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Endocrine > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Pre diabetes definition

A

Impaired fasting glucose = >6.1 and 7.8 but

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2
Q

Definition of type 1 DM

A

Chronic hyperglycaemia caused by absolute insulin deficiency due to autoimmune destruction of beta cells

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3
Q

Aetiology of type 1 DM

A

Genetics
HLA D3 or D4

Monozygotic twins = 36%
Mother =1-2%
Father = 3-6%

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4
Q

Signs and symptoms of type 1DM

A

Polyuria - excess urine output at 2.5/3l every 24hr
Polydipsia - excess thirst from fluid and electrolyte loss
Polyphagia - excess hunger, blood glucose can’t enter the cells due to lack of insulin
Weight loss - perceived lack of BG means that fatty acids and proteins are broken down

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5
Q

Islet cell autoantibodies in type 1

A

ia2 - tyrosine phosphatase
IAAs- insulin molecule
GAD - glutamic acid decarboxylase

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6
Q

What the patient needs to know about insulin regimens?

A
  1. Educate to self adjust dose in light of exercise and calorie intake
  2. Avoid binge drinking
  3. Inject at variable sites (outer thigh/ abdomen)
  4. Phone support (trained nurse)
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7
Q

Monitor blood glucose

A

Fingerprint glucose if type 1 DM

  1. Glycated haemoglobin relates to mean glucose levels over previous 8 weeks 48-57mmol/l
  2. Be sure to ask about hypoglycaemic attacks. Hypoglycaemia awareness may diminish control if is too tight or with time in type 1 due to decreased glucagon secretion.
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8
Q

Subcutaneous insulins

A
  1. Ultra fast Acting ( Humalog, novorapid)
  2. Isophane insulin - favoured by nice as cheap variable leak at 4-12 hr
  3. Premixed insulins - with ultra fast component (30% short, 70% long novomix 30)
  4. Long acting recombinant human insulin analogue - insulin glargine, insulin detemir
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9
Q

Diagnosis of diabetes

A

Symptomatic patients if
- plasma glucose in a random sample is >11.1mmol/l or 2hrs after an OGTT
- fasting plasma glucose >7mmol/l
-hbA1c >6.5%
In a symptomatic individuals two diagnostic tests at different occasions

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10
Q

Type 2 Diabetes features

A

85% of cases
maturity onset
insulin resistance and B-cell insulin secretory dysfunction
no associate autoantibodies

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11
Q

Genetics in type 2 diabetes

A

identical twins near 100% concordance

70-100% risk if both parents have

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12
Q

Secondary diabetes mellitus

A
  1. Due to pancreatic disorders causing insuling deficiency
    a. pancreatitis
    b. carcinoma of the pancreas
    c. cystic fibrosis
    d. haemochromatosis (bronze diabetes)
    e. pancrectomy
  2. Due to insulin resistance
    a. endocrine causes (cushings, thyrotoxocis, acromegaly, pheochromocytoma, PCOS
    b. drugs (steroids, thiazides)
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13
Q

Microvascular Complications of Diabetes

A

progress dependent on degree of glycaemic control

  1. retinopathy
  2. neuropathy
  3. Nephropathy
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14
Q

Retinopathy

A

annual retinal screening

  1. hyperglycaemia increases blood flow to the retina
  2. dilation of retinal cappillaries –> microaneurysms
  3. Increased vasoactive substances + clots cause vessels to close up –> haemorrhagic
  4. hypoxia occurs –> causes release of VEGF –> neovascularisation
  5. new vessels are fragile and leaky –> blurred vision and retinal leakage
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15
Q

Background (early) vs proliferative (late) retinopathy

A

background changes
- microaneurysms (dots), haemorrhages (blots), and hard exudates (lipid deposits) - refer if near the macula for

pre-proliferative
- cotton wool spots (eg infarcts), haemorrhages, venous bleeding- signs of retinal ischaemia

proliferative
- new vessels form

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16
Q

Nephropathy

A

increased blood flow due to hyperglycaemia
increased glomerular pressure –> hypertrophy (thickening) of epithelium and endothelium
glomerular sclerosis & loss of nephrons
Look for microalbuminaemia vs macroalbuminaemia

delayed by ACE I/ ARBS

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17
Q

Types of neuropathys in Diabetes

A
  • Peripheral sensory neuropathy “glove and stockings (tingling and pain worse at night)
  • mononeuropathy
  • diabetic amytrophy
  • autonomic neuropathy
18
Q

Peripheral sensory neuropathy and Treatment

A
  • Insiduous, symmetric
  • affects all sensory modalities
  • impaired vibration sense
  • wasting of intrinsiv muscles
  • painful, sharp burning

ANTI-DEPRESSANTS
paracetemol–> tricyclic –> dluoxetine –> anticonvulsants (gabapentin) –> opiates

19
Q

Mononeuropathies and Tbx

A
  • median nerve/carpal tunnel syndrome
  • occur suddenly

Self limiting

20
Q

Diabetic amytrophy and Tbx

A
  • painful wasting of quadricepts involvement of lumobosacral plezxus

related to poor diabetic control –> convert to insulin treatment and physio

21
Q

Autonomic neuropathy and tbx

A
  • abnormal autonomic function
  • impotence
  • postural hypotension
  • resting tachycardia
  • gastroparesis

depends on the cause

  • support stockings
  • sildenafil devices for impotence
  • metoclopramide for gastroparesis
22
Q

risk factors for diabetic foot disease

A
  • PVD
  • neuropathy
  • callus
  • males
  • previous amputation
23
Q

Diabetic foot is the result of:

A

-ischaemia and/ or neuropathy +/- infection

24
Q

Ischaemic foot features

A
  • BETWEEN TOES
  • cold/cool
  • atrophic/hairless
  • foot pulses absent
  • painful
  • history of claudication and/or rest pain
25
Q

Neuropathic foot

A
  • PRESSURE POINTS
  • warm
  • dry skin
  • foot pulse palpable
  • ulcer is painless
26
Q

Risk assessment of diabetic foot

A

low risk –> no sensation impairment, foot pulses present, annual checkup

moderate risk –> sensation impaired and foot pulses absent but NO skin callys - annual check up by podiatrist

high risk –> sensation impaired and foot pulses absent, skin callus and foot ulcer - see podiatrist

27
Q

Treatment of foot disease

A

education, sensible footwear, podiatrist, multidisciplinary foot clinic

28
Q

Management of active foot disease

A 
debridement 
pressure relief 
antibiotics where indication 
arterial reconstruction where indicated 
total contact cast and no weight bearing
29
Q

Charcot foot

A
  • fracture and acute inflammation
  • red, swollen, oedematous
  • can be painful
  • skin temp 2-8 degrees higher than contralateral foot
  • often difficult to distinguish from infection

total contact cast and no neuropathy

30
Q

Mechanism of HHS (hyperosolic hyperglycaemic state)

A
  1. relative insulin deficiency
  2. less BG can enter muscle
  3. body perceives you are in a glucose deficient state
    - increase gluconeogenesis and glycogenolysis (liver) + decreased protein synthesis and increased proteolysis (in muscle)
  4. presence of some insulin inhibits lipolysis - no ketone body production
  5. result is osmotic diuresis –> leads to dehydration
31
Q

Diabetic ketoacidosis mechanism

A
  1. absolute insulin deficency
  2. less blood glycose utilities by muscle and cells
  3. body perceives you are in a glcusoe deficient state
    - gluconeogeneis
    - glycogenolysis
    + excess mobilisation of free fatty acids from adipose tissue provides the substrate for ketone production in lover
  4. ketons Bhydroxybutyrate, acetoacetate and acetone are excreted by the kidneys and buffered in the blood initially, eventually fails –> metabolic acidosis
  5. osmotic diuresis + ketonuria causes hypovolaemia
32
Q

HHS features

A
  • absence of significant ketones
  • acidosis not rpesent
  • high mortality
  • elderly
  • insidious onset
33
Q

Causes of HHS

A

infection - 60%
poor compliance - 30%
drugs

34
Q

Treatment of HHS

A

Identify and treat the precipitant

  1. fluid
    - 0.9% crystalloid
    - aim for postivie fluid balance within 3-6L with 12 hrs
    - switch to NaCl if postive fluid balance but osmolality rising –> 0.45% Na
  2. Insulin
    - only start once glucose is not falling with fluid
  3. prophylaxis
    - LMWH
    - Foot protection
35
Q

Criteria for DKA

A
  1. metabolic acidosis
  2. plasma glucose high
  3. urinary plasma ketones
36
Q

Signs and symptoms

A

(dka)
- Dizziness, dehydration, diuresis
K- kussmauls breathing (deep fast breath to offset co2), ketotich breath
A- abdominal pain (disrupts enteric nervous system)

37
Q

treatment (FUCKING)

A 
identify precipitant agent 
F- fluids (crystalloid) 
U- urea 
C- creatine/cathetirise 
K- K+ (iv KCL)
I- IV insulin 
N- Nasogastric tube 
G- glucose 
H- heparin
38
Q

Hypoglycaemia (whipples triad)

A
  1. symtpoms of low blood glucose (neuroglycopaenic

2. meausre plasma glucose

39
Q

Edinburgh hypoglycaemic scale

A
  1. 0 mmol/l - autonomic - sweating, palpitations, shaking, hunger, 70-80% may have no symptoms
  2. 5mmol/l - neuroglycopenic - confusion, dorwsiness, odd behaviour, speech difficulty
40
Q

Treatment of hypoglycaemia

A

15-20g of CHO, assess response 15mins later to ensure glucose >4mmol/l, then give longer actin

Process repeated

41
Q

Hypos and driving

A

BM> 5mmol/l before driving, carry CHO, identifiers 2 hours at a time

In the event of a hypo

  1. stop the car where it is safe to do so
  2. keys out the ignition, move to the passenger seat
  3. check the glucose levels, and treat , wait 10 minutes, check
  4. wait another 40 minutes to make sure still above 5

allow 1 hypo in 12 months
Bm monitoring evidence

42
Q

Dietary advice

A

encourage high fibre, low glycaemic index sources of carbohydrates
include low-fat dairy products and oily fish
control the intake of foods containing saturated fats and trans fatty acids
limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
discourage use of foods marketed specifically at people with diabetes
initial target weight loss in an overweight person is 5-10%

Endocrine (7 decks)

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