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MSPA-Endocrinology > DM 1 and 2 > Flashcards

DM 1 and 2 Flashcards

1
Q

What is the action of insulin ?

A

Insulin mediated signalling cascades facilitates the GLUT4 translocation to the cell membrane and facilitates glucose transport into the myocytes, adipocytes and other insulin responsive cells.

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2
Q

What is the action of glutamic acid decarboxylase enzyme ?

A

It is responsible for releasing GABA within the pancreatic Islets of Langerhan’s which stimulates beta cells to secrete insulin and promote regeneration of beta cells.

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3
Q

What are the key antibodies involved in immune mediated destruction of pancreatic beta cells in T1DM ?

A

GAD65 antibody and Islet cell antibody.

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4
Q

What is the gene complex involved in the autoimmune response in type 01 DM ?

A

The HLA gene complex subunits such as DR3 and DR4 which code for MHC-II : a molecule responsible for recognising foreign molecules and maintaining cell tolerance.

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5
Q

What is the Islet histology in T1DM ?

A

Leukocytic infiltration.

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6
Q

What are the four clinical symptoms of T1DM ?

A

Polyphagia, Polyuria, Polydyspia, and Glycosuria

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7
Q

What is the cause of weight loss in uncontrolled diabetes ?

A

When there is lack of glucose availability for energy production. The myocytes induce proteolysis and adipocytes induce lipolysis to produce enery which leads to weight loss.

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8
Q

What is the mechanism of polyphagia in DM ?

A

It is the increased lipolysis and proteolysis for energy production due to lack of glucose availability is what causes polyphagia.

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9
Q

What is the mechanism of polyuria, polydyspia and glycosuria in DM ?

A

The increased circulating glucose get filtered by the kidney sometimes. Since glucose is osmotically active it draws water with it leading to glycosuria and polyuria. This water loss leads to polydipsia.

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10
Q

What is the histology of the pancreatic Islet of patients with T2DM ?

A

Due to excessive insulin production by the beta cells in T2DM, the pancreatic Islets are replaced by amyloid polypeptide deposits. This leads to the histology showing variable number of beta cells and amyloid polypeptides.

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11
Q

What is the diagnostic value of the FBG in diabetes ?

A

126 mg/dl

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12
Q

What is the diagnostic value of the random BG in diabetes ?

A

200 mg/dl and symptoms.

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13
Q

What is the PPBS value for the 2 hour glucose tolerance test ?

A

200 mg/ dl

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14
Q

What is the HbA1c level in diabetes ?

A

> 6.5%

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15
Q

What are the triggers of DKA ?

A
  • Poor compliance to insulin therapy, stress and infections that demand more insulin.
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16
Q

What are the types of ketone bodies ?

A

Aceto acetic acid and beta hydroxy butyric acid.

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17
Q

What causes acidity in DKA ?

A

It is the increased keton bodies.

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18
Q

Why does DKA typically do not happen in T2DM ?

A

Due to the presence of some endogenous insulin the lipolysis responsible for the production of ketones are inhibited.

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19
Q

What is the cause of Kussmaul respiration in DKA ?

A

It is the hyperventilation occurs to compensate for Ketones induced metabolic acidosis of DKA.

20
Q

What gives sweet and fruity smell to breath in DKA ?

A

The presence of acetone which is a metabolite of the ketone body component aceto acetic acid.

21
Q

What are the symptoms of moderate to severe DKA ?

A

Moderate: abdominal pain, nausea and vomiting
severe: delirium and psychosis.

22
Q

What are the complications of DKA ?

A
  • Acute extracellular cerebral edema
  • cardiac arrhythmia due to potassium imbalance
  • Mucoremycosis
23
Q

What are the metabolic features seen in DKA ?

A
  • Low PH and low HCO3 ( Metabolic acidosis)
  • High anion gap.
  • High ketones
  • If the DKA is precipitated by infection high WBC can be seen.
24
Q

What is the mechanism of hyperkalemia in DKA ?

A

The DKA causes extracellular H+ increase which will cause an increase in exchange of extracellular H+ for intracellular potassium leading to hyperkalemia. In addition, the lack of insulin mediated activation of the Na/K+ ATPase pump impairs the transport of pottasium irons from the ECS to the ICS.

25
Q

What is the Tx of DKA ?

A

IV fluids to correct dehydration + IV K+ and small amount of dextrose to correct hyperkalemia + IV insulin.

26
Q

What is the DKA equivalent of T2DM ?

A

Hyperosmoler hyperglycemic state which causes extrem dehydration.

