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2 - CR/MET > Met PBLs > Flashcards

Met PBLs Flashcards

1
Q

Main energy fuels used during starvation

A

Amino acids from muscle
TAGs from adipose tissue
Ketones from the liver

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2
Q

Main substrates for gluconeogenesis

A

Lactate
Glycerol
Amino acids
Oxaloacetate

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3
Q

Features of Kwashiorkor

A

Ascites and pitting oedema
Hepatosplenomegaly
Dermatitis

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4
Q

How does starvation lead to ketosis?

A

Decreased glucose available for the brain
Brain can only use glucose and ketones for energy production
Large amounts of lipolysis releasing FFAs to the liver for metabolism produced large amounts of acetyl CoA
Excess acetyl CoA cannot be put into the Krebs cycle as oxaloacetate supplies are depleted due to it being used in gluconeogenesis
Therefore acetyl CoA is used to make ketone bodies

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5
Q

Ketone body examples

A

Acetoacetate

b-hydroyxbutarate

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6
Q

Why does feeding syndrome occur?

A

Insulin release in referring stimulates glycogen, fat and protein synthesis. These processes require vitamins and minerals such as phosphate, magnesium thiamine. Therefore large amounts of these substances enter cells upon feeding to deplete the plasma levels.
Leads to features associated with refeeding syndrome.

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7
Q

How is referring syndrome avoided?

A

Vitamin and mineral replacements

Slow increases in caloric intake

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8
Q

Causes of oedema

A

Increased capillary hydrostatic pressure
Reduced capillary oncotic pressure
Increased capillary permeability
Lymphatic blockage

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9
Q

AST

A

Aspartate + a-ketoglutarate –> oxaloacetate + glutamate
Uses vitamin B6 as cofactor
Found in the liver, muscles, bone, heart, pancreas

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10
Q

ALT

A

Alanine + a-ketoglutarate –> a-pyruvate + glutamate
Vitamin B6 cofactor
Found mostly in the liver
Raised to a greater extent in liver disease

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11
Q

AST/ALT ratio

A

Usually below 1

>1/2 = alcoholic causes or muscle disease

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12
Q

ALP

A

Raised in liver disease

Also in biliary obstruction and bone disease

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13
Q

GGT

A

Raised in liver disease
Also in biliary obstruction but not in bone disease
Large increases in excessive alcohol consumption

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14
Q

INR

A

Modified PT

Intrinsic pathway

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15
Q

What is in pabrinex?

A

Thiamine, riboflavin, pyridoxine, nicotinamide, vitamin C, glucose

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16
Q

Why is terlipressin used?

A

Reduces bleeding from oesophageal varices

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17
Q

Actions of Lactulose

A

Increases water excretion due to osmotic effect

Acidifies gut contents so reduces ammonia absorption to prevent hepatic encephalopathy

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18
Q

Metabolic diseases causing cirrhosis

A

Haemochromatosis
Wilson’s disease
Alpha-1-antitrypsin deficiency

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19
Q

Why does he have high urea?

A

Increased protein intake due to bleeding from varices

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20
Q

Treatments of ascites

A

Diuretics
Paracentesis
TIPS
Albumin supplements

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21
Q

Humalog

A

Fast acting insulin analogue

Must eat immediately after

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22
Q

Glargine insulin

A

Long acting insulin with a peak less profile that mimics the tonic release from beta cells

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23
Q

DKA treatment

A

Fluid and electrolyte replacement

Short acting insulin

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24
Q

How does alcohol lead to ketoacidosis?

A

Ethanol metabolism leads to increased NADH/NAD ratio
Inhibits Krebs cycle, glyconeogenesis and fatty acid oxidation
Causes fatty acid synthesis and ketogenesis

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25
Q

Actions of GKRP

A

Controls location of GK

GK involved in glycolysis and glycogen synthesis as well as sensing of glucose levels

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26
Q

Actions of PPARG

A

Transcription factor for lipid metabolism
–> increased lipid uptake and lipogenesis
Decreases circulating lipid levels

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27
Q

How does metformin work?

A

Activation of AMPK
Inhibits hepatic gluconeogenesis
Increases GLP-1 secretion
Increases GLUT4 translocation

28
Q

How does sitagliptin work?

A

Inhibits breakdown of GLP-1

Enhances insulin secretion

29
Q

How does pioglitazone work?

A

Increases PPARG transcription

Increases lipid uptake to decrease circulating FFA levels

30
Q

Define microalbuminaemia

A

Albumin excretion 30-300mg/day

ACR>3mg/mmol

31
Q

Define proteinuria

A

Albumin excretion >300mg/day

ACR>30mg/mmol

32
Q

How does the glomerular filtration barrier normally prevent passage of albumin into the urine?

