greenfylde
Mind Map by , created almost 6 years ago

Endocrine Mind Map on Diabetes, created by greenfylde on 12/08/2013.

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greenfylde
Created by greenfylde almost 6 years ago
Endocrine Glands
MARK BETTERTON
Biology F214: Section 1
emma_royal
Endocrine Hormones
Cassandra Bilodeau
Utilitarianism
ellie.blythe
Část 2.
Gábi Krsková
Endocrine System
Riki M
Diabetes Mellitus
Kirsty Jayne Buckley
GCSE AQA Biology 3 Kidneys & Homeostasis
Lilac Potato
B1.2: Responses to a changing environment
benprice99
Endocrine diseases
Anna4anatomy
Diabetes

Annotations:

  • think of as vascular disase commonest metabolic disorder in ocmmunity high lvls of morbidity (much avoidable) from complications common cause of admission health cost enormous (2bn /yr in UK)
1 pathophys
1.1 insulin -> decrease blood glucose lvls

Annotations:

  • control of this occurs in Beta-cell (direct response to portal glucose lvls) and is achived by:  -reducing hepatic glucose output -increasing peripheral glucose intake -a wide variety of other actions which regulate fat and protein metabolism -insulin produciton and activity are goverened principally by  1. circulating glucose lvls 2. diet 3. weight
2 diagnosis
2.1 WHO criteria

Annotations:

  • symps of hyperglycemia (eg polyruia, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy) AND raised venous glucose detected once - fasting > 7mmol/L or random >11.1moml OR raised venous glucose on 2 separate occasions- fasting >7mmol/L, random >11.1mmol/L or OGtt- 2h valve >11.1 mmol/L
2.2 Real criteria
2.2.1 HBA1c
2.2.1.1 >48

Annotations:

  • normal <42
2.2.2 Fasting plasma glucose
2.2.2.1 >7 mmol/L

Annotations:

  • <6
2.2.3 random plasma glucose
2.2.3.1 >11.1 mmol/L

Annotations:

  • normal <7.8
3 T1
3.1 epidem
3.1.1 common (less common approaching equator)
3.2 autoimmune destruction of B-cells
3.3 characterised clinically by:
3.3.1 onset in youth (but can occur at any age)
3.3.1.1 peak at 4-5 and early teens
3.3.2 absolute req for insulin
3.3.3 rapid onset (wk-mo)
3.3.4 often precipated by concurrent illness
3.3.5 risk of ketoacidosis (DKA)
3.4 genetic/immunological considerations

Annotations:

  •  ; 50% concord only in identical twins
3.4.1 HLA DR3 and HLA DR4
3.4.2 evidence of immune activation w/destruction of B-cells (insulitis).

Annotations:

  • offers the possiblity of pre-clin diag +/-intervention?
3.5 cause
3.5.1 unknown

Annotations:

  • theories incl viruses (mumps, coxsakie B, measles) and cows milk/ breast milk
3.6 manage
3.6.1 adminstered insulin

Annotations:

  • individualised)
3.6.1.1 requires motivation, assisted by self-blood glucose monitoring
3.6.2 food + exercise
3.6.3 reduction of risk factors for complications

Annotations:

  • eg reduce BP
4 T2
4.1 epidemiology
4.1.1 common
4.1.1.1 2-4% european adults
4.1.1.2 10% elderly
4.1.1.3 12-20% ethnic minories
4.2 characterised clinically by
4.2.1 onset in OLDER (uncommon before 35)
4.2.2 RELATIVE insulin deficiency (insulin insensitivity/resistance)
4.2.3 generally OVERWEIGHT
4.2.4 may be present for many years prior to diagnosis
4.2.5 rarely devel ketoacidosis but elderly in partic may devel HYPEROSMOLAR CRISIS (HONK)
4.3 genetic/histological considerations
4.3.1 BIG GENETIC LINK

Annotations:

  • almost 100% identical twin concordance
4.3.2 islet amyloid deposition

Annotations:

  • leads to 2ndry Beta-cell failure?
4.4 etiology
4.4.1 GENETICS +ENVIRONMENT espec obesity
4.5 Management principles
4.5.1 weight redution
4.5.2 approp diet
4.5.3 reduce risk factors for complics
4.5.3.1 eg decrease BP, statins
4.5.4 altered lifstyle

Annotations:

