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CBE > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Insulin effects

A

Muscle cells: Increased glucose uptake
Adipocytes: Suppression of lipolysis (Reduced FFA release)
Liver:
Suppression of glucose production
Promote glycogen production
Protein: Promotes protein synthesis/Inhibit protein breakdown

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2
Q

T1D and DKA

A
  1. almost insulin insuffiency
  2. minimal glucose uptake by cells
  3. Lipolysis, adipocytes release FFA
  4. Ketone bodies accumulation
  5. Acidosis due to ketone accumulation
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3
Q

Urine/Blood test for ketone bodies diagnosis

A

Can confirm DKA as cause of metabolic acidosis
Typically for T1, not characteristic for T2.

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4
Q

Blood gas test

A

Tests H+ concentration, pH in blood.

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5
Q

C-peptide telling T1 and T2 apart

A

C-peptide levels will be low in T1.

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6
Q

What is C-peptide?

A

part of proinsulin, cleaved from insulin prior to secretion

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7
Q

What is LADA?

A

Latent Autoimmune Diabetes in Adults.

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8
Q

Diagnostic marker for T1DM and LADA

A
  1. C-peptide insufficiency
  2. Islet cell autoantibodies (eg. anti-GAD)
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9
Q

Why monitor diabetes?

A

Resolve acute complications:
Avoid hyper/hypoglycaemia
Ketone meter - identify early DKA
Prevent chronic complications:
CVD, nephropathy, neuropathy, retinopathy

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10
Q

Glucose sensor complication

A

15 minute lag due to sampling site being the interstitial fluid, issue with acute hypoglycaemia

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11
Q

Glucometer complication

A

Inaccurate results if poor perfusion of peripheries

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12
Q

The test to measure average glucose levels

A

HbA1c (1-2 months)

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13
Q

HbA1c test underlying mechanism

A

Glucose will spontaneously bind to haem, glycate haemoglobin.
Percentage of glycated haem – indicate blood glucose

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14
Q

HbA1c test complication

A

Affected by RBC turnover.

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15
Q

Measurement of HbA1c and Accuracy

A

Using Cation Exchange HPLC: RBC lysis then measure Hb
(+ve) glycated haemoglobins will move faster than non-glycated.
Ability to separate from other Hb subtypes.

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16
Q

lower HbA1c clinical relevance

A

A lower level of HbA1c indicates a significantly lower risk of diabetic complications (Long term - chronic).

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17
Q

Fructosamine test underlying mechanism

A

Glucose will also glycate plasma proteins.
Including albumin, globulins.

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18
Q

Fructosamine test complication

A

Not accurate for rapid glucose change, abnormal protein turnover.

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19
Q

Diabetic nephropathy underlying mechanisms

A
  1. Ischaemic damage (renal arteriole atherosclerosis)
  2. Glomerular sclerosis (Glycation-induced inflammation)
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20
Q

Outcomes of diabetic nephropathy

A
  1. Progressive fall in eGFR, creatinine accumulation.
  2. Proteinuria
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21
Q

Microalbuminuria detection clinical relevance

A

prevent/delay diabetic nephropathy

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22
Q

Microalbuminuria underlying mechanism

A

Increase in Glomerular Permeability, protein leakage
Tests ACR or PCR

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23
Q

How to reverse microalbuminuria?

A

Control blood pressure.
Treat with ACE-I, relieve renal burden.

24
Q

Urinary ACR test complications

A
  1. Avoid dilute sample, take in morning
  2. Acute illness can have elevated ACR (UTI), avoid false positives.
25
Q

Hepatic stellate cell function

A

a major source of extracellular matrix proteins, such as collagen

26
Q

kupffer cells function

A

The macrophage of the liver.
Prolonged inflammation in the liver can lead to liver damage and fibrosis.

27
Q

Liver functions

A
  • Glucose production
  • Ketone production (from acetyl-CoA)
  • Albumin production
  • Lipoprotein production
  • Bile acid
28
Q

How does the liver detoxify substances

A

conjugation to make substances more water soluble for excretion:
Bilirubin - bind with glucuronic acid
Steroid hormones/T4 - bind with sulphate

29
Q

Liver - general drug metabolism pathway

A

Uses enzyme cytochrome p450:
1. Hydroxylation (OH)
2. OH –> OR
3. R = glucuronic acid, GSH (glutathione), Sulphate

30
Q

Liver - paracetamol metabolism

A
  1. Portions of paracetamol are conjugated with sulphate and glucuronic acid
  2. toxic byproduct (NAPQI) is conjugated by GSH (glutathione)
31
Q

Paracetamol overdose

A

GSH is depleted, NAPQI will bind to cell constituents:
- nephro/hepatotoxicity

32
Q

Liver function tests (examples):

A

Anion transport: Bilirubin
Cholestasis: GGT, Alk Phos
Hepatocyte damage: Serum Aminotransferases
Protein synthesis: Pro-Thrombin, Albumin

33
Q

Markers of cholestasis

A

GGT, Alk Phos: Increased synthesis
GGT locates on the cell membrane, obstruction and damage (inflammation) of bile duct flow will make GGT lining the bile duct leak into bloodstream.
Alk Phos works similarly.

