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Year 1 > Clinical Diabetes > Flashcards

Clinical Diabetes Flashcards

1
Q

What is diabetes?

A

Issues with production or response to insulin which leads to increase in blood glucose over a period of time.

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2
Q

What are the symptoms of diabetes?

A

Polyuria, polydipsia, weight loss (type 1 diabetes) and hypertension and increased risk of stroke.

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3
Q

What is polyuria?

A

Excessive urination even with restricted fluid intake due to high blood glucose levels which increases blood pressure and reduces water resorption in the kidneys.

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4
Q

What is polydipsia?

A

Excessive thirst.

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5
Q

What is diabetes insipidus?

A

Rare form of diabetes caused by neurological or nephornic dysfunction. Neurological is insufficient ADH mutation that affects water reabsorption and increases glucose retention. Nephronic is issue with the kidney or ADH that affects water reabsorption and increases glucose retention.

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6
Q

What is the cause of death commonly before age 70?

A

High blood glucose.

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7
Q

What is the prevalence of diabetes?

A

Greater in western countries and higher income. It increases the risk of blindness, lower limb amputation, stroke, heart attack and death before 70 years of age due to high glucose production

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8
Q

What is Type 1 diabetes?

A

Autoimmune condition associated with a genetic mutation causing issue with insulin production. Commonly diagnosed in younger people and can present in children as sudden weight loss. Insulin injections is needed to sustian life.

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9
Q

What is Type 2 diabetes?

A

Issue with insulin resistance, but may be related to insulin production. Commonly in obese children or adults where the body does not respond well to insulin. Insulin can improve QOL.

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10
Q

What is gestatinal diabetes?

A

Occurs in pregnancy where hormonal imbalance creates insulin resistance which resolves with birth

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11
Q

What is MODY?

A

Maturity onsent diabetes of the young which is very rare and linked to genetic mutation.

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12
Q

What is LADA?

A

Late autoimmune diabetes in adults which has the symptoms of both Type 1 and Type 2 Diabetes

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13
Q

What is Neonatal diabetes?

A

Occurs pre-6 months in infants caused by genetic mutation leading to impaired insulin porduction which is transient or permanent.

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14
Q

What causes Type 1 diabetes?

A

Genetics, environmental factors and autoimmune disease.

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15
Q

What is Phase 1?

A

Beta cells that die by natural causes or infection undergo apoptosis and removed by macorphages. Instead, natural dendritic cells enter and activate to take them up and present to B and T cells.

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16
Q

What is Phase 2?

A

Priming of B and T cells which undergo proliferation and infiltrate the islets of Langerhan and destroy the beta cells. There is a balance betwen regulation and activation of lymphocytes.

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17
Q

What is Phase 3?

A

Short phase of regulation however CD8+ T cells increase the activity of cytotoxic T cells. NK and macrophages potentiate the effect.

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18
Q

What increases the risk of diabetes in geneticlaly susceptible individuals?

A

Ratio of islet antigen cells to antibodies

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19
Q

What is the genetic link to Type 1 diabetes?

A

HLA which has two variants implicated in type 1 diabetes. There is HLA Class 1 nolecule DQ8 and HLA CLass 2 Molecule A2. Mutation to CTLA4, PTPN22 and IL2Ra.

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20
Q

What allelic variant is assoicated with Type 1 diabetes?

A

Mutation of autoregulatory proteins for immune response. CTLA-4 (Cytotoxic T cell associated antigen) is responsible for switching off T cells and this mutation disregulates T cell activity.

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21
Q

What are the environmental factors for diabetes?

A

Chemicals, bacteria, nutrition and most importantly, Enterovirus infection in childhood coupled with either:
Antiviral innate immunity where interferons and inflammatory ctokines are produced result in production of antiviral T cells. Beta cells block gamma interferon by producing beta interferon
adaptive immunity such as bystander activation or molecular mimicry causes autoreactive T cells against the beta cells.

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22
Q

What is the antiviral innate immune response?

A

Production of interferons and inflammatory cytokines.

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23
Q

What is the treatment for Type 1 diabetes?

A

Insulin

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24
Q

What is the prevalence of Type 2 diabetes?

A

2/3 in developing countries, expected to reach 370m by 2030 and have complications when presenting.

25
Q

What is the cause of Type 2 diabetes?

A

There is a chronic increase in blood glucose levels due to insulin insensitivity that are dysregulated. This causes beta cell function in type 2 diabetes to decline further over time.

26
Q

What is the driving factor for type 2 diabetes?

A

Obesity increases the levels of white fat deposits in liver and skeletal muscles which reduces insulin sensitivity and increases the productino of pro-inflammatory cytokines that affect beta cells.

26
Q

What causes insulin insufficency in type 2 diabetes?

A

Dysregulation of blood glucose levels that are high due to insulin insensitivity. Beta cells continue to produce high levels of insulin consistently, in a condiiton called hyperinsulinemia which exhausts and impairs function of beta cells over time.

27
Q

What are ceramides?

A

Bioactive lipids synthesised from FFas which increase action of the PKB/AFT pathway to decrease GLUT4 translocation and glycogenolysis and increase glucnoegenesis and lipolysis in Type 2 diabetes which contirbutes to insulin insensitivity.

28
Q

How do free fatty acid intakes affect insulin?

