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2 - CR/MET > Met physiology > Flashcards

Met physiology Flashcards

1
Q

Toxic sources of acid

A

Methanol poisoning –> formic acid

Ethylene glycol poisoning –> glycol acid, oxalic acid

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2
Q

Death zones of acidity/alkalinity

A

> 8

<6.8

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3
Q

Normal anion gap

A

with K+ = 8-12mEq/L

without K+ = 12-16mEq/L

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4
Q

Causes of normal gap acidosis

A 
Diarrhoea
Laxative abuse 
Fistulas 
NG tube 
Carbonic anhydrase inhibitors 
Renal tubular acidosis 
Ureteric diversion 
Excessive HCl intake
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5
Q

Causes of low anion gap acidosis

A 
Ketoacidosis
Lactic acidosis 
Ethylene glycol poisoning 
Methanol poisoning 
Uraemia 
Isoniazid 
Iron overload 
Salicyclates 
Aspirin 
Paraldehyde
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6
Q

Causes of low gap acidosis

A 
Hypoalbuminaemia 
Haemorrhage 
Nephrotic syndrome
Intestinal obstruction 
Liver cirrhosis
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7
Q

Where is bicarbonate reabsorbed?

A

PCT
70-90%
Via carbonic anhydrase

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8
Q

Types of carbonic anhydrase

A

CA IV = through membrane

CA II = within cell

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9
Q

Which cells function more in acidosis?

A

Alpha intercalated cells

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10
Q

Which cells function more in alkalosis?

A

Beta intercalated cells

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11
Q

How do potassium levels change with acid base balance?

A 
Acidosis = hyperkalaemia 
Alkalosis = hypokalaemia
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12
Q

Features of acromegaly

A 
Acral enlargement 
Sweating 
Menstrual upset 
Headache 
Arthritis 
Carpal tunnel 
Diabetes 
Impotency 
Hypertension 
Visual changes 
Sleep apnoea 
Coronary artery disease
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13
Q

Which cells release GH?

A

Somatotrophs

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14
Q

What inhibits GH release?

A

Somatostatin

IGF-1

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15
Q

How do the adrenal glands develop?

A

From the gonadal ridges
Become invaded by primordial germ cells but gonads split off
Then becomes invaded by neural crest cells (become the medulla)
Becomes surrounded by a layer of mesenchymal cells (becomes the capsule)

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16
Q

Blood supply within the adrenal gland

A

Sub scapular plexus in ZG
Venous sinusoids in ZF
Medullary plexus in ZR and medulla

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17
Q

Steroidogenic pathway

A

Cholesterol –> pregnenolone –> steroids

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18
Q

What enzyme inactivates cortisol in the kidney? Why does it do this?

A

11bHSD-2
Converts it to cortisone
Prevents excessive activation of the mineralocorticoid receptor

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19
Q

Causes of primary hyperaldosteronism?

A

Conn’s syndrome
Adrenal adenoma
Bilateral adrenal hyperplasia

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20
Q

Glucocorticoid remediable aldosteronism

A

Promotor regions for CYP11B2 and CYP11B1 get switched around
Causes ACTH release to stimulate aldosterone release
Treatment with glucocorticoid drugs to suppress ACTH

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21
Q

Symptom of apparent mineralocorticoid excess

A

Inhibition of 11b-HSD2
Allows cortisol to activate the mineralocorticoid receptor
E.g. liquorice consumption

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22
Q

Features of Liddle syndrome

A 
Low renin 
Low aldosterone 
Hypertension 
Metabolic alkalosis 
Hypokalaemia
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23
Q

HPA axis

A

CRH –> ACTH –> cortisol
Cortisol inhibits CRH and ACTH
ACTH inhibits CRH
ACTH inhibits itself

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24
Q

What else stimulates the HPA axis?

A

CRH stimulated by stress, catecholamines, AgII and ghrelin

ACTH stimulated by AgII, IL-1, IL-2, IL-6

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25
Q

What else inhibits the HPA axis?

A

CRH inhibits by ANP, opioids and oxytocin

ACTH inhibited by CRIF

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26
Q

Causes of Cushing’s syndrome

A 
Iatrogenic (too much drug) 
Pituitary adenoma 
Ectopic ACTH tumour (commonly lung) 
Adrenal adenoma 
Bilateral adrenal hyperplasia
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27
Q

Features of Cushing’s syndrome

A 
Hypertension 
Hyperglycaemia 
Moon face
Thin skin 
Proximal myopathy 
Osteoporosis 
Ulcers
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28
Q

Features of Addison’s disease

A 
Fatigue 
Myalgia 
Anorexia 
Weight loss 
Hyper pigmentation
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29
Q

Features of Addisonian crisis

A

Low BP
Low glucose
Low Na
High K

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30
Q

Addison’s disease replacement steroids

A 
Hydrocortisone = cortisol 
Fludrocortisone = aldosterone
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31
Q

Congenital adrenal hyperplasia

A

Due to 21-hydroxylase deficiency
Cannot produce GCs or MCs from pregenonlone
Instead produces large amounts of androgens
–> salt loss, virilisation, adrenal hyperplasia

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32
Q

Noradrenaline synthesis pathway

A

L-tyrosine –> L-dopa –> dopamine –> noradrenaline –> adrenaline

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33
Q

Noradrenaline vs adrenaline effects

A

Noradrenaline more with BP control

Adrenaline more with glucose control

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34
Q

Where are chromaffin cells found/

A

Adrenal medulla
Sympathetic chain
Organ of Zuckerkandl
Bladder wall

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35
Q

Symptoms of catecholamine excess

A 
Hypertension 
Hyperglycaemia 
Tachycardia 
Dyspnoea 
Diaphoresis 
Weight loss
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36
Q

How are catecholamines inactivated?

