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Met physiology Flashcards

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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
What else inhibits the HPA axis?
CRH inhibits by ANP, opioids and oxytocin | ACTH inhibited by CRIF
26
Causes of Cushing's syndrome
``` Iatrogenic (too much drug) Pituitary adenoma Ectopic ACTH tumour (commonly lung) Adrenal adenoma Bilateral adrenal hyperplasia ```
27
Features of Cushing's syndrome
``` Hypertension Hyperglycaemia Moon face Thin skin Proximal myopathy Osteoporosis Ulcers ```
28
Features of Addison's disease
``` Fatigue Myalgia Anorexia Weight loss Hyper pigmentation ```
29
Features of Addisonian crisis
Low BP Low glucose Low Na High K
30
Addison's disease replacement steroids
``` Hydrocortisone = cortisol Fludrocortisone = aldosterone ```
31
Congenital adrenal hyperplasia
Due to 21-hydroxylase deficiency Cannot produce GCs or MCs from pregenonlone Instead produces large amounts of androgens --> salt loss, virilisation, adrenal hyperplasia
32
Noradrenaline synthesis pathway
L-tyrosine --> L-dopa --> dopamine --> noradrenaline --> adrenaline
33
Noradrenaline vs adrenaline effects
Noradrenaline more with BP control | Adrenaline more with glucose control
34
Where are chromaffin cells found/
Adrenal medulla Sympathetic chain Organ of Zuckerkandl Bladder wall
35
Symptoms of catecholamine excess
``` Hypertension Hyperglycaemia Tachycardia Dyspnoea Diaphoresis Weight loss ```
36
How are catecholamines inactivated?
By COMT = catechol-O-methyltransferase
37
What is a phaeochromocytoma?
Tumour of the chromatin cells of the adrenal medulla
38
Treatment for phaeochromocytoma
``` Alpha blockers Beta blockers MUST HAVE BOTH Avoid opiates Surgical resection ```
39
How much calcium is protein bound?
Around 50%
40
What happens to calcium levels in acid-base changes?
``` Acidosis = more ionised Alkalosis = less ionised ```
41
Where do the parathyroid glands originate from?
3rd and 4th pharyngeal pouches
42
Cell types in parathyroid gland
Chief cells | Oxyphil cells
43
How is PTH made?
PreproPTH --> proPTH by RER --> PTH by Golgi Releases in vesicles
44
How does the CASR work?
``` GPCR Calcium binding activates PLC Inhibits cAMP signalling Reduces PTH secretion and transcription Increases breakdown of stored PTH ```
45
Other regulators of PTH release?
Supressed by activated vitamin D Stimulated by phosphate Inhibited by cinacalcet
46
Actions of PTH
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
47
How is calcium absorbed in the kidney?
65% in PCT by voltage gradient 20% in LoH by voltage gradient 10% in DTC by PTH control
48
PTH action on the bone
Stimulate RANKL production | Dow regulate OPG (inhibits osteoclasts)
49
What stimulates vitamin D activation?
PTH
50
What inhibits vitamin D activation?
High calcium High phosphate FGF23 High 1,25(OH)2 D
51
Vitamin D2 vs D3
``` D2 = ergocalciferol from vegetables D3 = cholecalciferol from meat ```
52
Inactive forms of vitamin D
1, 24, 25 | 24, 25
53
Effects on vitamin D receptor activation
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
54
FGF23 function
Increases renal phosphate excretion
55
Symptoms of hypercalcaemia
Polyuria and polydipsia Kidney stones Osteoporosis Mood disorder
56
Primary vs secondary vs tertiary
``` Primary = absence of hypocalcaemia Secondary = compensation for hypercalcaemia Tertiary = autonomous PTH following chronic secondary ```
57
Symptoms of hypocalcaemia
Convulsions Arrhythmias Tetany Parasthesia
58
Treatment of hypoparathyroidism
PTH infusion Calcium supplmenets Alfacalcidiol
59
What is mutated in familial hypocalciuric hypocalcaemia?