27
Q

What is the mechanism of hyperosmolar hyperglycemic state ?

A

HIgh glucose in the blood drives the ICS fluid to the intravascular space which leads to cellular dehydration and polyuria. This severe dehydration leads to neurologic complications, coma and death.

28
Q

What are the lab findings seen in hyperosmolar hyperglycemic state ?

A
  • > 600 mg/dl glucose.
  • > serum osmolality
  • With no acidosis
29
Q

What is the management of hyperosmolar hyperglycemic state ?

A

IV fluids and insulin therapy.

30
Q

What are the neuroglycopenic symptoms of hypoglycaemia ?

A
  • Focal neuro deficit
  • confusion and coma.
31
Q

How to differentiate hypoglycaemia due to endogenous or exogenous insulin ?

A
  • High insulin + normal C-peptide = exogenous insulin .
  • High insulin + high C-peptide = either insulinoma or salfanyluria induced pancreatic release of insulin.
32
Q

What is non-enzymatic glycozilation?

A

It is the non enzymatic formation of glycosilated proteins and lipids which are pro inflammatory and cause hyaline arteriolosclerosis, sclerosis of basement membrane causing hypoxia, nodular glomerular sclerosis which are called Kimmelstile willson nodules.

33
Q

What is the mechanism of glucose induced osmotic damage?

A

when glucose enters the cells it is normally converted to an alcohol called sorbitol by the enzyme aldose reductase. The sorbitol drives more water into the cell leading to osmotic damage in cells that lack the enzyme sorbitol dehydrogenase which convert sorbitol to fructose.

34
Q

What are the tissues that lack sorbitol dehydrogenase?

A
  • Lens- resulting in cataract
  • Shwann cells - causing sensory and autonomic neuropathy.
35
Q

What is the cause of gestational diabetes ?

A

In pregnancy the placenta produces human placental lactogen which causes insulin resistance. Some pregnant patients are not able to produce extra insulin to overcome the insulin resistance leading to gestational diabetes.

36
Q

What is the cause of diabetes in cushing’s syndrome and glucocorticoid therapy ?

A

corticosteroid induced insulin resistance.

37
Q

What is Whipple’s triad ?

A

It consist of symptoms of hypoglycaemia, low blood glucose level < 2.2 mmol/L, and relief of symptoms by the correction of the low blood glucose. Without the presence of Whipple’s triad hypoglycaemia can not be diagnosed.

38
Q

What is Non-islet Cell Tumour Hypoglycaemia (NICTH)?

A

It is more likely to develop in patients with large tumour burden. In NICTH, the tumor cells overexpress the IGF-II gene.Normal IGF-II binds to become an inactive complex. The abnormal big IGF-II binds differently and causes hypoglycemia by direct interaction with IGF and insulin receptors.

39
Q

What is Non-insulinoma pancreatogenous hypoglycemia
?

A

Spells of neuroglycopenia due to endogenous hyperinsulinism which occurs usually post prandially.

40
Q

What is nesidioblastosis ?

A

Nesidioblastosis is defined as the proliferation of both ductular and islet cells, with hypertrophy of beta cells in islets and the formation of ductuloinsular complexes. The imaging will be normal in this case and the Tx is partial pancreatectomy.

41
Q

what is the definition of postprandial vs fasting hypohlycemia ?

A

When the hypoglycemia occurs > 5 hrs after food is considered fasting and < 5hrs is considered post prandial.

42
Q

What is the first steps in the evaluation of a patient presenting with non- diabetic hypoglycemia ?

A
  • Mixed meal diagnostic test / Extended OGTT.
43
Q

What is the fist step in the diagnosis of post prandial hypoglycemia ?

A

Take a regular meal or similar meal that triggered hypoglycemia and take the blood sample every 30 min to 1 hr until the glucose is <60 mg/dl ( the critical sample).

44
Q

What are the components that needs to be analysed in the blood sample of patient presenting with non-diabetic hypoglycemia ?

A
  • Plasma glucose, C-peptide, insulin and cortisol ( more important in fasting hypoglycemia than PP hypogylcemia).
45
Q

What are the cause of post prandial hypoglycemia ?

A
  • NIPHS
  • Insulin autoimmune syndrome
  • Post gastric bypass or beriatric surgery
  • Insulinoma
  • Hereditary fructose intolerance
  • Facticious hypoglycemia
  • Post prandial syndrome( Dx of exclusion).
46
Q

What is the management of post-prandial syndrome ?

A

Acarbose.

MSPA-Endocrinology (10 decks)

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