A

By COMT = catechol-O-methyltransferase

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37
Q

What is a phaeochromocytoma?

A

Tumour of the chromatin cells of the adrenal medulla

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38
Q

Treatment for phaeochromocytoma

A 
Alpha blockers 
Beta blockers 
MUST HAVE BOTH 
Avoid opiates 
Surgical resection
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39
Q

How much calcium is protein bound?

A

Around 50%

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40
Q

What happens to calcium levels in acid-base changes?

A 
Acidosis = more ionised 
Alkalosis = less ionised
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41
Q

Where do the parathyroid glands originate from?

A

3rd and 4th pharyngeal pouches

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42
Q

Cell types in parathyroid gland

A

Chief cells

Oxyphil cells

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43
Q

How is PTH made?

A

PreproPTH
–> proPTH by RER
–> PTH by Golgi
Releases in vesicles

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44
Q

How does the CASR work?

A 
GPCR
Calcium binding activates PLC 
Inhibits cAMP signalling 
Reduces PTH secretion and transcription 
Increases breakdown of stored PTH
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45
Q

Other regulators of PTH release?

A

Supressed by activated vitamin D
Stimulated by phosphate
Inhibited by cinacalcet

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46
Q

Actions of PTH

A

Decreases kidney calcium excretion
Increases kidney phosphate excretion
Increases bone calcium and phosphate resorption
Increases intestinal calcium and phosphate absorption
Vitamin D activation
PCT gluconeogenesis

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47
Q

How is calcium absorbed in the kidney?

A

65% in PCT by voltage gradient
20% in LoH by voltage gradient
10% in DTC by PTH control

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48
Q

PTH action on the bone

A

Stimulate RANKL production

Dow regulate OPG (inhibits osteoclasts)

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49
Q

What stimulates vitamin D activation?

A

PTH

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50
Q

What inhibits vitamin D activation?

A

High calcium
High phosphate
FGF23
High 1,25(OH)2 D

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51
Q

Vitamin D2 vs D3

A 
D2 = ergocalciferol from vegetables 
D3 = cholecalciferol from meat
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52
Q

Inactive forms of vitamin D

A

1, 24, 25

24, 25

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53
Q

Effects on vitamin D receptor activation

A

Increased gut reabsorption of calcium and phosphate
Reduced PTH transcription
Increased bone resorption - increases RANKL
Increased FGF23 release to promote renal phosphate loss
Increased amino acid uptake

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54
Q

FGF23 function

A

Increases renal phosphate excretion

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55
Q

Symptoms of hypercalcaemia

A

Polyuria and polydipsia
Kidney stones
Osteoporosis
Mood disorder

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56
Q

Primary vs secondary vs tertiary

A 
Primary = absence of hypocalcaemia 
Secondary = compensation for hypercalcaemia 
Tertiary = autonomous PTH following chronic secondary
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57
Q

Symptoms of hypocalcaemia

A

Convulsions
Arrhythmias
Tetany
Parasthesia

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58
Q

Treatment of hypoparathyroidism

A

PTH infusion
Calcium supplmenets
Alfacalcidiol

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59
Q

What is mutated in familial hypocalciuric hypocalcaemia?

A

CASR receptor

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60
Q

Causes of respiratory acidosis

A

CNS depression
Chest wall abnormalities
NM disease
Lung disease –> COPD, severe asthma

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61
Q

Causes of metabolic alkalosis

A 
Diuretics (Cl- loss) 
Vomiting 
Hyperaldosteronism 
Liquorice 
Barter's/Liddle/Gitelman's 
Milk alkali syndrome 
Bicarbonate therapy 
Dialysis
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62
Q

Causes of metabolic alkalosis

A 
Anxiety, pain 
CVA 
Fever and sepsis 
Pregnancy 
Altitude 
Asthma, PE, pneumonia 
Salicyclates, progesterone
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63
Q

Levels of cortisol in the day

A 
Morning = 150-500
Evening = 25-125 
Stress = 650-2500
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64
Q

Genomic effects of GCs

A

Trans-activation
Binds to GC response elements
Stimulates/inhibits transcription

Transrepression
Blocks actions of cytokines/prostinoids/mitogens
Blocks transcription of target genes

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65
Q

Where does the pituitary develop from?

A

Oral ectoderm

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66
Q

What does somatostatin inhibit?

A

GH and TSH

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67
Q

What inhibits and stimulates PRL?

A 
Stimulates = dopamine 
Inhibits = TRH
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68
Q

What stimulates ACTH?

A

CRH, AVP

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69
Q

What stimulated GnRH?

