weeks 24-28

= complete clinical management of diabetic patient

• Therapy→ Lifestyle, Medication, Bariatric Surgery
• Education
• Monitoring
• Evaluation- annual

• healthy eating patterns→ nutrient dense foods in appropriate portion sizes
• address individual needs
• maintain pleasure of eating

20-25 kcal/kg/KG

Mediterranean 📷→ rich in monounsaturated fatty acids, omega-3 (fish)

sodium reduction <2,300 mg/day

saturated fat, cholesterol, trans-fat

Patient compliance→ Patient education is very important

psycho-social care

physical activity

children → 60min per day

Aduls → 150min / week

• Encourage children with diabetes or prediabetes to engage in at least 60 minutes of physical activity daily.
• Advise adults with diabetes to perform at least 150 minutes per week of moderate-intensity aerobic physical activity spread over 3 days with no more than 2 consecutive days without exercise.
• Encourage adults with type 2 diabetes to perform resistance training twice per week.

• low-glycemic Carbs should be eaten
• no artificial (free) sugar (<10% of total energy)
• no processed foods→ often with sugar
• high fiber→ Veggies

• low trans-fats and saturated fats
• high unsaturated, polyunsaturated fats→ fish, coconut oil, nuts, seeds
• omega-3

avoid carbohydrate sources high in protein

< 2.300 mg

• only moderate
• patient education→ delayed hypoglycemia

• attitude towards DM and Tx
• Depression assessment
• cognitive impairment in older patients

decreased mortality, better glycemic control, improved lipid profile, improved quality of life

10-15% in the first 3-6 months

• exercise
• diet
• obstetric surgery→ most superor glycemic control
• medication→ Glucosidase inhibitor

BMI> 40

BMI 35-40 with inadequately controlled glycemia

‣

💬

⇒ BENEFITS: 📷

• denutrition, malnutrition, eating disorders
• Endocrine diseases: Adrenal insuff., pituitary dysfunction, thyroid diseases
• renal failure
• hepatic failure
• severe infections
• extrapancreatic tumor
• Insulinoma
• stomach surgery
• hemodialysis
• sustained physical activity

• transient neonatal hypoglycemia - resolves in 3-5 days
• persistent (recurrent) hypoglycemia - doesnt resolve in 5-7 days

• biochem (high insulin+C-pep; low Gluc)
• Localization: CT, Octreoscan (scinti[labeled somatostatin analog], endoscopic or intraoperator US)

• mild-moderat: 15-20 mg carbohydrates
• severe→ iv glucose and/or glucagon

• Diazoxide (K+ channel blocker)→ 10-25 mg/kg/day
• Ocreotide (Somatostatin analog)→ 1-20 mcg/kg/day
• tumor removal

Mediteranean diet 📷

A food is considered functional if it positively affects one or more specific bodily functions, going beyond basic nutritional benefits, and is relevant to improving health, well-being, and disease risk reduction.

Diabetology focuses on the health benefits of live microorganisms, such as lactic acid bacteria and bifidobacteria, which can lower cholesterol and blood pressure, improve immune function, prevent infections and colon cancer, reduce allergies and inflammation. Yoghurt consumption can also improve mineral absorption, help with irritable bowel syndrome and colitis, prevent gastrointestinal infections, and reduce oxidative stress.

Fibers → ↑ activity of intestinal flora

• abdominal obesity
• aterogenic dyslipidemia (high TG, low HDL)
• Gluc intol + insulin resistance
• HT
• Prothrombitic + proinflammatory state
• endothelial dysfunction
• Non-alcoholic fatty liver disease (NAFLD)
• Albuminuria

• Lifestyle optimization (diet+physical activity)
• weight loss and maintenance
• BP control
• lipids control
• DM2 prevention

• Hyperlipidemia→ elevated Cholesterol and/or Triglycerides
• Dyslipidemia→ Hyperlipidemia plus decreased HDL

cLDL= Cholesterol- HDL- TG/5

if TG >400 mg/dl

HDL→ brings to liver ''good''

LDL→ brings to tissue and arteris ''bad''

=Protein component of lipoproteins

• structural→ ensures stability
• functional→ binding to receptors

"B stands for bad"

Apo-B→ main protein of LDL

Apo-A→ main protein of HDL

• Chol <190
• TG<150
• HDL male >40 female >50
• LDL <100

• Pt. with high to very high CV risk (CVD, DM, CKD, Chromic Inflamm, Hypertension)

• age: males >40 females >50
• relatives of patients with severe forms of dyslipidemias and/ or premature CVD

(note: LDL is the primary goal in CVD prevention)

very high <55mg/dl

high <70 mg/dl

moderate <100 mg/dl

low <116 mg/dl

no smoking, diet, physical activity, body weight, blood pressure, DM-control, decr. alcohol

→ all have a pos. effect on lipid profile

• monounsaturated fats→ olive oil, avocado, nuts, egg yolk
• polyunsaturated fats→ vegetable and seed oils, linseeds, 🐟

• saturated→ animal fat butter, cream lard, coconut oil
• trans fats→ refined shizzle

• consume low-fat milk
• avoid salad dressings
• low-fat yogurt
• olive oil instead of butter
• bake,boil, steam veggies
• no excessive fast food
• cut visible fat of the meat
• consume less meat

• decrease total cholesterol, LDL, TG
• prevent plaques in arteries
• lower BP
• lowers risk for arrhythmia

statins

Mechnism: inhibition of HMG-CoA reductase→ lowers cholesterol de-novo synthesis→ higher cholesterol uptake by the liver by incr. LDL-R expression on hepatocytes

→ titration to max. tolerated dose

Ezetimibe

Mechanism: inhibits intestinal uptake of fat without lowering fat-soluble vitamin uptake

10 mg/day

→ can also be given as monotherapy if statins not tolerated

PCSK-9 inPCKShibitors

⇒ Evolocumab + Alirocumab

• Mechanism:

normal action PCSK-9 → inactivates LDL receptor on hepatocytes → less LDL into liver, more remain in blood

MABs→ inhibit PCSK-9 → decreased LDL-receptor breakdown

>880 mg/dl→ fibrates

>200 mg/dl

statins as first-line treatment

if LDL is within target: add Fenofibrate