CASR receptor
60
Causes of respiratory acidosis
CNS depression Chest wall abnormalities NM disease Lung disease --> COPD, severe asthma
61
Causes of metabolic alkalosis
``` Diuretics (Cl- loss) Vomiting Hyperaldosteronism Liquorice Barter's/Liddle/Gitelman's Milk alkali syndrome Bicarbonate therapy Dialysis ```
62
Causes of metabolic alkalosis
``` Anxiety, pain CVA Fever and sepsis Pregnancy Altitude Asthma, PE, pneumonia Salicyclates, progesterone ```
63
Levels of cortisol in the day
``` Morning = 150-500 Evening = 25-125 Stress = 650-2500 ```
64
Genomic effects of GCs
Trans-activation Binds to GC response elements Stimulates/inhibits transcription Transrepression Blocks actions of cytokines/prostinoids/mitogens Blocks transcription of target genes
65
Where does the pituitary develop from?
Oral ectoderm
66
What does somatostatin inhibit?
GH and TSH
67
What inhibits and stimulates PRL?
``` Stimulates = dopamine Inhibits = TRH ```
68
What stimulates ACTH?
CRH, AVP
69
What stimulated GnRH?
Kisspeptin
70
GHRH receptor mutation
``` Mosaic = McCune-Albright syndrome Germline = death ```
71
ACTH independant Cushing's syndrome
= low ACTH Steroid therapy Adrenal tumour Adrenal hyperplasia
72
ACTH dependant Cushing's syndrome
Pituitary tumour | ACTH secreting lung tumour
73
Congenital hyperbilirubinaemia
= Gilbert's disease
74
Types of viral hepatitis
A and E = acute B and C = chronic D only occurs with B
75
Nodule size in cirrhosis
``` Macro = autoimmune Micro = alcohol ```
76
Alcohol metabolic pathway
``` 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 ```
77
Hepatitis C treatment
PegInterverfon + ribacvarin + protease inhibitors Transplant
78
Hepatits B treatment
Entecavir
79
Drugs causing cirrhosis
Amiodarone | Methotrexate
80
What cytokine is involved in cirrhosis?
TGFb
81
Contraindications for liver transplant
Active sepsis Malignancy outside the liver Non-Ccompliance with drugs Severe CR problems
82
Bladder afferent nerves
Pelvic nerves | --> pontine micrurition centre
83
Parasympathetic nerves --> bladder
S2-4 pelvic splanchnic nerves
84
Sympathetic nerves --> bladder
Hypogastric plexus
85
Somatic nerves --> bladder and sphincter
S2-4 pudendal nerve
86
M receptors on bladder
M3
87
Beta receptors on bladder
Beta 3
88
Alpha receptors on sphincter
Alpha 1
89
Storage symptoms
Increased frequency Nocturne Urgency Incontinence
90
Voiding symptoms
``` Hesitancy Straining Poor flow Intermittent flow Incomplete emptying Terminal dribbling Dysuria Haematuria ```
91
Outflow problems
Bladder neck obstruction Stricture Meatus problem Foreskin problem
92
Pump problems
Bladder failure OAB Cardiac failure Medications
93
Control problems
``` Stroke Spinal cord injury Parkinson's MS Tumour ```
94
Constituent problems
UTI Cancer Inflammation Stones
95
BPH drugs
``` Alpha blockers (tamsulosin, doxazosin) 5 alpha reductase inhibitors (finasteride) ```
96
OAB drugs
Anticholinergics (oxybutynin, solifenacin) --> reduce bladder contractility B3 agonist (mirabegron) --> increases bladder capacity Botox --> prevents contraction
97
Neurogenic bladder
Above pons = safe Below T12 = safe --> flaccid bladder Lesions between are unsafe --> loss of sympathetic relaxation --> spastic bladder
98
Acute renal failure causes
``` Sepsis Hypo perfusion Toxicity Obstruction Primary renal disease ```
99
Consequences of acute renal failure
Increased retention of salt, water, electrolytes Acidosis Toxins
100
Presentation of acute renal failure
``` Acutely unwell Hypertensive Oliguric Acute urine on dipstick Normal sized kidneys ```
101
Systemic manifestations of acute kidney failure
``` Pulmonary oedema Hyperkalaemia --> arrhythmia Acidosis Uraemia Encephalopathy Pericarditis Effusions ```
102
Common causes of chronic renal failure
Hypertension Diabetes Polycystic kidneys GN
103
CKD staging
``` 1 = GFR >90 2 = GFR 60-90 3 = GRR 30-60 4 = GFR 15-30 5 = GFR <15 ```
104
When is haemodialysis performed?
