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Neurophysiology, synaptic pharmacology and endocrinology - 2nd semester summary £10.49   Add to cart

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Neurophysiology, synaptic pharmacology and endocrinology - 2nd semester summary

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Neurophysiology, synaptic pharmacology and endocrinology - 2nd semester summary Includes bullet points, key diagrams and images

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  • June 8, 2023
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  • 2019/2020
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Semester 2 Summary

Glucose Homeostasis

 Blood glucose 3.4-5.8mmol/L
 Glycogen- glycogenesis and glycogenolysis
 Fat- lipogenesis and lipolysis
 Protein- gluconeogenesis and proteolysis
 Insulin- secreted by β cells decrease BG
 Glucagon- secreted by α cells increases BG
 Cortisol- glucocorticoid increases BG
 Adrenaline- increase BG and fatty acids
 Growth hormone- secreted by APG increases BG and fatty acid+protein
synthesise
 Somatostatin- secreted by δ cells from raised glucose+amino acids. Inhibits
digestion, absorption and secretion of pancreatic hormones
 Pancreatic polypeptide- secreted by F cells in response to raised amino acids
reducing appetite
 GLP-1- secreted from ileum from L cells. Increases insulin secretion and slow
absorption from GIT

Insulin Secretion

 GLUT-4 uptake glucose into β cells
 Glucose metabolised into ATP
 Increase ATP opens ATP dependant potassium channels
 Potassium gate closed so cell depolarises
 Voltage gated calcium channels open
 Calcium influx causes calcium release from ER
 Vesicles containing insulin by exocytosis

GLP-1

 Incretin gut hormone
 Increases insulin secretion, inhibits glucagon secretion, stimulates β
proliferation and slow GI absorption
 Receptors are GPCRs act via Gs causing cAMP rise in β cells and gene expression
like GLUT-2
 Rapidly hydrolysed by DPP-4




Diabetes Mellitus

,  Primary diabetes mellitus- type 1 and 2
 Secondary diabetes mellitus- pancreatic disease, endocrine disease or drug
induced
 Gestation diabetes- 2nd or 3rd trimester

Type 1

 Polyuria, polydipsia, weight loss, blurred vision, DKA, hyperventilation, muscle
catabolism, high BG, hyperosmolality and potassium loss
 DKA- ketone bodies, acetoacetate and hydroxybutyrate created from fat
breakdown
 DKA symptoms- polyuria, polydipsia, nausea, tiredness, abdominal pain, dry
mouth, ketone breath, confusion and tachycardia

Type 2

 Bacteria infections, HONK (hyperosmolar non-ketotic) but not many
 HONK- endogenous insulin inhibits hepatic ketogenesis but not hepatic
glycogenolysis and glucogenesis
 HONK symptoms- polydipsia, polyuria, dry skin and drowsiness

Diagnosis

 Random venous >11.1mmol/L
 Fasting venous >7.0mmol/L
 GTT >11.1mmol/L




Complications

, Microvascular

 Endothelial of retina, kidney and PNS allows glucose to enter cell without insulin
 Retinopathy- blurred vision, cataracts and glaucoma. Small haemorrhages and
harden exudates causes no blood supply an new fragile vessels form and break
 Risk- high BG, high BP, nephropathy and smoking
 Treatment- good GP and BP control, screening and laser treatment
 Nephropathy- HbA1c aim <7% target <6% and BP<120/70mmHg
 Proteinuria- albumin in urine
 High BP- ACEIs (captopril and ramipril) and CCBs (amlodipine and felodipine
renoprotective)
 Neuropathy- decreased vibrational sense, tingling and itching
 Autonomic nerve damage- orthostatic hypotension, diabetic diarrhoea and
erectile dysfunction
 Treatment- BG and BP control, analgesics, wound management and foot
inspection
 Diabetic foot- peripheral vascular and neuropathy
 Risk factors- ulceration, amputation and poor BG or BP control

Macrovascular Disease

 Statins if high risk of CV disease mainly type 1
 Target 140/80 or 130/80 if related disease
 Risk- retinopathy, nephropathy, high BP/BG and cholesterol
 Treatment- antihypertensive if BP over 130/80




Type 1 Therapeutics

 Rapid acting- Novorapid, Humalog or Apidra

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