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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Where does the pancreas sit ?

A
  • Behind the stomach
  • In the duodenum
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2
Q

What is the endocrine function of the pancreas

A

-Pancreatic islets (islets of Langerhans) specialized tissues contain endocrine cells

  • Alpha (α) cells produce glucagon (a hyperglycemic hormone) essential for controlling blood glucose levels. (20%)
  • Beta (β) cells produce insulin (antagonistic to glucagon or a hypoglycemic hormone) (= 70%)
  • Delta Cells (δ) produce somatostatin, which inhibits both glucagon and insulin. (<10%)
  • PP cells (gamma cells or F cells) producing pancreatic polypeptide (<5%)
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2
Q

What is the exocrine function of the pancrease?

A
  • Sceret Pancreatic juicefrom the duct.
  • This is full of bicaronbanate (alkalitic) to neutralise the acidicity of the stomach acid.
  • Protease, lipase, amylase
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3
Q

Explain the physiology of blood sugar homeostasis after eating food.

A
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4
Q

Explain what happens if a meal is skipped eg fasting in regards to blood sugar homeostasis.

A
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5
Q

effects of insulin

A
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6
Q

effects of glucagon

A
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7
Q

What happens when hyperglycemia occurs to maintain homestasis ?

A
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8
Q

What happens when hypoglycemia occurs to maintain homeostasis?

A
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9
Q

What are the symtoms of diabetes (the three Ps)

A

Polyuria—huge urine output
Polydipsia—excessive thirst
Polyphagia—excessive hunger and food consumption

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10
Q

What calle release insulin ?

A

Beta cells - Insulin release

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11
Q

What cells release glucagon ?

A

Alpha cells -Glucagon release

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12
Q

Explain the difference between Glycogenolysis and gluconeogenesis.

A
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13
Q

What is Glycogenesis ?

A

Glycogenesis is the process of storing excess glucose for use by the body at a later time.

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14
Q

What is glycolysis ?

A

Glycolysis is the process in which glucose is broken down to produce energy.

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15
Q

What happens in type 1 diabetes mellitus?

A

Autoimmune: destruction of β-cells – results in lack of insulin.

No or very little insulin.

Glucose stays in blood
Sudden onset.

Insulin dependent

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16
Q

What are the three factors that can cause type diabetes?

A
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17
Q

What antigen is detected in T1DM (genetic factor)?

A

human leukocyte antigen (HLA)

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18
Q

Who is at risk of T2DM ?

A
19
Q

What happens in T2DM ?

A

Insulin resistance: tissues are less responsive to insulin leading to impaired glucose uptake by adipocytes and muscle. Mechanism not well understood.

Slow onset.

20
Q

Explain clinical characteristics differences between type 1 and type 2 diabetes.

A
21
Q

What is double diabetes ?

A
  • Type 1 diabetes is diagnosed
  • Use of Insulin can lead to weight gain
  • Development of Type 2 DM
22
Q

Explain Gestational Diabetes

A

Gestational diabetesis high blood sugar (glucose) that develops during pregnancy and usually disappears after giving birth.

23
Q

How do you test for Gestational diabetes?

A

NICE: 75g glucose Oral Glucose Tolerance Test. Reading after 2 hours.

24
Q

What is Latent Autoimmune Diabetes (LAD)

A
25
Q

Explain Alzheimer’s Diabetes

A

Insulin resistance specific to the brain

People with diabetes more likely to develop Alzheimer’s than those without

Damage to blood vessels in brain?

Treatment with insulin? Intranasal delivery or sensitizers (THROUGH THE NOSE)

26
Q

Explain Diabetes and mental health

A

Diabetes: depressive episodes are prolonged and 2x more likely

More prone to diabetes if you have depression (60% increase)

27
Q

How to test for Diabetes ?

A
  • Fasting Glucose Levels
  • Glucose Tolerance Tests
  • HbA1c:
    Tests for glycosylation of Hb - THIS WILL TEST OVER 3 MONTHS BECAUSE RBC LAST FOR 120 DAYS.

Renal function:
- glucose levels in urine (>10mmol/L)
- Urea electrolytes
Plasma Lipid levels

28
Q

What are the complications of DM ?

A

Acute
Diabetes ketoacidosis (DKA) (comomnly t1DM)

Diabetic nonketotic Hyperosmolar hyperglycaemic state(HHS)
(Commonly T2Dm).

Chronic

Microvascular

Macrovascular

29
Q

Explain KETOACODIS

A

Diabetic ketoacidosis:
Lack of insulin leads to increased amounts of glucagon which stimulates production of glucose by glycogenolysis / gluconeogenesis in the liver and muscle cells; and breakdown of fatty acids in adipocytes to ketones.
Usually happens in type 1 rather than type 2 DM.