A

Kisspeptin

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70
Q

GHRH receptor mutation

A 
Mosaic = McCune-Albright syndrome 
Germline = death
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71
Q

ACTH independant Cushing’s syndrome

A

= low ACTH
Steroid therapy
Adrenal tumour
Adrenal hyperplasia

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72
Q

ACTH dependant Cushing’s syndrome

A

Pituitary tumour

ACTH secreting lung tumour

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73
Q

Congenital hyperbilirubinaemia

A

= Gilbert’s disease

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74
Q

Types of viral hepatitis

A

A and E = acute
B and C = chronic
D only occurs with B

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75
Q

Nodule size in cirrhosis

A 
Macro = autoimmune 
Micro = alcohol
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76
Q

Alcohol metabolic pathway

A 
Ethanol to acetaldehyde
--> alcohol dehydrogenase in the cytoplasm 
--> MEOS in microsomes 
--> catalase in peroxisomes 
Acetaldehyde --> acetate
--> aldehyde dehydorgnase 
--> NAD --> NADH
Large amounts of NADH promote fatty acid synthesis --> steatosis
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77
Q

Hepatitis C treatment

A

PegInterverfon + ribacvarin
+ protease inhibitors
Transplant

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78
Q

Hepatits B treatment

A

Entecavir

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79
Q

Drugs causing cirrhosis

A

Amiodarone

Methotrexate

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80
Q

What cytokine is involved in cirrhosis?

A

TGFb

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81
Q

Contraindications for liver transplant

A

Active sepsis
Malignancy outside the liver
Non-Ccompliance with drugs
Severe CR problems

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82
Q

Bladder afferent nerves

A

Pelvic nerves

–> pontine micrurition centre

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83
Q

Parasympathetic nerves –> bladder

A

S2-4 pelvic splanchnic nerves

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84
Q

Sympathetic nerves –> bladder

A

Hypogastric plexus

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85
Q

Somatic nerves –> bladder and sphincter

A

S2-4 pudendal nerve

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86
Q

M receptors on bladder

A

M3

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87
Q

Beta receptors on bladder

A

Beta 3

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88
Q

Alpha receptors on sphincter

A

Alpha 1

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89
Q

Storage symptoms

A

Increased frequency
Nocturne
Urgency
Incontinence

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90
Q

Voiding symptoms

A 
Hesitancy 
Straining 
Poor flow 
Intermittent flow 
Incomplete emptying 
Terminal dribbling 
Dysuria 
Haematuria
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91
Q

Outflow problems

A

Bladder neck obstruction
Stricture
Meatus problem
Foreskin problem

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92
Q

Pump problems

A

Bladder failure
OAB
Cardiac failure
Medications

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93
Q

Control problems

A 
Stroke
Spinal cord injury 
Parkinson's 
MS 
Tumour
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94
Q

Constituent problems

A

UTI
Cancer
Inflammation
Stones

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95
Q

BPH drugs

A 
Alpha blockers (tamsulosin, doxazosin) 
5 alpha reductase inhibitors (finasteride)
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96
Q

OAB drugs

A

Anticholinergics (oxybutynin, solifenacin) –> reduce bladder contractility
B3 agonist (mirabegron) –> increases bladder capacity
Botox –> prevents contraction

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97
Q

Neurogenic bladder

A

Above pons = safe
Below T12 = safe –> flaccid bladder
Lesions between are unsafe –> loss of sympathetic relaxation –> spastic bladder

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98
Q

Acute renal failure causes

A 
Sepsis 
Hypo perfusion 
Toxicity 
Obstruction 
Primary renal disease
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99
Q

Consequences of acute renal failure

A

Increased retention of salt, water, electrolytes
Acidosis
Toxins

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100
Q

Presentation of acute renal failure

A 
Acutely unwell 
Hypertensive 
Oliguric 
Acute urine on dipstick 
Normal sized kidneys
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101
Q

Systemic manifestations of acute kidney failure

A 
Pulmonary oedema 
Hyperkalaemia --> arrhythmia 
Acidosis 
Uraemia 
Encephalopathy 
Pericarditis 
Effusions
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102
Q

Common causes of chronic renal failure

A

Hypertension
Diabetes
Polycystic kidneys
GN

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103
Q

CKD staging

A 
1 = GFR >90 
2 = GFR 60-90
3 = GRR 30-60
4 = GFR 15-30
5 = GFR <15
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104
Q

When is haemodialysis performed?

A

3x per week

For 4 hours

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105
Q

Complications of haemodialysis

A

Thrombosis
Infection at access site
Lack of access
Hypotension

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106
Q

Advantages of haemodialysis

A

Hospital or home based

Less time than CAPD

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107
Q

Disadvantages of haemodialysis

A

Requires access to circulation

Limited by staff and space

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108
Q

When is CAPD performed?

