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T year LOBs medicine > endocrinology > Flashcards

endocrinology Flashcards

1
Q

what is the underlying issue in type one diabetes?

A

There is severe insulin deficiency due to pancreatic beta cell destruction

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2
Q

what genes can increase the susceptibiltiy of type 1 diabetes?

A

Mainly HLA DR

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3
Q

what can cause the beta cell destruction in type 1 diabets?

A

Can be immune mediated or idiopathic

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4
Q

what is the underlying issue in type 2 diabetes?

A

Insulin resistance or a less severe insulin deficienc. often there are defects in secretion

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5
Q

What are causes of type 2 diabetes?

A

Low birth weight and poor nutrition show an association
Insulin resistance is worsened by ageing, in activity and obesity.
genetic links with TCF 7 and KCNQ1

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6
Q

what is often the presentation of a patient with new onset type 1 diabetes?

A

Triad: polyuria, weight loss, thirst
juvenille onset
Severe cases: DKA
weight loss, blurred vision, nausea, abdo pain

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7
Q

what is often the presentation with new onset type 2 diabetes>

A

Often asymptomatic for many years
Frequent UTI’s and infections
fatigue, blurred vision, polydipsia, polyuria
Older age

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8
Q

what is the diagnostic criteria for type 1 diabetes?

A

two of:

  • a random plasma glucose of 11 or higher
  • a fasting plasma glucose of over 6.9
  • a 2 hour plasma glucose of over 11
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9
Q

what is the criteria for the diagnosis of type 2 diabetes?

A

A fasting plasma glucose of over 6.9
a random plasma glucose of over 11
2 hour post load glucose of over 11

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10
Q

what is the diagnosis for impaired glucose tolerance?

A

Oral glucose tolerance test at fasting below 7 and two hours later between 7.8-11

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11
Q

what drugs can cause drug induced diabetes?

A 
corticosteroids
glucocorticoids decrease insulin action
GH decreases insulin action
thiazide diuretics decrease insulin action and secretion 
beta blockers
statins
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12
Q

what are the signs of DKA?

A
  • hyperventilation
  • weakness
  • sweet smelling breath
  • nausea and vomiting
  • sometimes abdominal pain
  • dry skin
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13
Q

what blood results are seen in DKA?

A
  • hyperglycaemia
  • acidotic
  • ketonaemia
  • low bicarbonate
  • hypokaelaemia
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14
Q

What is the pathophysiology of DKA?

A
  1. insulin deficiency
  2. raised glucose and ketone bodies
  3. insulin deficiency leads to increased lipolysis and more FFA taken up by the liver which are converted to ketones in the mitochondria
  4. hyperglycaemia leads to osmotic diuretisis and electrolye depletion.
    Renal hypoperfusion

Also increase in counter regulatory hormones

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15
Q

what can trigger DKA in a patient?

A

They have un-diagnosed diabetes
There insulin therapy has been interrupted
intercurrent illness has caused extra stress
Drugs that affect carb metabolism: corticosteroids, thiazides and dobutamine

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16
Q

What general test results would be seen in DKA?

A
  • ketones and glucose in urine
  • acidosis
  • hypokalaemia
  • low bicarbonate
  • high blood ketones
  • low oxygen sats can be seen
  • elevated anion gap
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17
Q

what are the test results seen in mild DKA?

A 
Plasma glucose >13.9
ph 7.25-7.3
bicarbonate 15-18
positive urine ketone
positive serum ketone
anion gap over 10
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18
Q

what are the test results in severe DKA?

A

plasma glucose >13.9
serum bicarbonate <19
positive urine ketone
positive serum ketones

arterial pH <7
anion gap over 12
mental state affected

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19
Q

what is emergency management of DKA?

A
  1. soluble insulin iv 0.1kg/hr
  2. fluid and electrolyte replacement with 0.9% nacl
    adjust KCL amount according for hypokalaemia
  3. give sodium bicarbonate if necessary
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20
Q

in management of DKA in what order should insulin and potassium treatment be given and why?

A

insulin should always be given first because it causes an uptake of potassium into cells causing a further fall in plasma potassium

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21
Q

what is hyperosmolar hyperglycaemic state?

A

A complication of type 2 diabetes where there is uncontrolled hyperglycaemia causing a hyperosmolar state in the abscnece of significant ketosis.

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22
Q

what is the pathophysiology of a hyperglycaemic hyperosmolar state?

A

insulin deficiency with increased counter regulatory hormones
unlike DKA the insulin deficiency is less severe so still suppresses lipolysis and ketogenesis but is bad enough to stop regulation of hepatic glucose

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23
Q

what are signs of a hyperglycaemic hyperosmolar state?

A 
dehydration
coma
dry mucous membranes
poor skin turgor
hypotension
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24
Q

what are the test results in a hyperglycaemic hyperosmolar state?

A

elevated glucose above 33
negative ketones in urine and serum
elevated urea and creatinine due to volume depletion
high serum osmolality

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25
Q

what are simliarities and differences in test results of DKA and hyperglycaemic hyperosmolar states?