  • reqs high lvls motivation. diet, exercise, etc
4.5.5 most can be managed w/o drug therapy but few are
4.5.6 some req insulin (?slow onset type 1 diabetes?)
5 complications
5.1 acute
5.1.1 Diabetic Ketoacidosis (DKA)
5.1.1.1 cause
5.1.1.1.1 due to INADEQUATE circulating INSULIN (insulin deficiency -> body starves)
5.1.1.1.1.1 triggers: infect, missed insulin, onset of undiagd DM (usually)
5.1.1.1.2 use of fats for fuels, and inability (due to insulin lack) to clear fat breakdown products (acetoacetic acid + Beta-hydroxybutyrate)
5.1.1.2 presentation
5.1.1.2.1 often precipitated by illness
5.1.1.2.2 DEHYDRATION an important feature
5.1.1.2.3 onset over days weeks
5.1.1.2.4 in many centres carry a 5% mortality
5.1.1.2.5 symps
5.1.1.2.5.1 polyuria/polydypsia
5.1.1.2.5.2 vomiting
5.1.1.2.5.3 abdopain, anorexia
5.1.1.2.5.4 SOB
5.1.1.2.6 signs
5.1.1.2.6.1 tachycardia
5.1.1.2.6.2 hypervent
5.1.1.2.6.3 hypotension
5.1.1.2.6.4 sweet breath
5.1.1.2.6.5 confusion, unconsciousness
5.1.1.3 manage
5.1.1.3.1 treat underly cause
5.1.1.3.2 in large amounts (watch K+)
5.1.1.3.3 insulin admin in modest amounts
5.1.2 Hyperosmolar non-ketotic crisis (HONK)
5.1.2.1 etiology less clear
5.1.2.2 profound DEHYDRATION
5.1.2.3 usually in ELDERLY
5.1.2.4 more common in T2DM
5.1.2.5 often related to infect/sudden loss of mobility (stroke, etc)
5.1.2.6 onset over wks
5.1.2.7 manage principles
5.1.2.7.1 as for DKA but FLUID more important, LESS INSULIN req'd
5.1.3 Hypoglycemia
5.1.3.1 due to insuffic glucose supply in the face of ADEQUATE/EXCESS INSULIN
5.1.3.2 anyone on glucose loweirng hterapy (tablets/insulin)
5.1.3.3 presentation
5.1.3.3.1 rapid onset
5.1.3.3.2 EMERGENCY! brain dam + death in severe prolonged
5.1.3.3.3 symps/signs
5.1.3.3.3.1 autonomic- sweat, anx, hunger, tremor, palps, dizzy
5.1.3.3.3.2 neuroglycopenic- confusion, drowsy, visual trouble, seizures, coma
5.1.3.3.3.3 blood glucose <3mmol/L
5.1.3.4 2 types
5.1.3.4.1 Fasting- b/c insulin
5.1.3.4.1.1 b/c increased activity, missed meal, accdental or non-accidental overdose
5.1.3.4.2 Post prandial
5.1.3.4.2.1 after gastic/bariatric surg or in T2DM
5.1.3.5 managment
5.1.3.5.1 rapid + adequate admin of soluble carb (lucozade, soda- small)
5.1.3.5.1.1 if can't swallow - IV 25-50mL glucose or glucagon 1mg IM if no IV access
5.1.3.5.2 occasionally glucagon req'd
5.1.3.5.3 always follow w/longer acting carb- Toast
5.2 chronic

Annotations:

  • NB- may be present at diagnosis w/T2DM
5.2.1 macrovascular
5.2.1.1 both types assoc'd w/increased risk of mac vasc disease: STROKE 2x, MI 4x
5.2.1.2 glycemic control NOT known to influence risk
5.2.1.3 reduction in other risk factors critical
5.2.1.3.1 smoking, BP, lipids, etc
5.2.1.4 diabetic amputations largely avoidable by identification of the 'at risk foot' + adequate preventive care
5.2.2 microvasc
5.2.2.1 both types affected
5.2.2.2 glycemic control MAIN risk factor
5.2.2.2.1 high glucose in blood damages small vssls
5.2.2.3 nephropathy
5.2.2.3.1 30% T1DM
5.2.2.3.2 characterisitic histo appearances of glomerulus (glomerulosclerosis)
5.2.2.3.3 test: urine: creatinine ratio >30mg/mmol
5.2.2.3.4 progression can be slowed by BLOOD PRESSURE CONTORL
5.2.2.3.4.1 but <120 NOT bettter than <140 and has increased risk of serious adverse event from therapy
5.2.2.3.5 high risk of CHD
5.2.2.3.6 manage: inhibit renin-angiotensisn to protect kidneys
5.2.2.3.6.1 candesartan (AZA blocker, decrease albumin excr)
5.2.2.3.6.2 + can combine w/ ACEi
5.2.2.4 retinopathy
5.2.2.4.1 commonest cause of blindness in <65 in devel'd world
5.2.2.4.2 charac'd by ISCHEMIA and LEAKY vssls -> growth of NEWbut fragile VSSL -> HAEMORRHAGE scarring and traction
5.2.2.4.2.1 microaneurysms- dots
5.2.2.4.2.2 hameorrhages- blots
5.2.2.4.2.3 hard exudates- lipid deposits
5.2.2.4.3 at least 95% have retinopathy after 20y
5.2.2.4.4 blindness preventable by annual screening + early laser therapy
5.2.2.5 neuropathy