A

Four daily exchanges

0.5h for each exchange

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109
Q

Principles of CAPD

A 
Fluid pumped into abdominal cavity 
Peritoneum acts as exchange membrane 
Contains high amounts of glucose 
Can also contain buffers and amino acids 
Fluid equalises in concentrations 
Can then be drained and replaced
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110
Q

Advantages of CAPD

A

Can be done at home

Less CV demanding

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111
Q

Disadvantages of CAPD

A

Patient competence
Risk of membrane failure
Abnormal glycosylation

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112
Q

Creatinine vs GFR

A

In early kidney disease, large GFR drops will have a low impact on creatinine levels
In late kidney disease small drops in GFR can cause large increases in creatinine

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113
Q

Caveats of using creatinine

A

Product from muscle so depends on persons muscularity

Drugs such as trimethoprim inhibit tubular secretion

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114
Q

Glucose absorption threshold

A

10mmol/L

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115
Q

NIS function

A

Sodium and iodine into follicular cell

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116
Q

Pendrin function

A

Iodine from cell –> colloid

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117
Q

TPO function

A

Iodine oxidation

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118
Q

DUOX1 and 2 function

A

Oxidising agents

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119
Q

IYD function

A

Recycles iodine

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120
Q

How does TSH lead to thyroid hormone synthesis?

A

Binds to TSHR
Acts via cAMP cascade
Upregulation of all the components in thyroid hormone synthesis

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121
Q

D1 enzyme

A

Found peripherally

Upregulated by hyperthyroidism

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122
Q

D2 enzyme

A

Found in brain and pituitary
Down regulated in hyperthyroidism
Up regulated in hypothyroidism

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123
Q

D3 enzyme

A

Deactivation of thyroid hormones
T4 –> rT3
T3 –> T2

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124
Q

How is T4 excreted?

A

Glucoronidation by the liver

Gut excretion

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125
Q

How does T3 alter gene transcription?

A

Binds to thyroid hormone receptor in nucleus
Releases homodimer
Binds retinoic acid and co-activation molecule
Binds to thyroid response elements
Stimulates or inhibits gene transcription

126
Q

Features of hyperthyroid

A 
Tachycardia 
Increased risk of AF 
Increased BMR 
Increased appetite 
Heat intolerance 
Weight loss 
Myopathy 
Hyperglycaemia 
Seizures 
Proptosis 
Pretibila myxoedema 
Osteoporosis 
Hypercalcaemia 
Amenorrhoea 
Gynaecomastia
127
Q

Causes of hyperthyroidism

A 
Grave's disease
Toxic multi nodular goitre 
Toxic adenoma 
Excess iodine 
Amiodarine 
HCG 
Stroma ovarii
TSHoma 
Hamburger thyrotoxicosis
128
Q

Treatment of hyperthyroidism

A

Thionamide drugs –> carbomaxole, propylthiouracil
Radioactive iodine
Thyroidectomy

129
Q

Features of hypothyroidism

A 
Pale and dry skin 
Hair and eyebrows loss 
Hypercarotenaemia
Bradycardia 
Hypothermic J waves 
Sensitivity to cold 
Reduced appetite 
Weight gain 
Constipation 
Slowed relaxing reflexes 
Growth retardation 
Delayed puberty 
Decreased GLUT4 stimulation
130
Q

Causes of hypothyroidism

A 
Hashimoto's disease
Iodine deficeincy 
Lithium 
Cabbage 
Infiltrative disease
Pendred's disease
Hypopituitarism
131
Q

Hypothyroidism treatment

A

Levothyroxine

132
Q

When does hyper acute rejection occur?

A

Immediately after the transplant
When there are pre-existing antibodies present in the blood
May be ABO incompatibility
Type II hypersensitivity

133
Q

When does acute rejection occur?

A 
One week - 6 months after transplant 
Due to helper T cell activation 
May be due to MHC incompatibility 
May be cellular or antibody mediated 
Type IV hypersensitivity
134
Q

When does chronic infection occur?

A

Months to years after transplant

Due to immunological and non-immunological factors

135
Q

Characteristics of hyperacute rejection

A

Neutrophil invasion
Intravascular coagulation
Intra-tissue haemorrhage

136
Q

Characteristics of acute rejection

A

Cell mediated
Infiltration of lymphocytes
Macrophage activation

Antibodies mediated
–> endarteritis
C4d production

137
Q

Important complement protein in rejection

A

C4d

138
Q

Reasons for chronic rejection

A 
Damaged graft 
Surgical complications 
Recurrence of original disease
Infection 
Inadequate immunosuppression
139
Q

Immunosuppression drugs

A

Block TCR = alemtuzumab
Blocks transcription factor production = calcineurin inhibitors (tacrolimus, cyclosporin)
Inhibits gene transcription = corticosteroids
Anti-IL2 receptor antibodies = basiliximab
Prevents B/T cell activation = rapamycin (sirolimus), everolimus
Prevent T cell proliferation = azathiprone, MMF

140
Q

Most important HLAs to match

A

A, B, DR

141
Q

Preventing transplant rejection

A

Hyper acute –> ABO matching and direct cross match
Acute –> HLA matching and minimising ischaemia
Chronic –> best quality organ, minimising surgical damage, minimise drug toxicity

142
Q

Complications of transplant

A 
Viral infection --> CMV, warts
Bacterial infection --> UTI, RTI
Protozoa --> pneumocystis 
Cardiovascular disease 
Diabetes 
Osteoporosis 
Cushing's syndrome 
Tumours --> skin, solid organ, PTLD
143
Q

Option for non-compatible transplants

A

Plasma exchange
IV immunoglobulins
Organ exchange scheme

144
Q

Advantages of live donation

A

Donor can be screened for organ function
Shorter cold ischaemia time
Elective procedure

145
Q

Order of kidney connection

A

Vein
Artery
Ureter

146
Q

How do the 3 germ layer contribute to the gut?

