Problem 7

Question 1

What are the islet beta auto-antibodies

Answer 1

insulin autoantibodies, antibodies to tyrosine phosphatase IA-2, antibodies to glutamic acid decarboxylase, and others

Question 2

When does hyperglycemia become apparent

Answer 2

when insulin secretory capacity becomes inadequate to enhance peripheral glucose uptake and to suppress
hepatic and renal glucose production

Question 3

Why does weight loss occur in diabetes

Answer 3

from the persistent catabolic state and the loss of

calories through glycosuria and ketonuria

Question 4

What is the classic presentation of diabetes type I

Answer 4

polyuria
polydipsia
polyphagia
weight loss

Question 5

When can we say the patient has diabetic ketoacidosis

Answer 5

if (1) the arterial pH is below 7.3
(2) the serum bicarbonate level is below 15 mEq/L
and (3) ketones are elevated in serum or urine.

Question 6

Can diabetic ketoacidosis occur if the patient is treated

Answer 6

yes
if treatment ometted
or insulin injections are not enough because of stress hormones (glucagon, GH, catecholamines, cortisol)

Question 7

What about the anion gap for ketoacidosis

Answer 7

elevated

Question 8

What causes vomiting

Answer 8

Vomiting and increased insensible water losses caused

by tachypnea can worsen the dehydration

Question 9

What causes electrolyte abnormalities in diabetes

Answer 9

occur through a loss of electrolytes in the urine and
transmembrane alterations resulting from acidosis. As hydrogen ions accumulate as a result of ketoacidosis, intracellular potassium is exchanged for hydrogen ions.

Question 10

What about K concentration

Answer 10

intracellular is depleted

serum levels can be high low or normal depending on how long it has been for ketoacidosis

Question 11

How is respiration with ketoacidosis

Answer 11

deep kussmaul respiration

Question 12

What is the most serious DKA treatment complication

Answer 12

cerebral edema and cerebral herniation because of rapid fluid shifts

Question 13

What is the treatment for DKA

Answer 13

careful replacement of fluid deficits
correction of acidosis and hyperglycemia via insulin administration
correction of electrolyte imbalances
and monitoring for complications of treatment.

Question 14

What is a dermatological manifestation of hyperinsulinism and insulin resistance

Answer 14

Acanthosis nigricans
presents as hyperkeratotic pigmentation in the nape of the neck and in flexural areas and is noted as a sign in the metabolic syndrome.

Question 15

Le diagnostic du diabete

Answer 15

Glycémie à jeun ≥7,0 mmol/l
Glycémie ≥11,1 mmol/l, lors d’un test de tolérance au glucose, 2 heures après ingestion de 1,75 g/kg (maximum 75 g) de glucose
Hémoglobine glyquée ≥6,5% (48 mmol/mol)
Glycémie ≥11,1 mmol/l à n’importe quel moment, accompagnée de symptômes classiques d’hyperglycémie

Question 16

Insuline pour couvrir les besoins de repas

Answer 16

insuline sous forme d’analogue rapide

Question 17

Insuline pour corriger les glycemies elevees

Answer 17

insuline sous forme d’analogue rapide

Question 18

Les insulines rapides pour l’enfant

Answer 18

l’insuline lispro (Humalog®)
aspart (Novorapid®)
glulisine (Apidra®)
En plus, l’adjonction de niacinamide et de L-arginine à l’insuline aspart, a permis récemment d’accélérer l’entrée en action de cette dernière et a mené au développement d’une insuline encore plus rapide, la Fiasp

Question 19

Les symptômes/signes d’hypoglycémies consistent en…

Answer 19

des manifestations adrénergiques telles que des tremblements, sudations, tachycardie
puis de neuroglucopénie avec trouble de la concentration, vision trouble, confusion et changement de l’état de conscience.

Question 20

Type 2 diabetes

Answer 20

characterized by two underlying defects. The earliest
abnormality is insulin resistance, which initially is compensated for with an increase in insulin secretion. Type 2 diabetes mellitus then develops due to a defect in insulin secretion that prevents such secretion from
matching the increased requirements imposed by the insulin-resistant state.

