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MET2 > DM > Flashcards

DM Flashcards

1
Q

What causes DMT1? [1]

What population normally effects? [1]

A
  • Autoimmune disruption of the pancreatic β cells within the islets of Langerhans: causes Insulin deficiency
  • Genetic factors include HLA-D
  • Seen in young and fitter populations
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2
Q

What causes DMT2? [1]

What % of people with DM have DMT2? [1]

Which patient population is it in? [1]

A

Caused by: abnormal insulin action & β cell dysfunction due to a mix of genetic and environmental factors

80% of diabetes is DMT2

Used to be common In elderly - now commonly young people. Due to obesity.

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3
Q

Name some risk factors for DMT2 [4]

A

Family history of diabetes
Ethnicity

Overweight
Unhealthy diet
Physical inactivity
Increasing age
High blood pressure
Impaired glucose tolerance (IGT)*
History of gestational diabetes
Poor nutrition during pregnancy

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4
Q

How does obesity cause extrinsic insulin resistance? [3]

How does obesity cause intrinsic insulin resistance? [3]

What is net effect of obesity and insulin? [1]

A

Which aspects of obesity causes extrinsic insulin resistance? [3]
* Accumulation of lipids and FFA
* Chronic inflammation
* Altererd adipokiine (cytolines from FA)

How does obesity cause intrinsic insulin resistance? [3]
* Mitochondrial dysfunction
* Ox stress
* ER stress

Overall: causes hyperinsulinaemia, whcih increases lipid synthesis and insulin resistance

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5
Q

How do B pancreatic cells first react to being insulin resistant? [3]

A

B cells:
* become bigger
* increase in number
* produce more insulin

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6
Q

Whats difference between insulin resistance and DMT2?

A

Insulin resistance: adapt by : become bigger, increase in number and produce more insulin (compensatory hyperinsulinaemia)

DMT2: resistance AND failure

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7
Q

How does islet compensation occur if there is impaired function of B-cells?

A

As the impacts of obesity occur the susceptible cells will decrease in number/function –> B-cell apoptosis

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8
Q

Impaired genetic comepensation: genetic component

How do most of the genes assocaited with DMT2 infuence the disease? [2]

A

impairing insulin secretion rather than insulin action

Gene risk variants are to do with the regulators of β cell turnover or regeneration

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9
Q

Impaired genetic comepensation: environmental component

Which envrionmental factors within body influence DMT2 infuence? [4]

A

Increased circulating FFAs (lipotoxicity)

Hyperglycaemia (glucotoxicity)

Combination of the two (glucolipotoxicity)

Hyperinsulinemia

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10
Q

What is Monogenic diabetes? [1]

Specifically how is it caused / insulin affected? [2]

A

Caused by a mutation in a single gene (one of over 40 genes): Means theres 40 types of MODY

Most cases are Maturity Onset Diabetes of the Young (MODY)

Caused by:
* prevent the insulin sensing glucose metabolism in B-cells

  • Due to: impairment of insulin secretion/pancreatic βcell dysfunction
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11
Q

What may cause gestational diabetes? [2]

A

excessive proinsulin that may induce β cell stress

high concentrations of hormones may affect β cell function and peripheral insulin sensitivity

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12
Q

Many women with GD experience pregnancy-related complications including WHAT? [3]

A

Many women with GD experience pregnancy-related complications including
* high blood pressure,
* large birth weight babies
* obstructed labour

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13
Q

What is LADA?

What are characteristics of LADA? [2]

A

Latent Autoimmune Diabetes of Adults (LADA): Features of both Type 1 and Type 2 (type 1.5)

Immunologically similar to T1 - produce DMT1 antibodies but destruction is slower than in T1.

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14
Q

What values for resting and random plasma glucose and values do you use for DM? [2]

A

Plasma glucose:
- fasting >7 mmol/L
- random >11.1 mmolL

Need one AND symptoms (Thirst, Increased urination, recurrent infections, weight loss drowsiness)

If asympotamic need more measurements

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15
Q

What scores in oral glucose tolerance test would you use?

A
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16
Q

What % HbA1c is used as cut off for diabetes? [1]

A

An HbA1c of 48 mmol/mol (6.5%) is recommended as the cut point for diagnosing diabetes

17
Q

How can you treat DMT1?

Currently? [2]
Future? [2]

A

Insulin - short acting and long acting.
- Pumps
- Injections - pens
- Short / Fast acting: Humalog
- Long acting: Glargine

Islet transplantation
- Only patients matching a strict list of criteria, including being at risk of frequent and secere hypos/hypers.

Possible future treatment: immunotherapy

SGLT Inhibitors:.
* Prevent co-reabsorption of glucose in the PCT with Na.
* Encourages glycosuria -> wee out the excess glucose. Lowers blood glucose levels. Restores GFR in diabetics
* E.g.

18
Q

What is the first line of treatment for DMT2? [1]

A

Metformin

19
Q

MoA of Metformin [3]

A

Inhibits gluconeogenesis in the liver
Inhibits CAMP + PKA pathway.
Also increases glucose transport - increasing uptake at skeletal muscle. Opposes insulin resistance through various mechanisms.