A

Converted into LCA-coA which undergoes beta oxidation excessively in mitochondria of cells that increases levels of reactiive oxygen species and cellular stress. It increases levels of PKC, JKNT and IKKB which impair insulin receptor signalling. FFAs can be synthesised to form ceramides which increase hyperglyceimia by affecting the PKB/Akt pathway to increase gluconeogenesis and lipolysis and decrease glucose translocation and glycogen synthesis.

29
Q

What is the role of the PKB/Akt pathway?

A

Gluconeogenesis, lipolysis, trasnslocation of GLUT4 for glucose uptake and glycogenesis.

30
Q

Which part of the PKB/Akt pathway is affected by FFAs?

A

Reduced translocation of GLUT4 receptor to the membrane for glucose uptake and glycogen synthesis. Increased gluconeogesis and lipolysis which contributes to hyperglycemia.

31
Q

What is protein kinase C?

A

Entry of freee fatty acids that undergo reactions to form DAG -> PKC which inhibits insulin singalling and the insulin recepotr substrate 1.

32
Q

What reduces the effect of the insulin receptor substrate 1 in Type 2 diabetes?

A

From the precursor free fatty acids -> LCA- coA -> Dialglycerol (DAG). This forms PKC, JNK and IKKB which inhibit IRS1 for insulin signalling.

33
Q

What causes insulin sensitivity?

A

White fat which increases inflammatory cytokine production and gluconeogenesis and lipolysis which reduces insulin sensitivity.

34
Q

What is glucolipotoxicity?

A

High levles of hyperglyceimia and hyperlipidaemia in type 2 diabetes due to levels of FFAs which reduces insulin sensitivity in cells and overexhausts beta cells to produce insulin to no effect and leads to impaired function.

35
Q

What affects gene and protein expression?

A

Inflammation, obesity, excess diet, family history and Mitochondrial dysfunction due to oxidative stress. Results in glucolipotoxicity which causes insulin resistance and leads to beta cell dysfunction.

36
Q

What is lean diabetes?

A

Greater likelihood for beta cell dysfunction and can lead to Type 2 diabetes. Greater in Asians and Africans with younger onset age and strong family history.

37
Q

Crossover with Type 1 and Type 2 diabetes?

A

Decreased insulin output over time. Levels of C-peptide in urine is high when there is high insulin production.

38
Q

What is LADA?

A

Latent autoimmune diabetes/Type 1.5. Characterised by polyupia, polydyspuria, blurred vision. However, there is weight loss which is indicative of not being Type 2 diabetes. It is caused by autoimmune destruction of beta cells.

39
Q

What is the cause of LADA?

A

Insulin resistance and insulin deficiency due to autoimmune destruciton.

40
Q

What factors cause LADA?

A

Fetal malnutrition, smoking and excess weight which causes insulin resistance. There is genetic suscpetibility with mutation to HLA DR-DQ that causes islet autoimmunity and insulin deficiency.

41
Q

How can diabetes affect the body?

A

Blindness, stroke, cardiovascular disease, neuropathy, nephropathy, foot ulcers and cognitive defect.

42
Q

What is the cause of the mutlisystem effects of diabetes?

A

Diabetes affects the large and small blood vessels due to glucolipotoxicity. This causes both hypertension and atherosclerosis

43
Q

What is normal kidney functino?

A

Unfiltered “dirty” blood enters via renal artery. Waste products exit via the ureter and filtered blood leaves through renal vein.

44
Q

What forms a nephron?

A

Glomeruli and tubules.

45
Q

How does diabetes affect the kidney?

A

Glucolipotoxicity causes hypertension and affects chemical composition of glomeruli and increases cellular stress. Leads to damage and protein leakage which over time forms scar tissue and causes renal failure

46
Q

What is diabetic neuropathy?

A

Glucolipotoxicity reduces blood flow in vessles and cause them to disappear and nervs to shrivel. Results in tingling pain or loss of sensation.

47
Q

What is large fibre neuropathy?

A

Ability to sense vibration caused by type 2 diabetes

48
Q

What is small fibre neuropathy?

A

Pain, temp and control body function caused by type 2 diabetes

49
Q

What is proximal motor neuropathy?

A

Hips, buttocks and thigh are affected and causes muscle weakness and pain. It is typically one sided and rare caused by Type 2 diabetes

50
Q

What is entrapment neuropathy?

A

Compression of nerves caused by type 2 diabetes

51
Q

What is diabetic foot syndrome?

A

Peripheral nerve damage or arterial disease due to glucolipotoxicity causes ulceration and infection. Failure to deal with infection such as fungus increases risk of amputation.

52
Q

What is noraml retina function for sight?

A

Retina most posteriorly converts light into electrical signals to the brain to form images which requires constant blood supply.

53
Q

What is diabeteic retinopathy?

A

High blood glucose damages retina blood supply.

54
Q

What is background retinopathy?

A

Tiny vessel bulges but no damage.

55
Q

What is pre-proliferative retinopathy?

A

Severe damage to the vessels causes blood to leak into the eye.

56
Q

What is proliferative retinopathy?

A

Scar tissue forms and new weaker blood vessels form which allow extensive leakage of blood into the eye.

57
Q

What is the measure of blood sugar levels?

A

GLucose binds to Hb which forms glycated Hb as a measure for blood sugar level control. High levels increase the risk of retinopathy development.

Year 1 (191 decks)

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