Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

UG Biochemistry > 8. Diabetes Mellitus > Flashcards

8. Diabetes Mellitus Flashcards

(42 cards)

Start Studying
1
Q

Define diabetes mellitus

A

Metabolic disease of multiple causes

Characterised by;

  • chronically elevated blood glucose level
  • disturbances in carb/fat/protein metabolism

Caused by;
- defects in insulin secretion, insulin action, both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Briefly describe glucose homeostasis + regulation

A

Blood glucose levels maintained in narrow range: 3.5-6.5mmol/L

Tightly regulated by insulin + counter regulatory hormones;

  • insulin = decreases blood glucose (smaller level IGF1 too)
  • glucagon, GH, T3+4, catecholamines, steroids = increase blood glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe insulin + its actions

A

Insulin = hormone of plenty

  • secreted by beta cells of pancreas
  • peptide hormone (secreted as prohormone)

Actions; OVERALL = DECREASE BLOOD GLUCOSE
RAPID;
- increased transport of glucose, a acids + K+ into insulin sensitive cells
- includes striated muscle, adipose tissue + liver cells

INTERMEDIATE;

  • stimulation of protein synthesis
  • activation of glycolysis + glycogen synthesis
  • inhibition of GNG

DELAYED;
- increase in lipogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the effects of insulin on adipose tissue, striated muscle tissue + liver tissue

A

Adipose tissue;

  • increased glucose uptake
  • increased lipogenesis
  • decreased lipolysis

Striated muscle;

  • increased glucose uptake
  • increased glyogen synthesis
  • increased protein synthesis

Liver;

  • decreased GNG
  • increased glycogen synthesis
  • increased lipogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the processes that happen during insulin deficiency

A

Decreased glucose uptake
Increased protein catabolism = increased plasma a acids
- both cause hyperglycemia + glycosuria

Increased lipolysis = increased plasma FFAs

All result in dehydration + acidosis = coma + death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the pathogenesis of diabetes

A

Insulin resistance > relative insulin deficiency > absolute insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is diabetes mellitus classified?

A

Type I
Type 2

Gestational
Genetic-MODY
Iatrogenic
Secondary causes
Associated diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes type 1 diabetes, how does it present + what are the risk factors?

A

Cause;

  • absolute insulin deficiency
  • B cells destroyed by autoimmunity

Presentation;

  • acute
  • commonly presents as complications like DKA

Risk factors;

  • positive family history
  • younger patient group
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes type 2 diabetes, how does it present + what are the risk factors?

A

Cause;

  • relative insulin deficiency
  • insulin resistance

Presentation;
- hyperglycemia: polyuria, polydipsia, nocturia, blurred vision, weight loss

Risk factors;

  • overweight
  • middle/older age group
  • strong family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the old diagnostic criteria for DM?

A

Old criteria based on glucose

Any 2 of the following;

  • symptoms, e.g. polyuria, polydipsia, unexplained weight loss
  • random plasma glucose >= 11.1mmol/L
  • fasting plasma glucose >= 7.0mmol/L
  • 2hr level in OGTT >11.1mmol/L (2hr after 75g anhydrous glucose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the new diagnostic criteria for DM?

A

New criteria based on HbA1c

WHO 2011 decision to accept use of HbA1c testing in diagnosing DM

Recommended cut off point for DM = 48mmol/mol (6.5%)
- lower value does not exclude DM diag using glucose

Treat as high risk = 42-47mmol/mol (6.0-6.4%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is HbA1c?

A

HbA1c = glycated Hb, Hb covalently bound to glucose

Formed in non-enzymatic glycation pathway by Hb exposure to plasma glucose
- after prolonged exposure to high conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is HbA1c used to diagnose diabetes + what does it indicate?

A

Test measures the beta-N-1 deoxyfructosyl component of Hb

Measured to identify the 3 month average glucose concentration; (HbA1c ~~ Glucose levels)

  • diag test for DM + assessment test for glycemic control in diabetics
  • limited to 3 month average as RBC lifespan = 4 months (~120 days) but don’t all lyse at same time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where does the term HbA1c come from?

A

HbA separates into fractions on cation exchange chromatography > based on order of elution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why were the units for HbA1c changed?