3x per week | For 4 hours
105
Complications of haemodialysis
Thrombosis Infection at access site Lack of access Hypotension
106
Advantages of haemodialysis
Hospital or home based | Less time than CAPD
107
Disadvantages of haemodialysis
Requires access to circulation | Limited by staff and space
108
When is CAPD performed?
Four daily exchanges | 0.5h for each exchange
109
Principles of CAPD
``` 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 ```
110
Advantages of CAPD
Can be done at home | Less CV demanding
111
Disadvantages of CAPD
Patient competence Risk of membrane failure Abnormal glycosylation
112
Creatinine vs GFR
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
113
Caveats of using creatinine
Product from muscle so depends on persons muscularity | Drugs such as trimethoprim inhibit tubular secretion
114
Glucose absorption threshold
10mmol/L
115
NIS function
Sodium and iodine into follicular cell
116
Pendrin function
Iodine from cell --> colloid
117
TPO function
Iodine oxidation
118
DUOX1 and 2 function
Oxidising agents
119
IYD function
Recycles iodine
120
How does TSH lead to thyroid hormone synthesis?
Binds to TSHR Acts via cAMP cascade Upregulation of all the components in thyroid hormone synthesis
121
D1 enzyme
Found peripherally | Upregulated by hyperthyroidism
122
D2 enzyme
Found in brain and pituitary Down regulated in hyperthyroidism Up regulated in hypothyroidism
123
D3 enzyme
Deactivation of thyroid hormones T4 --> rT3 T3 --> T2
124
How is T4 excreted?
Glucoronidation by the liver | Gut excretion
125
How does T3 alter gene transcription?
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
Features of hyperthyroid
``` Tachycardia Increased risk of AF Increased BMR Increased appetite Heat intolerance Weight loss Myopathy Hyperglycaemia Seizures Proptosis Pretibila myxoedema Osteoporosis Hypercalcaemia Amenorrhoea Gynaecomastia ```
127
Causes of hyperthyroidism
``` Grave's disease Toxic multi nodular goitre Toxic adenoma Excess iodine Amiodarine HCG Stroma ovarii TSHoma Hamburger thyrotoxicosis ```
128
Treatment of hyperthyroidism
Thionamide drugs --> carbomaxole, propylthiouracil Radioactive iodine Thyroidectomy
129
Features of hypothyroidism
``` 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
Causes of hypothyroidism
``` Hashimoto's disease Iodine deficeincy Lithium Cabbage Infiltrative disease Pendred's disease Hypopituitarism ```
131
Hypothyroidism treatment
Levothyroxine
132
When does hyper acute rejection occur?
Immediately after the transplant When there are pre-existing antibodies present in the blood May be ABO incompatibility Type II hypersensitivity
133
When does acute rejection occur?
``` 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
When does chronic infection occur?
Months to years after transplant | Due to immunological and non-immunological factors
135
Characteristics of hyperacute rejection
Neutrophil invasion Intravascular coagulation Intra-tissue haemorrhage
136
Characteristics of acute rejection
Cell mediated Infiltration of lymphocytes Macrophage activation Antibodies mediated --> endarteritis C4d production
137
Important complement protein in rejection
C4d
138
Reasons for chronic rejection
``` Damaged graft Surgical complications Recurrence of original disease Infection Inadequate immunosuppression ```
139
Immunosuppression drugs
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
Most important HLAs to match
A, B, DR
141
Preventing transplant rejection
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
Complications of transplant
``` Viral infection --> CMV, warts Bacterial infection --> UTI, RTI Protozoa --> pneumocystis Cardiovascular disease Diabetes Osteoporosis Cushing's syndrome Tumours --> skin, solid organ, PTLD ```
143
Option for non-compatible transplants
Plasma exchange IV immunoglobulins Organ exchange scheme
144
Advantages of live donation
Donor can be screened for organ function Shorter cold ischaemia time Elective procedure
145
Order of kidney connection
Vein Artery Ureter
146
How do the 3 germ layer contribute to the gut?
