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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
Hepatic stellate cell function
a major source of extracellular matrix proteins, such as collagen
26
kupffer cells function
The macrophage of the liver. Prolonged inflammation in the liver can lead to liver damage and fibrosis.
27
Liver functions
- Glucose production - Ketone production (from acetyl-CoA) - Albumin production - Lipoprotein production - Bile acid
28
How does the liver detoxify substances
**conjugation to make substances more water soluble** for excretion: **Bilirubin - bind with glucuronic acid** Steroid hormones/T4 - bind with sulphate
29
Liver - general drug metabolism pathway
Uses **enzyme cytochrome p450**: 1. Hydroxylation (OH) 2. **OH --> OR** 3. R = glucuronic acid, GSH (glutathione), Sulphate
30
Liver - paracetamol metabolism
1. Portions of paracetamol are conjugated with sulphate and glucuronic acid 2. toxic byproduct (NAPQI) is conjugated by GSH (glutathione)
31
Paracetamol overdose
GSH is depleted, NAPQI will bind to cell constituents: - nephro/hepatotoxicity
32
Liver function tests (examples):
**Anion transport**: Bilirubin **Cholestasis**: GGT, Alk Phos **Hepatocyte damage**: Serum Aminotransferases **Protein synthesis**: Pro-Thrombin, Albumin
33
Markers of cholestasis
**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
Comparing Alk Phos with GGT in indicating cholestasis
**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
Bilirubin Clearance pathway (normal)
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
Liver enzyme - conjugation of bilirubin
UDP-glucuronyl transferase (UGT)
37
Cholestatic Jaundice (stool)
Pale stool, because no bilirubin is secreted via bile duct.
38
Pre-hepatic jaundice cause
Haemolysis (RBC breakdown)
39
Pre-hepatic jaundice
Unconjugated Hyperbilirubinaemia
40
Hepatocellular Jaundice cause
- viral hepatitis - malignancy - autoimmune - inherited disorders
41
Hepatocellular Jaundice
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
What is kernicterus
Premature babies cannot conjugate bilirubin, don't have UGT yet.
43
Treating kernicterus
phototherapy, bilirubin breakdown and urinary excretion.
44
Gilbert's syndrome (genetic)
Mild **unconjugated bilirubin build-up in plasma**: Reduced expression of UGT1A1, **reduced conjugation ability by liver**.
45
Cholestasis meaning
Obstructed bile flow
46
Cholestatic Jaundice Causes
**Intra-hepatic:** Blocked canaliculus, cirrhosis **Post hepatic:** Block in bile duct gall stones, pancreatic tumour.
47
Cholestatic Jaundice
stagnates the excretion of conjugated bilirubin from the liver - **mainly conjugated bilirubin** in the blood. - much more presence of bilirubin in the urine.
48
serum aminotransferases
**Elevate due to hepatocyte damage: Though not necessarily** AST:ALT >1 could indicate **alcoholism** or **advanced cirrhosis** (Larger affect on ALT)
49
Plasma albumin changes
Only present in **chronic liver disease**.
50
How does alcohol lead to alcoholic liver disease
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
Who gets non-alcoholic fatty liver disease
Closely related to T2DM and obesity.
52
Development of NAFL
1. steatosis 2. Steatohepatitis (NASH) 3. Cirrhosis 4. Hepatocellular cancer (HCC)
53
Biochemical Diagnosis of NAFLD
1. Raised serum aminotransferases (ALT, AST) 2. Raised Alk Phos and GGT 3. Hyperinsulinaemia/glycaemia (HOMA-IR)
54
Hepatic Insulin Resistance
Cannot suppress glucose production. Promotes **liver lipogenesis** (Trig synthesis and transported into circulation via VLDL)
55
Why does hepatic insulin resistance lead to liver lipogenesis?
Partially because of peripheral IR: **FFA release from peripheral tissue** is absorbed by the liver, **increased FFA stimulates lipogenesis**.
56
Leptin in non-alcoholic fatty liver
Elevated levels of leptin, correlated to steatosis.
57
Adiponectin
Insulin sensitiser

CBE (16 decks)

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