A

Negative charge of endothelial cells repeals anions like albumin
Large diameter too large to pass through the pores of the filtration barrier
Prevents passage of molecules with molecular weight >60,000Daltons

33
Q

Pathological changes seen in the glomerular filtration barrier in diabetes?

A

BM thickening
Glomerulosclerosis
Mesangial cell hypertrophy and increased matrix secretion

34
Q

How does kidney disease lead to hypertension?

A

Reduced GFR –> increased RAAS activation
Increased water and electrolyte retention
Increases SNS activity

35
Q

BP aim for diabetics

A

135/85

36
Q

First line BP lowering drug in diabetics

A

ACEI or ARB

37
Q

Causes of goitre

A

Follicular cell hypertrophy and hyperplasia due to increased TSH levels
Increased colloid accumulation in follicles
Inflammatory processes
Neoplastic processes

38
Q

Main cell type in Hashimoto’s

A

Lymphocytes

39
Q

Effects of thyroid hormones sytsemically

A

Increased BMR and non-shivering thermogenesis
Increased mitochondria number
Increased cardiac myocyte activity

40
Q

Effects of thyroid hormones on the liver

A

Antagonise insulin

Increase gluconeogenesis and glycogen breakdown

41
Q

Effects of thyroid hormones on muscle

A

Act alongside insulin

Increase uptake by increasing GLUT4 translocation

42
Q

Effects of thyroid hormones on adipose tissue?

A

Activate LPL

Increased removal of TAGs from lipoproteins

43
Q

When is ACTH released?

A

Begins at 3am
Peaks upon waking
Decreases throughout the day

44
Q

When is GH released?

A

In pulses

Mostly at night

45
Q

What inhibits PRL secretion?

A

Dopamine

46
Q

What are high PRL levels seen?

A

Pregnancy
Exercise
Stress
Antipsychotic drugs

47
Q

What does high PRL inhibit?

A

Kisspeptin

–> low oestrogen

48
Q

Symptoms of low ACTH

A 
Fatigue 
Weakness
Vomiting 
Abdominal pain 
Low blood sugar 
Low BP 
Weight loss 
Hyper pigmentation
49
Q

Symptoms of low TSH

A 
Tiredness 
Cold intolerance 
Dry skin 
Brittle hair 
Paleness 
Mental slowness
50
Q

Symptoms of low GH

A

Reduced strength and stamina
Reduced ability to exercise
Impaired lipid profile

51
Q

Symptoms of low FSH/LH

A

Loss of periods

52
Q

Symptoms of low oestrogen

A

Low libido

53
Q

Symptoms of tumour mass

A

Headaches

Visual disturbance

54
Q

Metabolic actions of GH

A

Stimulates protein synthesis
Increases gluconeognesis
Increases lipolysis
Increases ketogenesis

55
Q

IGFs

A

Types 1 and 2
Produced mainly by the liver
Some auto/paracrine release in peripheral tissues
Resemble proinsulin in structure
Counteract the diabetogenic effects of GH
Responsible for non-suppressible insulin like activity

56
Q

Metabolic actions of cortisol

A

Stimulate gluconeogensis
Stimulate muscle proteolysis
Stimulate lipolysis
Inhibition of glucose uptake by muscle and adipose tissue

57
Q

Insulin stress test

A

Measures functioning of HPA axis and GH axis
Blood taken
Fast acting insulin given
Blood taken again at 30 minute intervals

58
Q

Treatment

A 
TSS
Hydrocortisone 
Thyroxine 
Sex hormone replacement 
GH replacement
59
Q

Sympathetic detrusor innervation

A

Hypogastric nerve
Inhibitory
Beta 3 receptors

60
Q

Parasympathetic detrusor innervation

A

Pelvic nerves
Excitatory
M3 receptors

61
Q

Internal urethral sphincter innervation

A

Sympathetic
Hypogastric nevre
Alpha 1 receptor

62
Q

External urethral sphincter innervation

A

Somatic
Pudendal nerve
S2-4

63
Q

Tamsulosin

A

Alpha 1 blocker
Relaxes bladder neck and IUS
Eases urination

64
Q

Finasteride

A

5a reductase inhibitor
Reduces testosterone –> DHT
Reduces prostate size

65
Q

Surgical options for BPH

A

TURP
TUIP
Urolift

66
Q

Indications for prostate biopsy

A

High PSA

Abnormal digital rectal exam –> uneven texture

2 - CR/MET (8 decks)

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