``` Endoderm = mucosa, mucosal glands, submucosal glands Mesoderm = lamina propria, muscularis, submucosa, blood vessels, adventita/serosa Ectoderm = neurones and enteric nervous system ```
147
Foregut
--> upper duodenum | Supplied by coeliac trunk
148
Midgut
Upper duodenum --> proximal 2/3 of transverse colon | Supplied by SMA
149
Hindgut
Distal 1/3 of traverse colon --> anal aperture | Supplied by IMA
150
Imperforate anus
Failure of endodermal and ectodermal portions o the anal canal to communicate
151
Rectoanal atresia
Failure of recanalisation or defective blood supply
152
Persistent cloaca
Urethra, vagina and anus all open out into one cavity
153
Hirschsprung's disease
Absence of parasympatehctsi ganglia in the bowel walls Derived from neural crest cells Signs = failure to pass meconium, swollen belly, vomiting bile
154
Puborectalis
Forms a sling around the and-rectal junction to form the anorectal angle
155
Internal anal sphincter innervation
``` Sympathetic = excitatory = hypogastric nerve L1-2 Parasympathetic = inhibitory = pelvic nerves (S2-4) ```
156
External anal sphincter innervation
Inferior rectal brach of the pudendal nerve
157
How if faecal continence maintained?
Tonic contraction of both anal sphincters | Puborectalis (and EAS) muscle creating anorectal angle
158
How does the puborectalis create a flap valve?
Pushes the anterior rectal wall downwards onto the anal canal
159
What structures on the sigmoid colon and rectal walls also help with continence?
Valves of Houston | Lateral angulations
160
Valsalva manoeuvre
Holding breath and forcibly exhaling against a closed glottis to create a pushing down effect
161
What stimulates the closure reflex?
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
What drugs commonly cause constipation?
Opiates, anticholinergics, anticonvulsants, antidepressants
163
What endocrine conditions can cause constipation?
Diabetes, hypothyroidism
164
Passive vs urge incontinence
``` Passive = internal sphincter problem Urge = external sphincter problem ```
165
Causes of anal structural damage
Obstetric tear Iatrogenic tear Radiation damage Congenital defects
166
Hypersensitive rectal sensation
Urge incontinence
167
Hyposensitive rectal sensation
Evacuation difficulties, functional disorders, constipation
168
Orexigenic signals
SPY AgRP MHC
169
Where are oriexigenic centres found?
Medially
170
Anorexigenic signals
POMC | CART
171
Where are anorexigenic signals found?
Laterally
172
How does AgRP act?
As a melanocortin receptor antagonist
173
What is POMC converted to?
Alpha-MSH
174
How does serotonin act to control appetite?
Increases POMC signalling via HTr2c | Decreases AgRP signalling via HTr1b
175
Action of ghrelin on appetite
Stimulates NPY neurones
176
Where are PYY GLP1 released from?
Intestinal L cells
177
What is the action of GLP-1 and PYY?
Inhibit NPY signalling | Increased POMC signalling
178
Where is CCK produced?
Duodenal I cells
179
What is the action of CCK?
Increases POMC signalling Inhibits NPY signalling Also causes bile release from the gallbladder
180
Where is leptin produced?
Adipose tissue
181
How does leptin affect appetite?
Increases POMC signalling | Decreases NPY and AgRP signalling
182
Effect of insulin of AgRP levels
Decreases them
183
Leptin mutations
Defective leptin = ob | Defective receptor = db
184
When is malonyl CoA produced?
Produced when high levels of ATP are present | High levels suggest adequate energy supply
185
Effect of high malonyl CoA
Inhibits carnitine shuttle to inhibit fatty acid oxidation | Suppresses food intake by inhibiting NPY and stimulating POMC
186
Therapies to reduce appetite
``` GLP-1 agonists Leptin Cannabinoid antagonists SSRI derivatives Amphetamine derivatvies ```
187
PYY receptor
Y2R
188
Melanocortin receptor
MCR4
189
Metabolic syndrome
Insulin resistance Hypertension Dyslipidaemia Abdominal obesity
190
What is arachidonic acid produced from?
Omega 6
191
What does arachidonic acid produce?