Annotations:

  • REFER EARLY! GOOD CARE SAVES LEGS
5.2.2.5.1 common (up to 30%)
5.2.2.5.2 due to combo of METABOLIC + VASCULAR factors
5.2.2.5.3 anesthesia leads to increased INCIDENTAL DAMAGE + ULCERATION of peripheris
5.2.2.5.4 glove + stocking classical
5.2.2.5.4.1 numbness, tingling, pain eg worse at night
5.2.2.5.4.1.1 treat: paracetamol -> tricyclic -> amitryptilline -> gabapentin -> capsaicin cream -> baclofen-> SSRI (avoiding weight bearing helps)
5.2.2.5.5 EXAMINE FEET REGULARLY
5.2.2.5.5.1 ischemia -critical toes +/- absent dorsalis pedis pulsex
5.2.2.5.5.2 periph neruopathy- inj or infect over pressure points (eg MTP heads)
5.2.2.5.5.3 foot ulceration- typically painless, punched out ulcer in area of thick callus +/- superadded infection
5.2.2.5.5.3.1 artierial ulcer
5.2.2.5.5.3.1.1 deep, well demarcated 'punched out', necrosis, over pressure point
5.2.2.5.5.3.2 venous ulcer - superficial, Gaiter's area (medial malleolus), poorly demarcated, sloughy
5.2.2.5.5.4 causes: -> cellulitis, abscess + osteomyelitis
6 treatment
6.1 Insulin regimes
6.1.1 def for T1, maybe T2
6.1.2 combos of short acting (4-6hrs), intermediate acting (8-12h) and long acting (18-24hr) insulins. like do basal long act w/additnal per meal or based on carbs
6.1.3 attemps to mimic physiological profiles
6.1.4 info on how to give info (for pts) to practice for explanation station (+ safety issues - hypos and hypers)
6.1.4.1 http://www.patient.co.uk/medicine/insulin
6.1.4.2 hypos
6.1.4.2.1 feeling shaky or anxious, sweating, pale, hungry, palpitations, feeling dizzy.
6.1.4.3 hypers
6.1.4.3.1 causes
6.1.4.3.1.1 eat more than normal, or have a fever, or take too low a dose of insulin
6.1.4.3.2 symps
6.1.4.3.2.1 sleepy, flushed, fruity smell on yourbreath, polyuria, polydipsia, anorexia
6.2 oral hypoglycemic agens
6.2.1 only for T2 DM
6.2.2 insulin sensitisers- metformin, gamma-PPR agonists (glitazones)
6.2.3 Beta-cell stimulants- sulphonyureas
6.2.4 DPP-4 inhibitors ('gliptins')
6.2.5 SLGT-2 inhibitors
6.3 GLP-1 agonists
6.3.1 only for T2
6.3.2 -exenatide, liraglutide, lixisenatide
6.3.3 glucagon-like peptide analogues
6.4 blood glucose monitor
6.4.1 see notes for how
6.4.2 premeal :4-7mmol/L post meal 1-2hr: <9 (or8.5if T1) 8hrs fasting: 5-7
7 other causes

Annotations:

  • steroids; anti-HIV durgs; newer antipsychotics; thiazides pancreatitis, panc surg removal, trauma, panc destruc (hemochromatosis, CF), panc cancer cushings, acromegaly, phaeocrhomocytoma, hyperthyroidism, pregnancy others: acanthosis nigricans LADA- laten autoimmune diabetes in adults (if ketotic +/- a poor response to oral hypoglycemics) Imparied glucose tolerance (IGT) impaired fasting glucose (IFG) gestational diabetes (4% of pregs) (increased birhtweight, neonatal hypoglycemia, sacral agenesis)

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