A 
Endoderm = mucosa, mucosal glands, submucosal glands 
Mesoderm = lamina propria, muscularis, submucosa, blood vessels, adventita/serosa
Ectoderm = neurones and enteric nervous system
147
Q

Foregut

A

–> upper duodenum

Supplied by coeliac trunk

148
Q

Midgut

A

Upper duodenum –> proximal 2/3 of transverse colon

Supplied by SMA

149
Q

Hindgut

A

Distal 1/3 of traverse colon –> anal aperture

Supplied by IMA

150
Q

Imperforate anus

A

Failure of endodermal and ectodermal portions o the anal canal to communicate

151
Q

Rectoanal atresia

A

Failure of recanalisation or defective blood supply

152
Q

Persistent cloaca

A

Urethra, vagina and anus all open out into one cavity

153
Q

Hirschsprung’s disease

A

Absence of parasympatehctsi ganglia in the bowel walls
Derived from neural crest cells
Signs = failure to pass meconium, swollen belly, vomiting bile

154
Q

Puborectalis

A

Forms a sling around the and-rectal junction to form the anorectal angle

155
Q

Internal anal sphincter innervation

A 
Sympathetic = excitatory = hypogastric nerve L1-2
Parasympathetic = inhibitory = pelvic nerves (S2-4)
156
Q

External anal sphincter innervation

A

Inferior rectal brach of the pudendal nerve

157
Q

How if faecal continence maintained?

A

Tonic contraction of both anal sphincters

Puborectalis (and EAS) muscle creating anorectal angle

158
Q

How does the puborectalis create a flap valve?

A

Pushes the anterior rectal wall downwards onto the anal canal

159
Q

What structures on the sigmoid colon and rectal walls also help with continence?

A

Valves of Houston

Lateral angulations

160
Q

Valsalva manoeuvre

A

Holding breath and forcibly exhaling against a closed glottis to create a pushing down effect

161
Q

What stimulates the closure reflex?

A

Receptor adaption removed from rectus so inhibitory drive on IAS releases –> IAS contracts
Voluntary contraction of EAS
Smooth muscle in sigmoid colono realces –> reservoir function returns

162
Q

What drugs commonly cause constipation?

A

Opiates, anticholinergics, anticonvulsants, antidepressants

163
Q

What endocrine conditions can cause constipation?

A

Diabetes, hypothyroidism

164
Q

Passive vs urge incontinence

A 
Passive = internal sphincter problem
Urge = external sphincter problem
165
Q

Causes of anal structural damage

A

Obstetric tear
Iatrogenic tear
Radiation damage
Congenital defects

166
Q

Hypersensitive rectal sensation

A

Urge incontinence

167
Q

Hyposensitive rectal sensation

A

Evacuation difficulties, functional disorders, constipation

168
Q

Orexigenic signals

A

SPY
AgRP
MHC

169
Q

Where are oriexigenic centres found?

A

Medially

170
Q

Anorexigenic signals

A

POMC

CART

171
Q

Where are anorexigenic signals found?

A

Laterally

172
Q

How does AgRP act?

A

As a melanocortin receptor antagonist

173
Q

What is POMC converted to?

A

Alpha-MSH

174
Q

How does serotonin act to control appetite?

A

Increases POMC signalling via HTr2c

Decreases AgRP signalling via HTr1b

175
Q

Action of ghrelin on appetite

A

Stimulates NPY neurones

176
Q

Where are PYY GLP1 released from?

A

Intestinal L cells

177
Q

What is the action of GLP-1 and PYY?

A

Inhibit NPY signalling

Increased POMC signalling

178
Q

Where is CCK produced?

A

Duodenal I cells

179
Q

What is the action of CCK?

A

Increases POMC signalling
Inhibits NPY signalling
Also causes bile release from the gallbladder

180
Q

Where is leptin produced?

A

Adipose tissue

181
Q

How does leptin affect appetite?

A

Increases POMC signalling

Decreases NPY and AgRP signalling

182
Q

Effect of insulin of AgRP levels

A

Decreases them

183
Q

Leptin mutations

A

Defective leptin = ob

Defective receptor = db

184
Q

When is malonyl CoA produced?

A

Produced when high levels of ATP are present

High levels suggest adequate energy supply

185
Q

Effect of high malonyl CoA

A

Inhibits carnitine shuttle to inhibit fatty acid oxidation

Suppresses food intake by inhibiting NPY and stimulating POMC

186
Q

Therapies to reduce appetite

A 
GLP-1 agonists 
Leptin 
Cannabinoid antagonists 
SSRI derivatives 
Amphetamine derivatvies
187
Q

PYY receptor

A

Y2R

188
Q

Melanocortin receptor

A

MCR4

189
Q

Metabolic syndrome

A

Insulin resistance
Hypertension
Dyslipidaemia
Abdominal obesity

190
Q

What is arachidonic acid produced from?

A

Omega 6

191
Q

What does arachidonic acid produce?

A

Inflammatory mediators

Prostaglandins, leukotrienes

192
Q

What is omega 3 metabolised to?

A

Anti-inflammatory molecules such as resolvins and protectins

193
Q

Action of aspirin

A

Enhances the production of anti-inflammatory mediators from omega 3

194
Q

Where are flavonoids found?

