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Diabetes > Introduction > Flashcards

Introduction Flashcards

1
Q

What’s Diabetes

A

A clinical syndrome is characterized by chronic hyperglycemia as a result of relative absolute deficiency of insulin

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2
Q

Predisposed diabetes is

A

TYPE 1

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3
Q

Predetermined diabetes

A

Type 2

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4
Q

Diabetes can be a result of an absolute deficiency of insulin; here,

A

the pancreatic β-cells are not producing insulin due to the destruction of the β-cells (Type 1).

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5
Q

In relative deficiency of insulin

A

there is an amount of insulin being produced by the
β-cells

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6
Q

Type 1 diabetes is NOT strongly linked to

A

genetics

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7
Q

In type 1 there is exposure to toxins like

A

NITROSAMINES causing beta cell destruction

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8
Q

A global pandemic of diabetes what are some of the causes of type 2

A
  1. Lack of exercise
    2.Obesity
  2. SEDENTARY LIFESTYLE
    4.URBANIZATION
  3. Time of meals
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9
Q

Lack of insulin in the system will affect the metabolism of

A

carbohydrates,
fats,
amino acids

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10
Q

The number 1 structure affected in Diabetes is

A

BLOOD VESSELS

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11
Q

Why is wound healing difficult diabetes?

A

The hyperglycemia in diabetic patients provides a good medium for microbes to thrive,

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12
Q

Proteolysis also leads to reduced immunity since

A

proteins are the foundation of immunity.

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13
Q

Peripheral vascular disease OCCURS IN DM BECAUSE

A

insulin is low, there will be a breakdown of TG leading to more free fatty acids in the system that can lead to peripheral vascular disease which blocks the perfusion of blood to the extremities.

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14
Q

diabetic nephropathy due to

A

accumulation of sugar in the nephrons.

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15
Q

the body is able to maintain sugar level from

A

3.5 – 8mmol/L.

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16
Q

The body is able to maintain sugar levels by two simple methods;

A

• Intake of glucose and
• Utilization of glucose

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17
Q

Liver impairment will need

A

Glucose

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18
Q

Intake of glucose involves

A

1.From diet
2. GLUCONEOGENSIS when bodybis not getting glucose from food

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19
Q

In the adipose tissues, free fatty acids and glycerol
are produced from

A

breakdown of triglycerides (TG).

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20
Q

The substrates that move to the liver for hepatic Gluconeogensis are

A

GLYCEROL, PYRUVATE, LACTATE , and AMINO ACID

21
Q

Free fatty acids move into the liver to initiate

A

Ketogenesis to produce ketone bodies.

22
Q

In diabetes, there is no insulin to

A

push the glucose into the cells which leads to hyperglycemia

23
Q

What will availability of insulin do?

A

pushes glucose from blood into the cells hence reducing
** hyperglycemia and gluconeogenesis **

24
Q

Insulin inhibits

A

PROTEOLYSIS ie it is ANTIPROTEOLYTIC

25
Q

Insulin is Anabolic meaning

A

helps in the buildup of muscles rather than their breakdown.

26
Q

Insulin leads to the formation of

A

TRIGLYCERIDES

27
Q

Since insulin leads to TG formation it causes

A

WEIGHT GAIN

28
Q

β-cells do not produce direct insulin.

A

True They produce Proinsulin

29
Q

The pro-insulin gets into the blood and is cleaved to produce

A

insulin and a C-peptide.

30
Q

Significance of C-peptide

A

shows how much insulin is produced by the body.

31
Q

Phase 2 insulin is

A

Plateau ie basal insulin

32
Q

Phase 1 is characteristic of

A

soluble insulin.

33
Q

Type 2 diabetes causes WHAT COMPLICATION

A

HHS (Hyperosmolar Hyperglycemic State) just as type 1 cases DKA.

34
Q

CLINICAL IMPORTANCE OF C-PEPTIDE

A
  1. HELPS determine the amount of insulin produced since its in equimolar amounts
  2. Determine the secretory power of beta cells
    3.To differentiate between type 1 and type 2
35
Q

Causes of Type 2 diabetes

A

1.Genetic factors
2. Environmental factors
• Lifestyle
• Age
NB: Old age leads to reduction of β-cells.
Intake of fast foods causes the buildup of fat which opposes insulin action

36
Q

Narrate the Pathophysiology of Insulin resistance 1

A
  1. Abdominal fats oppose insulin action at the periphery. Fats in the abdomen are stored in adipocytes.
  2. When the adipocytes get full, there is a spillage of fats into the blood which is deposited in the muscles and liver. These fats oppose the antilipolytic action of insulin.
  3. Also, when the adipocytes are full, the walls of the cells stretch.
    This triggers the release of cytokines (Bad cytokines).
37
Q

Narrate the Pathophysiology of Insulin resistance 2

A

1.Resistin: This opposes the action of insulin in the periphery.

  1. Tumor necrosis factor alpha (TNF-α) or interleukin 6 (IL-6): Causes inflammation (pro-inflammatory agent)
  2. Plasminogen activator inhibitor I: Causes thrombosis (pro-thrombotic agent)
38
Q

Metformin is cardioprotective because

A

it inhibits plasminogen activator inhibitor I to prevent thrombosis.
Preventing occlusion

39
Q

What therapy prevents the overstretched cytokinesADIPOCYTES?

A

Statins

40
Q

Microvascular complications of diabetes

A

Retinopathy
• Nephropathy
• Neuropathy

41
Q

Macrovascular complications

A

Coronary heart disease
• Stroke
• Peripheral vascular disease (PVD)

42
Q

MOA of Metformin

A

-increases the sensitivity of insulin at the periphery.
- It inhibits gluconeogenesis in the liver.
-Metformin reduces the GI absorption of glucose.
- It also blocks the action of glucagon.

43
Q

Is metformin metabolised?

A

NO, it is excreted via the Kidneys unchanged.

44
Q

elimination half-life of metformin

A

1.3 – 4.5 hours

45
Q

Metformin does not cause hypoglycaemia because

A

it does not stimulate insulin secretion. does not cause weight gain but rather causes a reduction in weight.

46
Q

SE of Metformin

A

• GI disturbances – Diarrhea, abdominal cramping, nausea, etc. Hence, it is
advisable to take metformin with food.
• Lactic acidosis (rare) - because it reduces oxygen levels
• Vitamin B12 Deficiency
• Appetite decreased
• Diarrhoea (usually transient)
• Nausea and vomiting
• Taste altered

47
Q

What is the purpose of combining metformin and insulin in the treatment of diabetes?

A

This is done to preserve the β-cells. It reduces the burden on β-cells to produce insulin hence preventing their downregulation

48
Q

Contraindications of Metformin

A

-ACute MI
• Severe heart failure
• Liver disease
• Impaired renal function (eGFR < 30 mL/minute/1.73 m2)
• Acute metabolic acidosis (including lactic acidosis and diabetic ketoacidosis)

Diabetes (3 decks)

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