Question 21

What is MODY

Answer 21

Maturity-onset diabetes in youth could be considered in an adolescent who has a family history consistent with autosomal dominant inheritance of noninsulin-dependent diabetes with onset in the second or third decade of life

Question 22

ttt of monogenic diabetes like MODY

Answer 22

oral hypoglycemic agents that stimulate endogenous insulin secretion through binding to the sulfonylurea receptor

Question 23

What is the honeymoon phase

Answer 23

a time where residual function is present

so insulin requirements often decline temporarily 1 to 3 months after diagnosis.

Question 24

What are the acute complications of diabetes

Answer 24

acido-cetose

hypoglycemia

Question 25

Quelles sont les complications chroniques du diabete

Answer 25

micro: retinopathie, IR, neuropathie
macro: AVC, infarcts du myocarde, IAMI

Question 26

How to treat hypoglycemia

Answer 26

glucagon

glucose

Question 27

What is the recommended diet

Answer 27

50% to 55% carbohydrate calories, 20% protein, and approximately 30% fat.

Question 28

What is the relation between diabetes and thyroid

Answer 28

increased risk of thyroid auto-immune disease

same for celiac disease

Question 29

Why does blood cell count increase in keto-acidosis

Answer 29

elevation of the stress hormones epinephrine and cortisol

Question 30

What are the issues in adolescents

Answer 30

• menstrual irregualrities but normal ovulation
• a bit of delay for menarche
• hypogonadisme hypogonadotrope if uncontrolled
• hyperandrogenism with premenarcheal onsetof T1D and use of multiple insuline doses as risk factors
• increased risk of PCOS because of exogenous insulin
• hyperglycemia may cause early menopause

Question 31

Contraception and diabetes

Answer 31

In general, adolescents with diabetes duration of less than 20 years without vascular complications are eligible to use any method of contraception

Question 32

What are the main maternal problems in pregnant patients

Answer 32

A higher incidence of polyhydramnios and hypertensive disorders and progression of diabetes-related chronic complications, even if they have good metabolic control

Question 33

What are the foetal problems in pregnant patients

Answer 33

preterm delivery, including spontaneous and indicated
premature delivery
stillbirth and major malformations
macrosomie
RCIU

Question 34

Signes cliniques de la deshydratation chez l’enfant

Answer 34

Léthargie ou irritabilité
Diminution du pli cutané
Sécheresse des muqueuses
Enfoncement des globes oculaires
Absence de larmes
Diminution de la perfusion périphérique
Pouls radial rapide et faible
Hypotension
Oligurie, anurie

Question 35

Risk factors for ulcers in feet

Answer 35

• Previous foot ulceration
• Neuropathy (loss of protective sensation)
• Foot deformity: pied de charcot
• Vascular disease
• IR et dialyse

Question 36

Which med to avoid if history of ulceration

Answer 36

SGLT2 inhibitors

Question 37

What are the autonomic neuropathy symptoms

Answer 37

• Sweating is diminished or absent; as a result, the skin of the feet remains dry and has a tendency to become scaly and cracked, thereby allowing infection to penetrate below the skin.
• Lack of autonomic tone in the capillary circulation causes shunting of blood from arteries directly into veins, bypassing the tissues that need nutrition. This results in a foot that feels warm and has distended veins and bounding pulses.

Question 38

Quelle est la physiopathologie des ulceres du pied

Answer 38

1. les microtraumatismes d’origine mécanique ou sur des zones d’hyperpression passent inaperçus en raison de la neuropathie sensitive. L’artériopathie compromet la cicatrisation. La neuropathie réduit la réponse inflammatoire, et contribue à la déformation de l’architecture du pied
2. des callosités, phlyctènes et ulcérations se développent
3. ces lésions sont des portes d’entrée à l’infection. L’hyperglycémie entrave le fonctionnement des neutrophiles, et l’artériopathie compromet l’apport d’antibiotiques à la lésion. En raison de l’hyperkératose plantaire dure, l’infection se propage vers l’espace intermétatarsien où la résistance tissulaire est moindre ;
4. en cas d’évolution défavorable, l’infection peut perforer le dos du pied , atteindre l’os, se propager dans les tissus (dermo-hypodermite), puis infiltrer le système vasculaire et se disséminer (endocardite, infection d’implant, spondylodiscite).

Question 39

ttt d’un ulcere du pied diabetique

Answer 39

• retablir les conditions locales: oxygene, nutriments, antibiotiques par chirurgien vasculaire
• attelle ou chaussage par ortho
• soins pedicure-podologue