Increased glucose in the blood → osmotic diuresis and electrolyte loss (hyperglycaemic effect)
Lipolysis → increased free fatty acids → acetyl CoA → ketone bodies → metabolic acidosis
Acidosis
Dehydration and Vomiting → loss of electrolytes

30
Q

What are the pathogeneis of DKA ?

A

Hyperglycemia- kidneys excrete glucose (Renal threshold 10mmol). This osmotic diuresis – dehydration and marked electrolyte loss (Na, K and Cl).
Severe DKA may loose upto 6.5 L water and 400-500 mEq each of electrolyte over 24 hour period.
Breakdown of fat (lipolysis)into free fatty acid (FFA)and glycerol.
FFA are converted into ketone bodies (acetone, acetoacetic acid and beta-hydroxybutyric acid) by the liver.
Ketone bodies are acids and their accumulation in the circulation leads to metabolic acidosis.

31
Q

What is the treatment for DKA ?

A

admission to hospital for urgent treatment.
given insulin, fluids and nutrients through a drip via IV line.
monitored for complications, as DKA can sometimes affect brain, heart or lungs.

32
Q

What is hyperosmolar hyperglycaemia ?

A

The main triggers for hyperglycaemic hyperosmolar state is a relative insulin deficiency and inadequate fluid intake.
middle aged or elderly individuals with type 2 diabetes mellitus and it may be the presenting feature in around 25% of individuals.
HHS is the type 2 diabetes equivalent of diabetic ketoacidosis (DKA) in type 1 diabetes individuals.
most serious complication in patients with type 2 diabetes mellitus and whenever it occurs, it is a medical emergency
serious acute metabolic complication of diabetes mellitus that is characterized by hyperglycaemia (>600 mg/dl), hyperosmolarity (>330 mOsm/L) and, dehydration without ketosis or acidosis.
Its metabolic differences occur because in individuals with type 2 diabetes mellitus there is a small quantity of insulin remaining enough to suppress lipolysis and the associated acidosis.
This complication is more common is Afro-Caribbean.
HHS occurs less frequently when compared to diabetic ketoacidosis but once it occurs it has a higher mortality rate of about 15%.

33
Q

What is the pathogenesis of Pathogenesis of Hyperosmolar hyperglycaemic state(HHS)

A

Often in older people (age 50-70) with no know history of diabetes or with mild type II diabetes.
In DNHC the insulin level is too low to prevent hyperglycaemia, but high enough to prevent fat breakdown.
Hyperglycaemia predominates, ketosis is minimal or absent.
Ketosis or Acidosis does not occur because of difference in insulin level.
Altered sensorium

34
Q

What is the treatment for hyperosmolar hyperglycaemia state (HHS)?

A

fluid replacement
Correction of electrolytes imbalance
Insulin administration

35
Q

What is the difference between the pathogeneis of Pathogenesis of DKA and HHS

A
36
Q

What are some complications of DM?

A

Cataract
Depression
Glaucoma
Heart disease (angina, 94.2% MI, 62.5% stroke)
Hyper/hypoglycaemia: ketoacidosis/coma
Kidney disease
Peripheral neuropathy (↓ sensation) → amputation from infection
Microvascular blood flow problems leads to demyelination
Sexual dysfunction (neuropathy)
Retinopathy (retinal blood vessel damage, oedema, abnormal microvascular blood flow)

37
Q

What is Diabetes Insipudus ?

A
38
Q

What are the causes of Diabetes Insipidus ?

A
  • Central (neurogenic) – inadequate ADH released by hypothalamic neurons or posterior pituitary (e.g. tumour, physical damage, infection)
  • Nephrogenic – kidney unresponsive to ADH
  • Psychogenic - compulsive water drinking
39
Q

What medications can casue diabetes insidious?

A

Some medications, particularly lithium (used to help stabilise mood in some people with specific mental health conditions, such as bipolar disorder), can cause nephrogenic diabetes insipidus.

40
Q

What are the tests and measurements for Diabetes Inspididus ?

A
41
Q

What are the three types of Diabetes Inspidus ?

A

Central (neurogenic) diabetes insipidus - Decreased ADH secretion

Nephrogenic Diabetes Insipidus - Decreased effectiveness of ADH

Primary polydipsia - Pathological water drinking

42
Q

What is the treatment for Neurogenic (central) Diabetes Insipidus ?

A

Neurogenic (central) DI – treatment with desmospressin, a synthetic ADH analogue; surgery or radiotherapy to remove any associated tumour

43
Q

Treatment for Nephrogenic DI ?

A

low salt diet (less salt excreted in urine means less water excreted); adequate water ingestion to avoid dehydration. Medications called thiazide diuretics, which reduce the amount of urine the kidneys produce.

44
Q

Treatment for Psychogenic Diabetes Inspididus ?

A

Reduction in fluid intake; psychiatric support and treatment if the over drinking results from a mental health disorder

Endocrine (16 decks)

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