Inflammatory mediators | Prostaglandins, leukotrienes
192
What is omega 3 metabolised to?
Anti-inflammatory molecules such as resolvins and protectins
193
Action of aspirin
Enhances the production of anti-inflammatory mediators from omega 3
194
Where are flavonoids found?
Fruit and veg, tea, chocolate, wine, olive oil
195
Action of flavonoids
Inhibits NADPH oxidase that produces ROS | Decreases risk of MI and stroke
196
Where are sulforaphanes found?
In Brassica vegetables
197
Consequences of low B12 and folate
Low methionine and high homocysteine
198
Effects of high homocysteine
--> thiolactate | Damages endothelial cells
199
Fat soluble vitamins
A, D, E, K
200
Which vitamins can be stored?
Fat soluble | Not water soluble
201
Which vitamins can be toxic in excess?
Fat soluble | Not water soluble
202
Selenium deficiency
--> cardiomyopathy
203
Zinc deficiency
Growth retardation Alopecia Dermatitis
204
Copper deficiency
Defective keratinisation of hair
205
Vitamin A deficiency
Xerophthalmia
206
Vitamin D deficiency
Rickets | Osteomalacia
207
Vitamin E deficiency
Peripheral neuropathy
208
Vitamin K deficiency
Coagulopathy
209
Vitamin C deficiency
Scurvy
210
Vitamin B1 thiamine deficiency
Beri Beri Wernicke's encephalopathy Korsakoff syndrome
211
Vitamin B2 riboflavin deficiency
Angular stomatitis
212
Vitamin B3 niacin deficiency
Pellagra
213
Vitamin B6 pyridoxine deficiency
Neuropathy | Anaemia
214
Causes of vitamin D deficiency
``` Reduced sunlight exposure Obesity, smoking, alcohol Malabsorption Hyperparathyroidism Breast feeding Drugs ```
215
Role of vitamin B1
TTP cofactor for pyruvate --> acetyl CoA
216
Features of Beri Beri
Dry --> peripheral neuropathy Shoshin --> cardiac failure and lactic acidosis Wet --> cardiomegaly, tachycardia, peripheral oedema
217
Features of Wernicke's encephalopathy
Horizontal nystagmus Ophthalmoplegia Cerebellar ataxia
218
Features of Korsakoff's syndrome
Amnesia | Psychosis
219
Features of pellagra
``` Loss of appetite Weakness Abdominal pain Glossitis Casals neck Vaginitis Dermatitis Diarrhoea Dementia ```
220
Causes of B12 deficiency
Veganism Terminal ileum disorder Inadequate IF
221
Consequences of haemochromatotiss
Bronzed skin Cirrhosis Diabetes Cardiomyopathy
222
MUST assessment
BMI Recent weight loss Acute disease effects
223
Surrogate height measures
Knee height Ulna length Demispan
224
Surrogate weight measure
Mid upper arm circumference
225
Ascites weight estimation
14kg 6kg 2kg
226
Peripheral oedema weight estimation
``` Sacrum = 10kg Knee = 5kg Ankle = 1kg ```
227
Normal albumin level
35-50g/L
228
Consequences of feeding syndrome
``` Seizures Rhabdomyolysis Osteomalacia Cardiac failure Arrhythmias Tetany Paraesthesia ```
229
Indications for parenteral nutrition
``` Short bowel Ileus Motility disorder Ischaemia Perforation Pancreatitis Obstruction Fistulae Severe IBD ```
230
Problems with PN
``` Risk with placement Catheter related sepsis Disordered liver function Gut atrophy Psychological Cost ```
231
Indications for tube feeding
Unsafe swallow Head and neck cancer Cystic fibrosis
232
Obesogenic drugs
``` Corticosteroids Mood stabilsiers Diabetes medications Beta blockers Allergy relievers Anti-epileptics ```
233
Which diabetes drugs cause weight change?
``` Gain = insulin, sulfonylureas, TZDs Stable = metformin, DPP4 inhibitors Loss = SGLT-2 inhibitors, acarbose ```
234
What does the thrift gene hypothesis state?