A

Fruit and veg, tea, chocolate, wine, olive oil

195
Q

Action of flavonoids

A

Inhibits NADPH oxidase that produces ROS

Decreases risk of MI and stroke

196
Q

Where are sulforaphanes found?

A

In Brassica vegetables

197
Q

Consequences of low B12 and folate

A

Low methionine and high homocysteine

198
Q

Effects of high homocysteine

A

–> thiolactate

Damages endothelial cells

199
Q

Fat soluble vitamins

A

A, D, E, K

200
Q

Which vitamins can be stored?

A

Fat soluble

Not water soluble

201
Q

Which vitamins can be toxic in excess?

A

Fat soluble

Not water soluble

202
Q

Selenium deficiency

A

–> cardiomyopathy

203
Q

Zinc deficiency

A

Growth retardation
Alopecia
Dermatitis

204
Q

Copper deficiency

A

Defective keratinisation of hair

205
Q

Vitamin A deficiency

A

Xerophthalmia

206
Q

Vitamin D deficiency

A

Rickets

Osteomalacia

207
Q

Vitamin E deficiency

A

Peripheral neuropathy

208
Q

Vitamin K deficiency

A

Coagulopathy

209
Q

Vitamin C deficiency

A

Scurvy

210
Q

Vitamin B1 thiamine deficiency

A

Beri Beri
Wernicke’s encephalopathy
Korsakoff syndrome

211
Q

Vitamin B2 riboflavin deficiency

A

Angular stomatitis

212
Q

Vitamin B3 niacin deficiency

A

Pellagra

213
Q

Vitamin B6 pyridoxine deficiency

A

Neuropathy

Anaemia

214
Q

Causes of vitamin D deficiency

A 
Reduced sunlight exposure
Obesity, smoking, alcohol
Malabsorption 
Hyperparathyroidism 
Breast feeding 
Drugs
215
Q

Role of vitamin B1

A

TTP cofactor for pyruvate –> acetyl CoA

216
Q

Features of Beri Beri

A

Dry –> peripheral neuropathy
Shoshin –> cardiac failure and lactic acidosis
Wet –> cardiomegaly, tachycardia, peripheral oedema

217
Q

Features of Wernicke’s encephalopathy

A

Horizontal nystagmus
Ophthalmoplegia
Cerebellar ataxia

218
Q

Features of Korsakoff’s syndrome

A

Amnesia

Psychosis

219
Q

Features of pellagra

A 
Loss of appetite 
Weakness 
Abdominal pain 
Glossitis 
Casals neck 
Vaginitis 
Dermatitis 
Diarrhoea 
Dementia
220
Q

Causes of B12 deficiency

A

Veganism
Terminal ileum disorder
Inadequate IF

221
Q

Consequences of haemochromatotiss

A

Bronzed skin
Cirrhosis
Diabetes
Cardiomyopathy

222
Q

MUST assessment

A

BMI
Recent weight loss
Acute disease effects

223
Q

Surrogate height measures

A

Knee height
Ulna length
Demispan

224
Q

Surrogate weight measure

A

Mid upper arm circumference

225
Q

Ascites weight estimation

A

14kg
6kg
2kg

226
Q

Peripheral oedema weight estimation

A 
Sacrum = 10kg
Knee = 5kg 
Ankle = 1kg
227
Q

Normal albumin level

A

35-50g/L

228
Q

Consequences of feeding syndrome

A 
Seizures 
Rhabdomyolysis 
Osteomalacia 
Cardiac failure 
Arrhythmias 
Tetany 
Paraesthesia
229
Q

Indications for parenteral nutrition

A 
Short bowel 
Ileus 
Motility disorder
Ischaemia
Perforation 
Pancreatitis
Obstruction 
Fistulae 
Severe IBD
230
Q

Problems with PN

A 
Risk with placement
Catheter related sepsis 
Disordered liver function 
Gut atrophy
Psychological Cost
231
Q

Indications for tube feeding

A

Unsafe swallow
Head and neck cancer
Cystic fibrosis

232
Q

Obesogenic drugs

A 
Corticosteroids
Mood stabilsiers 
Diabetes medications 
Beta blockers 
Allergy relievers 
Anti-epileptics
233
Q

Which diabetes drugs cause weight change?

A 
Gain = insulin, sulfonylureas, TZDs
Stable = metformin, DPP4 inhibitors 
Loss = SGLT-2 inhibitors, acarbose
234
Q

What does the thrift gene hypothesis state?

A

Genes that predispose to obesity have a selective advantage in populations frequently experiencing starvation

235
Q

Autosomal dominant syndormes –> obesity

A

Prader Willi

Fragile X

236
Q

Autosomal recessive syndormes –> obesity

A

Bardet-Biedl
Alstom
= ciliopathies

237
Q

X linked syndromes –> obesity

A

Wilson-Turner

Borjeson-Forssman-Lehmann

238
Q

Orlistat

A

Gastric and pancreatic lipase inhibitor

239
Q

Lorcaserin

A

5HT antagonist

240
Q

Liraglutide

A

GLP-1 agonist

241
Q

Phentermine

A

Noradrenaline transporter inhibitor

242
Q

Topiramate

A

GABA agonist

243
Q

Naltrexone

A

Opioid receptor antagonist

244
Q

Bupropion

A

Noradrenaline transporter inhibitor

245
Q

Restrictive procedures

A

Gastric banding

Sleeve gastroplasty

246
Q

Malabsorptive procedures

A

Biliopancreatic diversion

Gastric bypass

247
Q

Normal fasting glucose levels

A

3.5-5.5mmol/L

248
Q

Normal glucose levels 2 hours after a meal

A

<8mmol/L

249
Q

Why is the brain dependant on glucose?