A

both have hypokalaemia
DKA has reduced bicarbonate
HONK has increeased urea
DKA has marked acidosis

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26
Q

what are the main macrovascular complications of diabetes?

A

Atherosclerotic process
MI
ischaemic stroke
gangrene and amputation

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27
Q

what is the process for the risk of macrovascular complications of diabetes?

A

hyperglycaemia leads to oxidative stress and the cytokine cascade
hyperglycaemia increases plasminogen activator inhibitor type 1 and decrease free tissue plasminogen activator
increased hypertension risk

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28
Q

what can be done to reduce the risk of macrovascular complications in diabetes?

A 
Good BP control
statins for lipid management
good glycaemic control
Ace inhibitor or AGII antagonist
low dose aspirin
smoking cessation
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29
Q

what are the main three microvascular complications of diabetes?

A

retinopathy
neuropathy
nephropathy

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30
Q

what changes can be seen in a diabetic eye exam and why?

A
  1. cotton wool spots due to micro infarcts leading to debris and ischaemia
  2. haemorrhages due to retinal capillary leakage
  3. microaneurysms due to damage to the small vessels of the retina
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31
Q

what is the process of damage in diabetic nephropathy?

A
  1. poor glycaemic control leads to kidney damage
  2. the afferent arteriole becomes vasodilated more than the efferent leading to increased intra-glomerular pressure
  3. shearing forces lead to mesangial cell hypertrophy and increased secretion of extracellular mesangial matrix material
  4. glomerular sclerosis and leakage

TGF beta is signalled causing fibrosis

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32
Q

what causes damage in diabetic neuropathy?

A

hyperglycaemia leads to formation of sorbitol and fructose. They accumulate in schwann cells causing damage.

33
Q

what are the clinical features of retinopathy?

A

Macula involvement means loss of central vision
macular oedema leading to loss of visual acuity
blurred vision

34
Q

what are the clinical features of nephropathy?

A
  • Protein in the urine

- fatigue, swelling, hypertension, oedema

35
Q

what are clinical features of neuropathy>

A

symmetrical sensory neuropathy

  • loss of pain, temp and vibration feeling
  • stocking and glove pattern of loss
  • muscle wasting of the foot

Acute painful neuropathy:
- bruning sensation in the shins and feet that is worse at night

Diabetic amyotrophy:
- painful wasting of the quads

Autonomic neuropathy:

  • postural hypotension
  • silent MI
  • incomplete stasis and emptying of the bladder
  • erectile dysfunction
36
Q

what is the prevention of diabetic retinopathy?

A

good glucose control
good BP control
candesartain can act as protection
Yearly eye screening

37
Q

what is prevention of diabetic nephropathy?

A
  • BP control
  • yearly albumin tests as this is an early sign
  • protein restricted diet
  • annual albumin to creatnine ratio
    avoid NSAIDS, radiocontrast and nephrotoxic drugs
38
Q

what is the pathogenesis of diabetic foot?

A

The peripheral neuropathy causing sugar build up in schwann cells
Vascular disease and an increase in thromboxane A2 which causes platelet aggregation and vasoconstriction

39
Q

what are the four main threats to a diabetic foot?

A
  1. infection
  2. ischaemia
  3. abnormal pressure
  4. wound environment
40
Q

what is a good diet for a diabetic patient?

A
  • low in sugar
  • high in starchy carbs especially those with a low glycaemic index
  • high in fibre
  • low in fat
41
Q

why should people on insulin and sulphonylureas be cautious when exercising?

A

risk of hypoglycaemia for 6-12 hours after excertion.

42
Q

how does metformin work?

A

activates AMP kinase to reduce gluconeogenesis and increase insulin sensitivity

43
Q

what are side effects of metformin?

A

weight loss
epigastric discomfort
diarrhoea

44
Q

when is metformin contraindicated?

A

hepatic and renal disease due to lactic acidosis

45
Q

how do sulphonylureas work?

A

act on beta cells to promote insulin secretion
- closes ATP sensitive potassium channels blocking efflux
calcium influx signals insulin release

46
Q

what patients cant have sulphonylureas?

A

no functioning beta cells

pregnancy

47
Q

what are unwanted effects of sulphoylureas?

A

weight gain

hypoglycaemic episodes

48
Q

how do thiazolidinediones/glitazones work?

A
  • reduce insulin resistance

- reduce hepatic glucose and enhance peripheral uptake

49
Q

what patients should not recieve thiazolidinediones/ glitazones?

A

heart failure

bladder cancer

50
Q

what are unwanted effects of thiazolidinediones/glitazones?

A 
weight gain
fluid retention
heart failure
mild anaemia
osteoporosis
51
Q

how do dipeptidyl peptidase 4 inhibitors work?

A

enhance the incretin effect to increase insulin secretion and lower glucagon secretion

52
Q

what is the incretin effect?

A

the insulin response to oral glucose is greater than to iv glucose because GIP and GLP1 increase insulin secretion . DPP4 inhibitors prevent there breakdown

53
Q

what type of treatment is a GLP1 agonist?