Genes that predispose to obesity have a selective advantage in populations frequently experiencing starvation
235
Autosomal dominant syndormes --> obesity
Prader Willi | Fragile X
236
Autosomal recessive syndormes --> obesity
Bardet-Biedl Alstom = ciliopathies
237
X linked syndromes --> obesity
Wilson-Turner | Borjeson-Forssman-Lehmann
238
Orlistat
Gastric and pancreatic lipase inhibitor
239
Lorcaserin
5HT antagonist
240
Liraglutide
GLP-1 agonist
241
Phentermine
Noradrenaline transporter inhibitor
242
Topiramate
GABA agonist
243
Naltrexone
Opioid receptor antagonist
244
Bupropion
Noradrenaline transporter inhibitor
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Restrictive procedures
Gastric banding | Sleeve gastroplasty
246
Malabsorptive procedures
Biliopancreatic diversion | Gastric bypass
247
Normal fasting glucose levels
3.5-5.5mmol/L
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Normal glucose levels 2 hours after a meal
<8mmol/L
249
Why is the brain dependant on glucose?
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
Cells in the pancreatic islets
``` Alpha cells --> glucagon Beta cells --> insulin Delta cells --> somatostatin PP (F) cells --> pancreatic polypeptide Epsilon cells --> ghrelin ```
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Insulin synthesis
Preproinsulin - -> proinsulin by ER - -> insulin by Golgi
252
Insulin amino acid lengths
Preproinsulin = 110 Proinsulin = 86 Insulin = 21+30 C peptide = 35
253
How is insulin released from vesicles?
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
Other signals causing insulin release
``` Arginine and leucine GLP-1 and GIP Fatty acids CCK Phospholipase C Acetylcholine ```
255
How does GLP1 act?
Through GLP-1R receptors | GCPR
256
How do leucine and arginine increase insulin secretion?
Act through glutamate dehydrogenase (GDH) | Can directly depolarise the membrane
257
How does phospholipase C lead to insulin secretion?
Cleaves PIP3 --> IP3 | IP3 binds to SER and causes calcium release
258
Insulin receptor type
Tyrosine kinase receptor
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Action of insulin binding to its receptor
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
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Actions of Akt
GLUT4 translocation in muscle and adipose tissue Stimulation of muscle glycogen synthesis Inhibit of lipolysis
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How does Akt stimulate glycogen synthesis?
Akt phosphorylates and inactviates glycogen synthase kinase that usually inactviates glycogen synthase
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How does insulin inhibit lipolysis?
Inhibits hormone sensitive lipase Inhibits TAG hydrolysis and release of FAs into the circulation Inhibits CPT-1
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Action of insulin on the liver
Enhances glucose uptake and glucokinase activity Increases glycogen synthesis Increases lipogenesis Inhibits gluconeogenesis
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Action of insulin on proteins
Stimulates amino acid uptake into cells Increases translate of mRNAs Inhibits catabolism of proteins Inhibits gluconeogenesis (uses proteins)
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Post-prandial metabolism
Insulin levels rise Increased uptake and TAG and glycogen synthesis Increased liver uptake and storage of glucose Inhibition of gluconeogenesis, glycogenolysis and lipolysis
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Metabolism during fasting
``` Low insulin levels Less tissue glucose uptake Glycogen breakdown Lipolysis releases FFAs Gluconeogenesis proceeds in the liver Lactate used in Cori cycle ```
267
Insulin resistance
Serine and threonine residues phosphorylated on IRS instead of tyrosine Act cannot be activated Reduced insulin action --> hyperglycaemia and dyslipidaemia
268
How is insulin switched off?
Serine/threonine kinases Endocytosis and degradation of receptor Dephosphorylation of tyrosine residues
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How many amino acids in glucagon?
29
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Synthetic pathway of glucagon
Preproglucagon - -> proglucagon - -> glucagon, GLP-1, GLP-2
271
Regulation of glucagon secretion
Low blood glucose levels Increased blood amino acids (alanine and arginine) Exercise Inhibited by insulin and somatostatin
272
Mechanism of action of glucagon
Binds to GPCR Alpha subunit detaches and activates adenylyl cyclase ATP --> cAMP Activates PKA
273
What does PKA activate?
PEPCK G-6-P Glycogen phosphorylase
274
How does glucagon inhibit glycolysis?