A

Cannot synthesis glucose
Cannot store it in large amounts
Cannot use other substrates except for ketones
Cannot extract glucose from the ECF at low concentrations

250
Q

Cells in the pancreatic islets

A 
Alpha cells --> glucagon 
Beta cells --> insulin 
Delta cells --> somatostatin 
PP (F) cells --> pancreatic polypeptide 
Epsilon cells --> ghrelin
251
Q

Insulin synthesis

A

Preproinsulin

  • -> proinsulin by ER
  • -> insulin by Golgi
252
Q

Insulin amino acid lengths

A

Preproinsulin = 110
Proinsulin = 86
Insulin = 21+30
C peptide = 35

253
Q

How is insulin released from vesicles?

A

Enters through GLUT1 channels
Glucokinase converts glucose –> acetyl CoA –> ATP
Rise in ATP:ADP ratio closes K+ channels
–> membrane depolasrisaion
–> calcium influx
Triggers vesicles to bind to membrane and release insulin
Occurs when glucose >5mmol/L

254
Q

Other signals causing insulin release

A 
Arginine and leucine 
GLP-1 and GIP 
Fatty acids 
CCK 
Phospholipase C 
Acetylcholine
255
Q

How does GLP1 act?

A

Through GLP-1R receptors

GCPR

256
Q

How do leucine and arginine increase insulin secretion?

A

Act through glutamate dehydrogenase (GDH)

Can directly depolarise the membrane

257
Q

How does phospholipase C lead to insulin secretion?

A

Cleaves PIP3 –> IP3

IP3 binds to SER and causes calcium release

258
Q

Insulin receptor type

A

Tyrosine kinase receptor

259
Q

Action of insulin binding to its receptor

A

Insulin binds to alpha portion
Tyrosine kinase domain in beta subunit phsophaorlyaes tyrosine residues on the C-terminus of the receptor for auto regulation
Also phosphorylates tyrosine resides on IRS
Leads to the activation of Akt

260
Q

Actions of Akt

A

GLUT4 translocation in muscle and adipose tissue
Stimulation of muscle glycogen synthesis
Inhibit of lipolysis

261
Q

How does Akt stimulate glycogen synthesis?

A

Akt phosphorylates and inactviates glycogen synthase kinase that usually inactviates glycogen synthase

262
Q

How does insulin inhibit lipolysis?

A

Inhibits hormone sensitive lipase
Inhibits TAG hydrolysis and release of FAs into the circulation
Inhibits CPT-1

263
Q

Action of insulin on the liver

A

Enhances glucose uptake and glucokinase activity
Increases glycogen synthesis
Increases lipogenesis
Inhibits gluconeogenesis

264
Q

Action of insulin on proteins

A

Stimulates amino acid uptake into cells
Increases translate of mRNAs
Inhibits catabolism of proteins
Inhibits gluconeogenesis (uses proteins)

265
Q

Post-prandial metabolism

A

Insulin levels rise
Increased uptake and TAG and glycogen synthesis
Increased liver uptake and storage of glucose
Inhibition of gluconeogenesis, glycogenolysis and lipolysis

266
Q

Metabolism during fasting

A 
Low insulin levels
Less tissue glucose uptake  
Glycogen breakdown 
Lipolysis releases FFAs
Gluconeogenesis proceeds in the liver 
Lactate used in Cori cycle
267
Q

Insulin resistance

A

Serine and threonine residues phosphorylated on IRS instead of tyrosine
Act cannot be activated
Reduced insulin action
–> hyperglycaemia and dyslipidaemia

268
Q

How is insulin switched off?

A

Serine/threonine kinases
Endocytosis and degradation of receptor
Dephosphorylation of tyrosine residues

269
Q

How many amino acids in glucagon?

A

29

270
Q

Synthetic pathway of glucagon

A

Preproglucagon

  • -> proglucagon
  • -> glucagon, GLP-1, GLP-2
271
Q

Regulation of glucagon secretion

A

Low blood glucose levels
Increased blood amino acids (alanine and arginine)
Exercise
Inhibited by insulin and somatostatin

272
Q

Mechanism of action of glucagon

A

Binds to GPCR
Alpha subunit detaches and activates adenylyl cyclase
ATP –> cAMP
Activates PKA

273
Q

What does PKA activate?

A

PEPCK
G-6-P
Glycogen phosphorylase

274
Q

How does glucagon inhibit glycolysis?

A

Inhibits PFK-1 by modulation of F-2,6-P2 levels

Inhibits pyruvate kinase

275
Q

How does glucagon increase lipolysis?

A

Activates hormone sensitive lipase

Activates CPT-1

276
Q

When are catecholamines releases?