From Drugs List:

Reduces hepatic glucose production and
increases skeletal muscle glucose uptake
Also lowers serum insulin

20
Q

Which treatments for DMT2

inhibitGNG [1]
increase insulin sensistivity [2]
stimulate insulin secretion [2]

two others? [2] ?

A

Inhibits GNG:
* Metformin: inhibits GNG at liver

Increases insulin sensitivity:
* Metformin
* Thiazolidinediones: Enhance GLUT4 uptake into the cell membranes (in adipocytes - so causes weight gain) via PPAR-y gene

Stimulation of insulin secretion:
* Sulfonylureas: close ATP sensitive K chance which regulates insulin secretion
* Prandial glucose regulators: same as above but faster

Others:
* GL1-P receptor agonists
* DPP-4 inhibitors: DPP-4 inhibits GL1-P

21
Q

What is the role of GLP-1? [4]

A

GLP-1
* Can inhibit glucagon secretion
* Can reduce gluconeogenesis.
* Can enhance insulin secretion + restore B-cell function/differentiation.
* Can increase insulin biosynthesis.

22
Q

When do you see DKA? [3]

A

DKA is a hallmark of DMT1 - it is usually seen in:
- Previously undiagnosed diabetes
- Interruption of insulin therapy
- The stress of intercurrent illness e.g. surgery or infection

23
Q

How does DKA occur?

A

In the absence of insulin there is an unrestrained increase in hepatic gluconeogenesis and peripheral glucose uptake by tissues such as muscle is reduced

High circulating glucose levels result in an osmotic diuresis (since increased glucose in urine which pull more water into urine) by the kidneys and consequent dehydration and loss of electrolytes

Peripheral lipolysis occurs leading to an increase in circulating free fatty acids (FFAs) which are then broken down to acetyl-coenzyme A (CoA), but little oxaloacetate within the liver cells and this, in turn, is converted to ketone bodies within the mitochondria. (no Kreb’s cycle)

Ketone bodies are in excess

Ketone bodies dissociate: H+

Causes metabolic acidosis w/ raised anion gap.

Vomiting leads to further electrolye loss

24
Q

What is the order of treatmnet for DKA? [3] What are complications of mismanaged treatment?

A
  1. Fluids
  2. Restore electrolytes - especially K+
  3. Insulin intravenously.

DKA patients have high extracelullar K+ but little intracellular. Need to he careful because if give insulin first, causes intracellular uptake of K but that would causes overall reduction in K and cardiac arrythmias

25
Q

How does XS alcohol cause hypoglycaemia (especially in DMT1?)

A

Alcohol broken down by alcohol dehydrogenase -> NADH:NAD ratio increased -> less gluconeogenesis -> hypo.

Dangerous overnight when the body uses stores for energy

26
Q

Why is hypoglycaemia dangerous with regards to awareness?

A

Not aware they are having a hypo - patients become progressively less aware:

(Thought to be due to body-wide adaptation to repeated insulin- induced hypoglycaemia and impaired counter reg hormone response)

27
Q

What are some chronic complications of diabetes?

  • Because of hyperglycaemia? [1]
  • Microvascular disease? [4]
  • Dyslipidaemia? [3]
A

Hyperglycaemia: Atherosclerosis and CVD events

Microvascular disease: Nephropathy, Neuropathy, Retinopathy Amputation

Dyslipidaemia: Ectopic fat deposition in muscle + liver, Exacerbation of insulin resistance

28
Q

MoA of diabetic retinopathy?

A

Hyperglycaemia -> increased PKA activity -> reduced retinal blood flow due to vc
PKA activity -> vascular permeability angiogenesis -> macular oedema.

29
Q

What is difference between non-proliferative and proliferative retinopathy?

A

Both occur because of damage to BV in back of eye

Non-profilerative: ‘Cotton wool’ dilation of retina veins causes internal haem. oedema causes vision loss

Proliferative: New BV proliferate near optic disc and bleed: detachment of retina

30
Q

MoA of diabetic nephropathy?

A

PKA activation -> collagen/fibronectin proliferation -> capillary occlusion -> thickening of glomerular basement membrane. PKA activation -> increase in NADPH -> ROS

31
Q

Characteristics of diabetic nephropathy? [4]

A

proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis

32
Q

MoA of diabetic neuropathy? [1] be aware but not too deep

Peripheral effects? [1]
Autonomic effects? [1]
Proximal effects? [1]
Focal effects [1]

A

Damage to nerve fibres and the BV supplying them

Peripherhal: causes pain or loss of feeling in the hands, arms, feet, and legs

Autonomic:

33
Q

How can diabetes increase chance of atheromatic plaque formation through Adva?

A

Hyperglycaemia and dyslipidaemia:
* endothelial cell dysfunction
* increased adhesion of monocytes and platelets

AGE modification of oxidised low-density lipoprotein (LDL) and their receptor (LDLR)
* enhanced LDL uptake into atherosclerotic plaques
* pro-inflammatory cytokine production

Glycation of apolipoprotein, LDL or LDLR
* impaired cholesterol efflux from atherosclerotic plaques
* impaired cholesterol clearance

34
Q

What is the most common cause of death
for patients with diabetes?

A

Heart attacks and strokes

35
Q

Diabetes made which disease worse? [1]

A

COVID

MET2 (52 decks)

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