A

an injectable treatment for type 2 diabetes

54
Q

how do GLP 1 agonists work?

A

its an analogue of GLP1 which is part of the incretin effect to increase insulin secretion, also delays gastric emptying and blunts appetite

55
Q

what are the unwanted effects of GLP1 analogues?

A

weight loss
acute kidney injury
acute pancreatitis
nausea

56
Q

what diabetic agents work by increasing insulin secretion?

A

GLP1 agonists
DPP4 inhibitors
sulphonylureas

57
Q

what are symptoms of hypoglycaemia?

A
  • nausea
  • confusion
    = tremor
  • sweating
  • hunger
  • anxiety
  • unsteady gait
58
Q

what are some causes of hypoglycaemia?

A
  • alcohol
  • insulin, quinine, sulphonyureas, salicylates, propranolol
  • Addisons
  • GH deficiency
  • non islet cell tumour
  • insulinoma
  • chronic renal failure
  • pancreatitis
59
Q

why can alcohol induce hypoglycaemia`/

A

It inhibits gluconeogenesis

60
Q

what is an insulinoma?

A

a pancreatic islet cell tumour that secretes insulin

61
Q

what is whipples triad for insulinoma?

A
  • fasting hypoglycaemia
  • hypoglycaemia is confirmed during these episodes
  • glucose will relieve symptoms
62
Q

why can sulfonylureas cause hpoglycaemia?

A

They promote insulin secretion due to a calcium influx

63
Q

what is the emergency management of hypoglycaemia?

A
  • stop any insulin treatment
  • 75ml 20% glucose over 10 minutes
  • recovery past 20 minutes give further 25g glucose with hydrocortisone
64
Q

what is the main way of determining who should get lipid lowering therapy?

A

QRISK2 tool

65
Q

what does the QRISK2 score take into account?

A 
Age
ethnicity
gender
smoking
diabetes
angina
CKD
AF
BP
RA
lipid profile
BMI
66
Q

who should the QRISK2 not be used on?

A
  • previous CVS condition
  • type 1 diabetes
    GFR <60
    familial hypercholesterolaemia
67
Q

what are symptoms of hypothyroidism?

A
  • tiredness
  • weight gain
  • cold intolerance
  • goitre
  • depression
  • coma
  • poor memory
  • hair dry and brittle
  • skin dry and coarse
  • myalgia
  • poor libido
  • puffy eyes
  • deafness
  • constipation
68
Q

what are common causes of weight gain?

A
  • pregnancy
  • hypothyroidism
  • steroids
  • cushings
  • menstruation
  • fluid retention
  • PCOS
69
Q

what are causes of hyperthyroidism?

A
  • Autoimmune in graves disease
  • toxic multinodular goite
  • adenoma
  • HCG stimulated gestations
  • exogenous iodine
70
Q

what are causes of hypothyroidism?

A
  • autoimmune
  • iodine deficiency
  • lithium
  • hashimotos
  • TSH deficiency
  • agenesis
  • amioderone
  • interferon
  • postpartum thyroiditis
  • radiation
71
Q

what are signs of hypercalcaemia?

A
  • tiredness
  • decreased concentration
  • confusion
  • renal colic
  • muscle weakness
  • osteopenia
  • osteoporosis
  • bone pain
  • abdo pain
  • peptic ulceration
  • polyuria and polydipsia
  • corneal calcification
  • bradycardia
72
Q

what are causes of hypercalcaemia?

A
  • primary hyperparathyroidism
  • ectopic PTH secretion
  • myeloma
  • small lung cancer producing PTH
  • lung lymphoma/ multiple myeloma producing PTH-RPor osteoclast activating factor
  • granulomatous disease as macrophages express 1 alpha hydroxylase
  • thyroxicosis
  • acromegaly
  • renal failure
  • addisons
73
Q

what are the findings in familial hypocalciuric hypercalcaemia?

A

normal to high PTH

high magnesium

74
Q

what is the emergency management for a patient with hypercalcaemia?

A
  • rehydrate using 0.9% saline
  • IV bisphosphonates often pamidronate
  • prednisolone if caused by myeloma, sarcoidosis, vit D excess
  • calcitonin
75
Q

what are major side effects of bisphosphonates?

A
  • jaw necrosis

- GI side effects

76
Q

what are signs of hypocalcaemia?

A
  • anxiety
  • tetany
  • convulsions
  • chvosteks sign
  • trousseaus sign
  • papilloedema
  • muscle cramps
  • intestinal colic
  • syncope
  • pruritis
77
Q

what are causes of hypocalcaemia?

A
  • high phosphate ie CKD
  • low PTH ie digeorges/ low magnesium
  • vit D deficiency
  • pseudohypoparathyroidism
  • calcitonin and bisphosphonate use
  • acute pancreatitis
  • low albumin plasma
78
Q

what is a definition of osteoporosis?

A

low bone mass so normally age related. Normal bone mineralisation

79
Q

in what main condition is bone mineralisation affected?

A

Osteomalacia

T year LOBs medicine (11 decks)

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