A

In response to stress and hypoglycaemia

277
Q

What amino acid is used in catecholamine synthesis?

A

Tyrosine and phenylalanine

278
Q

Metabolic actions of adrenaline

A

Inhibits insulin secretion
Stimulates glucagon secretion
Stimulates glycogen breakdown
Stimulates lipolysis

279
Q

Metabolic actions of cortisol

A

Inhibits glucose uptake
Stimulates lipolysis
Stimulates muscle proteolysis
Stimulates gluconeogenesis

280
Q

When is cortisol released?

A 
Trauma 
Infection 
Intense heat or cold 
Surgery 
Any debilitating disease
281
Q

Metabolic actions of growth hormone

A

Reduced glucose uptake
Increases lipolysis
Increases glycogen breakdown
Increases gluconeogenesis

282
Q

Metabolic actions of thyroid hormones

A 
Increase the number of mitochondria 
Increase insulin secretion 
Increase glucose uptake 
Increase glycolysis and gluconeogenesis 
Increase lipolysis 
--> increase BMR
283
Q

Metabolic actions of incretins

A

Increase insulin secretion
Inhibit gluconeogenesis
Promote satiety

284
Q

Mechanisms of insulin resistance

A

Diacylglycerol induced activation of protein kinase C

Pro-Inflammatory cytokines releases

285
Q

Normal mechanisms of islet compensation

A

Increase in size and number of beta cells

Increased beta cell function

286
Q

Beta cell adaption to insulin resistance

A

Increased GK activity
Increased malonyl CoA levels –> inhibition of CPT-1
Fatty acids binding to gRP40
GLP-1 binding to its receptor
Release of acetyl choline from parasympathetic nerve terminals

287
Q

Diagnosis of diabetes

A

Random blood glucose >11
Fasting blood glucose >7
Symptoms of hyperglycaemia

288
Q

HbA1c level for diabetes diagnosis

A

48mmol/mol

6.5%

289
Q

Biguanides

A 
Metformin 
Inhibit hepatic gluconeogensis
Reduce FA synthesis 
Increase GLP-1 levels 
Increase GLUT4 translocation
290
Q

Sulfonylureas

A

Glicazide
Increase insulin secretion
Inhibit K+ channels –> depolarisation

291
Q

Metglitinides

A

Repaglinine
Increase insulin secretion
Inhibit K+ channels –> depolarisation

292
Q

TZDs

A

Pioglitozone
Increase insulin sensitivity
Increase adipose storage of FFAs

293
Q

GLP-1 agonists

A

Exanatide
Increase insulin secretion
inhibit gluconeogenesis

294
Q

DPP-4 inhibitors

A

Sitagliptin
Increase insulin secretion
inhibit gluconeogenesis

295
Q

SGLT2 inhibitors

A

Decrease kidney reabsorption of glucose

296
Q

Alpha-glucosidase inhibitors

A

Acarbose

Decrease gut absorption of glucose

297
Q

How does ketoacidosis arise?

A

Continual use of fatty acids for energy production leads to ketone body formation

298
Q

Ketone bodes

A

Acetoacetate

b-hydroxybutarate

299
Q

Treatment of ketoacidosis

A

Fluids
Electrolytes
Insulin

300
Q

Hypoglycaemia Whipple triad

A

Low blood glucose
Symptoms and signs associated with low blood glucose
Resolution of signs and symptoms with carbohydrate ingestion

301
Q

Causes of hypoglycaemia

A 
Alcohol excess
Insulinoma 
Excessive exercise 
Reactive hypoglycaemia 
High dose insulin in T1DM
302
Q

Responses to hypoglycaemia

A

Decreased insulin secretion
Increased glucagon and adrenaline release
Carbohydrate ingestion

303
Q

Prolonged hypoglycaemia

A

GH and cortisol are released

304
Q

Symptoms of hypoglycaemia

A 
Trembling 
Palpitations 
Sweating 
Anxiety 
Tingling 
Difficulty concentrating 
Confusion 
Weakness 
Drowsiness 
Vision changes 
Difficulty speaking 
Dizziness 
Fitting 
Loss of consciousness
305
Q

How does hyperglycaemia cause damage?

A 
Activates protein kinase C 
Increases inflammation
Increases ROS production 
Increases endothelial permeability and occlusion 
Causes mitochondrial dysfunction
306
Q

Non-proliferative diabetic retinopathy

A

Dilation of retinal veins
Micro aneurysms
Internal haemorrhaging and oedema

307
Q

Proliferative diabetic retinopathy

A

New blood vessels from near optic disk and in the vitreous humour
These can rupture and bleed
Can lead to detachment of the retina

308
Q

Diabetic nephropathy features

A

Proteinuria
Glomerular hypertrophy
Decreased GFR
Renal fibrosis

309
Q

Sites of diabetic neuropathy

A

Peripheral nerves –> hands, feet, legs, arms
Autonomic nerves –> digestion, bladder control, erectile dysfunction, heart
Proximal –> thighs and hips
Focal –> any nerve in the body

310
Q

How does diabetes lead to atherosclerosis?

A

AGE formation
Oxidised LDL receptor to increase LDL uptake
Pro-Inflammatory cytokine production
Impaired cholesterol efflux from plaques

2 - CR/MET (8 decks)

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