A

Was reported as % but newer units were employed for global harmonisation

IFCC standardised units of mmol/mol

Dual reporting until June 2011

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What two ways is HbA1c testing carried out?

A

Fingerprick HbA1c;

  • convenient POCT
  • should only be used if national quality assurance guidelines are met in lab
  • must be confirmed by lab venous HbA1c test in all pts

Venous HbA1c testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What risk categories can HbA1c testing identify + what are the recommendations for these pts?

Study These Flashcards
A

HbA1c <48mmol/mol (6.5%);

  • may still fulfill WHO glucose criteria for diag of DM
  • use glucose test only if symptoms present/v high risk pt
  • not recommended routinely in this situation

HbA1c <42mmol/mol (6.0%);

  • may still have high diabetes risk
  • review personal risk + treat as high diabetes risk if clinically indicated
18
Q

When is HbA1c testing not appropriate?

Study These Flashcards
A

All children + young people

Any age suspected of having T1 DM

Symptoms of DM <2 months

High risk DM who are acutely ill (e.g. req hosp admission)

Taking medication that may cause rapid glucose rise, e.g. steroids, antipsychotics

Acute pancreatic damage inc pancreatic surgery

Pregnancy

Presence of genetic, hematological + illness related factors that influence HbA1c + its measurement, e.g. hemoglobinopathies

19
Q

What are the long standing complications of DM?

Study These Flashcards
A
  1. Macrovascular;
    - ischemic heart disease
    - peripheral vascular disease
  2. Microvascular;
    - nephropathy
    - retinopathy
    - neuropathy
20
Q

What are the acute complications of DM?

Study These Flashcards
A

Hypoglycemia (secondary to treatment)
Diabetic ketoacidosis (DKA)
Hyperosmolar non-ketotic coma (HONK)

21
Q

What is DKA?

Study These Flashcards
A

Diabetic Keto Acidosis = extreme metabolic state caused by insulin deficiency

Breakdown of FAs (lipolysis) produces ketone bodies (ketogenesis) = acidic

Acidosis occurs when ketone levels exceed body’s buffering capacity

22
Q

What are the causes of DKA?

Study These Flashcards
A

Common in T1 DM
Most common cause = omission of regular insulin
Ppted by infection + stress

23
Q

How does DKA present?

Study These Flashcards
A

Acute presentation

Polyuria + polydipsia
Weight loss, nausea, vomiting
Weakness + lethargy
Altered mental state

Characterist;

  • acetone on breath
  • Kussmaul respiration (deep hyperventilation)
24
Q

How serious is DKA?