34
Q

Comparing Alk Phos with GGT in indicating cholestasis

A

GGT is specific to liver and bile duct.
Alk Phos could rise in response to bone disease (Paget’s disease)

Alk Phos will not be affected by drugs and alcohol

35
Q

Bilirubin Clearance pathway (normal)

A
  1. Haem breaks down to bilirubin (unconjugated-albumin bound)
  2. bilirubin is transported to the liver
  3. bilirubin is conjugated by glucuronic acid in the liver
  4. bilirubin is no longer albumin-bound
  5. conjugated bilirubin -> biliary excretion (bile)
    rate limiting step: biliary excretion
  6. bile is metabolised in the intestines by bacteria.
  7. excreted as stool.
36
Q

Liver enzyme - conjugation of bilirubin

A

UDP-glucuronyl transferase (UGT)

37
Q

Cholestatic Jaundice (stool)

A

Pale stool, because no bilirubin is secreted via bile duct.

38
Q

Pre-hepatic jaundice cause

A

Haemolysis (RBC breakdown)

39
Q

Pre-hepatic jaundice

A

Unconjugated Hyperbilirubinaemia

40
Q

Hepatocellular Jaundice cause

A
  • viral hepatitis
  • malignancy
  • autoimmune
  • inherited disorders
41
Q

Hepatocellular Jaundice

A

Reduced liver processing (uptake and excretion):
Reduced excretion of conjugated bilirubin:
- conjugated bilirubin is returned to the plasma
- conjugated bilirubin is present in the urine

42
Q

What is kernicterus

A

Premature babies cannot conjugate bilirubin, don’t have UGT yet.

43
Q

Treating kernicterus

A

phototherapy, bilirubin breakdown and urinary excretion.

44
Q

Gilbert’s syndrome (genetic)

A

Mild unconjugated bilirubin build-up in plasma:
Reduced expression of UGT1A1, reduced conjugation ability by liver.

45
Q

Cholestasis meaning

A

Obstructed bile flow

46
Q

Cholestatic Jaundice Causes

A

Intra-hepatic:
Blocked canaliculus, cirrhosis
Post hepatic:
Block in bile duct gall stones, pancreatic tumour.

47
Q

Cholestatic Jaundice

A

stagnates the excretion of conjugated bilirubin from the liver
- mainly conjugated bilirubin in the blood.
- much more presence of bilirubin in the urine.

48
Q

serum aminotransferases

A

Elevate due to hepatocyte damage: Though not necessarily
AST:ALT >1 could indicate alcoholism or advanced cirrhosis (Larger affect on ALT)

49
Q

Plasma albumin changes

A

Only present in chronic liver disease.

50
Q

How does alcohol lead to alcoholic liver disease

A

Increases Triglycerides
1. Excessive alcohol promotes FA esterification (trig synthesis)
2. Promotes lipolysis and FFA accumulation
3. With more FFA and 3-GP, more triglyceride synthesis and VLDL delivery
4. ends with steatosis (fat droplets in hepatocytes)

51
Q

Who gets non-alcoholic fatty liver disease

A

Closely related to T2DM and obesity.

52
Q

Development of NAFL

A
  1. steatosis
  2. Steatohepatitis (NASH)
  3. Cirrhosis
  4. Hepatocellular cancer (HCC)
53
Q

Biochemical Diagnosis of NAFLD

A
  1. Raised serum aminotransferases (ALT, AST)
  2. Raised Alk Phos and GGT
  3. Hyperinsulinaemia/glycaemia (HOMA-IR)
54
Q

Hepatic Insulin Resistance

A

Cannot suppress glucose production.
Promotes liver lipogenesis (Trig synthesis and transported into circulation via VLDL)

55
Q

Why does hepatic insulin resistance lead to liver lipogenesis?

A

Partially because of peripheral IR: FFA release from peripheral tissue is absorbed by the liver, increased FFA stimulates lipogenesis.

56
Q

Leptin in non-alcoholic fatty liver

A

Elevated levels of leptin, correlated to steatosis.

57
Q

Adiponectin

A

Insulin sensitiser

CBE (16 decks)

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