Inhibits PFK-1 by modulation of F-2,6-P2 levels | Inhibits pyruvate kinase
275
How does glucagon increase lipolysis?
Activates hormone sensitive lipase | Activates CPT-1
276
When are catecholamines releases?
In response to stress and hypoglycaemia
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What amino acid is used in catecholamine synthesis?
Tyrosine and phenylalanine
278
Metabolic actions of adrenaline
Inhibits insulin secretion Stimulates glucagon secretion Stimulates glycogen breakdown Stimulates lipolysis
279
Metabolic actions of cortisol
Inhibits glucose uptake Stimulates lipolysis Stimulates muscle proteolysis Stimulates gluconeogenesis
280
When is cortisol released?
``` Trauma Infection Intense heat or cold Surgery Any debilitating disease ```
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Metabolic actions of growth hormone
Reduced glucose uptake Increases lipolysis Increases glycogen breakdown Increases gluconeogenesis
282
Metabolic actions of thyroid hormones
``` Increase the number of mitochondria Increase insulin secretion Increase glucose uptake Increase glycolysis and gluconeogenesis Increase lipolysis --> increase BMR ```
283
Metabolic actions of incretins
Increase insulin secretion Inhibit gluconeogenesis Promote satiety
284
Mechanisms of insulin resistance
Diacylglycerol induced activation of protein kinase C | Pro-Inflammatory cytokines releases
285
Normal mechanisms of islet compensation
Increase in size and number of beta cells | Increased beta cell function
286
Beta cell adaption to insulin resistance
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
Diagnosis of diabetes
Random blood glucose >11 Fasting blood glucose >7 Symptoms of hyperglycaemia
288
HbA1c level for diabetes diagnosis
48mmol/mol | 6.5%
289
Biguanides
``` Metformin Inhibit hepatic gluconeogensis Reduce FA synthesis Increase GLP-1 levels Increase GLUT4 translocation ```
290
Sulfonylureas
Glicazide Increase insulin secretion Inhibit K+ channels --> depolarisation
291
Metglitinides
Repaglinine Increase insulin secretion Inhibit K+ channels --> depolarisation
292
TZDs
Pioglitozone Increase insulin sensitivity Increase adipose storage of FFAs
293
GLP-1 agonists
Exanatide Increase insulin secretion inhibit gluconeogenesis
294
DPP-4 inhibitors
Sitagliptin Increase insulin secretion inhibit gluconeogenesis
295
SGLT2 inhibitors
Decrease kidney reabsorption of glucose
296
Alpha-glucosidase inhibitors
Acarbose | Decrease gut absorption of glucose
297
How does ketoacidosis arise?
Continual use of fatty acids for energy production leads to ketone body formation
298
Ketone bodes
Acetoacetate | b-hydroxybutarate
299
Treatment of ketoacidosis
Fluids Electrolytes Insulin
300
Hypoglycaemia Whipple triad
Low blood glucose Symptoms and signs associated with low blood glucose Resolution of signs and symptoms with carbohydrate ingestion
301
Causes of hypoglycaemia
``` Alcohol excess Insulinoma Excessive exercise Reactive hypoglycaemia High dose insulin in T1DM ```
302
Responses to hypoglycaemia
Decreased insulin secretion Increased glucagon and adrenaline release Carbohydrate ingestion
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Prolonged hypoglycaemia
GH and cortisol are released
304
Symptoms of hypoglycaemia
``` Trembling Palpitations Sweating Anxiety Tingling Difficulty concentrating Confusion Weakness Drowsiness Vision changes Difficulty speaking Dizziness Fitting Loss of consciousness ```
305
How does hyperglycaemia cause damage?
``` Activates protein kinase C Increases inflammation Increases ROS production Increases endothelial permeability and occlusion Causes mitochondrial dysfunction ```
306
Non-proliferative diabetic retinopathy
Dilation of retinal veins Micro aneurysms Internal haemorrhaging and oedema
307
Proliferative diabetic retinopathy
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
Diabetic nephropathy features
Proteinuria Glomerular hypertrophy Decreased GFR Renal fibrosis
309
Sites of diabetic neuropathy
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
How does diabetes lead to atherosclerosis?
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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