Study These Flashcards
A

If left untreated can be life threatening

25
Describe the pathophysiology of DKA
Normally, glucose in blood take up by muscle + adipose tissue under influence of insulin ``` If insulin deficient; Decreased glucose uptake in tissues, e.g. muscle Inc glucagon (excess) = inc GNG = inc glucose/ketones Increased lipolysis = increased FFAs + ketones ``` One of the ketone bodies = beta-hydroxybutyrate - predominant ketone in DKA - used as energy source in brain when low glucose - able to cross BBB: acts as iHDAC on HDAC 2 + 3 Accumulation of acidic ketones = acidosis; - causes vomiting + osmotic diuresis = hypovolemia - further concentrates ketones + glucose = increasing acidity
26
How can DKA be identified in the lab?
Unchecked GNG + glycogenolysis = hyperglycemia Osmotic diuresis, vomiting, poor intake = dehydration Unchecked ketogenesis = ketosis Dissociation of ketone bodies into H+ and anions = anion-gap metabolic acidosis Often a ppting event is identified e.g. infection, lack of insulin admin
27
What are ketone bodies? When and how are they produced?
3 water-soluble molecules containing the ketone group; - acetoacetate > acetone (spontaneous breakdown) - beta-hydroxybutyrate = predominant in DKA Characteristics; - all 3 interchangeable - ketone group = fruity smell - acidic Produced by liver from fatty acids; - during fasting/starvation - carb restrictive diets - prolonged intense exercise - alcoholism - untreated (or inadequately treated) type 1 DM - pregnancy
28
Define osmotic diuresis
Increased urination due to presence of certain substances in the filtrate causing water retention in the tubule E.g. glucose in tubules can't be reabsorbed = increased osmotic pressure = water retention in tubule = increased urine output
29
Define GNG
A metabolic pathway that generates glucose from non-carbohydrate carbon substrates, e.g. lactate, glycerol, glucogenic amino acids, lipids
30
What biochemical abns are found in DKA?
``` BLOOD; ABG analysis = acidosis Serum electrolytes analysis; - hyperkalemia - increased urea - increased creatinine - increased beta-hydroxybutyrate ``` URINE; Dipstick analysis; - ketones - glucose
31
What is the treatment for DKA?
``` IV insulin (for hyperglycemia) IV fluids (for dehydration) Antibiotics if underlying infection ``` Regular bedside monitoring of bloodsugar 2x daily urine dipstick for ketones Regular lab monitoring of electrolytes, phosphate, acid-base balance + beta-hydroxybutyrate
32
Describe HONK, its biochemical characteristics + treatment
Hyperosmolar non-ketotic coma Complication of DM when high blood sugar = high osmolarity without significant ketoacidosis Common in T2 DM Biochem; - high blood glucose >30mmol/L = high plasma osmolality - no ketones in urine - plasma ketones normal Treatment = IV fluids + insulin
33
What is the role of the lab in DM?
Diagnosis Monitoring/follow-up Acute complications Chronic complications
34
Give an example of the labs role in DM diagnosis
Random/fasting samples of glucose for diagnosis; - serum or plasma - GP/hospital samples Require grey topped fluoride tubes; - inhibits glycolysis - prevents glucose levels falling during long sample transit times Measured by enzymatic colorimetric assay
35
Give an example of the labs role in DM monitoring
Monitoring of glucose levels Short time monitoring; - in hospital emergency/inpatient - GP surgery - self monitoring by pts Glucose meters used for short term monitoring; - cap blood used as sample - metres not sensitive at lower range of blood glucose - lab has pivotal role in QC of meters Lab blood glucose always reliable at low glucose conc
36
How is HbA1c estimated in the lab for DM diagnosis/monitoring?
Many methods of estimation; - HPLC = gld std - immunoturbidimetric method: HbA1cAb - affinity chromatography - electrophoretic methods - methods based on chemical reactions
37
How is the lab involved in acute complications of DM?
``` Hourly electrolyte profile 12 hourly serum beta-hydroxybutyrate ABG CRP, Mg, PO4 Hourly blood glucose ```
38
How is the lab involved in chronic complications of DM?
DM long term complications = increased risk ischemic HD + CKD Assess IHD risk = fasting lipids Assess CKD risk = serum creatinine, eGFR, ACR ACR = albumin:creatinine ratio in urine; - no albumin in urine if kidney function normal - early sign of KD = leak of albumin into urine - levels of albumin so low not detected by dipstick
39
What diagnostic tests detect impaired glucose homeostasis + regulation? What doe these tests indicate?
Impaired fasting plasma glucose; - FPG 6.1-7 mmol/L - can indicate pre-diabetes Impaired glucose tolerance; - 2hr PPG (postprandial glucose) 7.1-11.1 mmol/L - if person doesn't produce/respond properly to insulin then elevated blood sugar from meal remains unregulated - indicates pre-diabetes/DM + if DM under control Oral glucose tolerance test; - evaluates ability to regulate glucose metabolism by anhydrous glucose challenge
40
When is the OGGT indicated for use?
- equivocal (unclear/indeterminate) fasting/random blood glucose result - unexplained glycosuria - gestational diabetes - diagnosis of acromegaly
41
Describe the prep + protocol for an OGGT
Prep; - normal diet 3 days, fast overnight for min 8 hrs - rest throughout test - smoking not allowed - water allowed Protocol; - baseline blood sample for glucose - 75g anhydrous glucose in 300ml of water orally over 5-10min - sample taken after 120min
42
How is an OGGT interpreted?
DM; - fasting glucose >7.1 mmol/L - 2H post glucose >11.1 mmol/L Impaired fasting glucose; - fasting glucose 6.1-7.1 - 2H post glucose <7.4 Impaired glucose tolerance; - fasting glucose <7 - 2H post glucose 7.4-11.1

UG Biochemistry (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions