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endocrinology > diabeties > Flashcards

diabeties Flashcards

1
Q

Where is insulin and glucagon released from

A

islet of langerhans

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2
Q

where does all glucose come from

A

LIVER

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3
Q

what does insulin do

A

Supresses hepatic glucose output
 Glycogenolysis
 Gluconeogenesis
Increases glucose uptake into insulin sensitive tissues (muscle, fat)
Suppresses Lipolysis

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4
Q

what does glucagon do

A

Increases hepatic glucose output
 Glycogenolysis
 Gluconeogenesis
Reduce peripheral glucose uptake
Stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
Lipolysis
Muscle glycogenolysis and breakdown

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5
Q

what is diabeties mellitus

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia
high sugar levels

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6
Q

how does diabeties mellitus cause morbidity

A

acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
Chronic hyperglycaemia leading to tissue complications

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7
Q

Complications of diabeties mellitus

A

stroke
blindness
diabaetic neuropathy
heart disease

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8
Q

types of diabetes

A

type 1
type 2 to include gestational and medication induced
MODY
pancreatic
endocrine diabeties
malnutrition related

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9
Q

symptoms of diabetes

A

polyuria
fatigue
fasting plasma glucose more than 7
Hba1c > 48mmol/ mol

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10
Q

treatment of type 1 diabetes

A

insulin treatment - basal bolus
once or twice daily of slow acting
ability to judge carbohydrate intake
awareness of blood glucose lowering effect of exercise

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11
Q

pathogenesis of type 1 diabates

A

Destruction of beta cells in the islet of langherhans caused by an autoimmune response

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12
Q

what would happen if you take too much insulin

A

cerebral dysfunction
hypoglycaemia
- release of glucagon
-sweating
-hunger
-loss of consciousness

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13
Q

failure of insulin secretion leads to

A

-Continued breakdown of liver glycogen
-Unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors
-Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake

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14
Q

failure to treat insulin resistance leads to :

A
  • increase in circulating glucagon, increases glucose
    -perceived ‘stress’ leads to increased cortisol and adrenaline
  • progressive catabolic state and increasing levels of ketones
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15
Q

aetiology of type 2 diabetes

A

genes and environment
impaired insulin secretion/ insulin resistance
impaired glucose tolerance
type 2 diabetes
progressive hyperglycaemia

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16
Q

impaired insulin action leads to

A

Reduced muscle and fat uptake after eating
Failure to suppress lipolysis and high circulating FFAs
Abnormally high glucose output after a meal

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17
Q

summary of type 1 diabetes

A

Severe insulin deficiency due to autoimmune destruction of the beta cell

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18
Q

signs and symptoms of type 1 dibaetes

A

polydipsia, polyuria, weight loss
- short history of severe symptoms

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19
Q

typical patient presenting with new T1DM

A

polydipsia, polyruia, rapid weight-loss, young, BMI >25
genetic history of disease

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20
Q

summary of type 2 diabetes

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

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21
Q

principles of treatment for diabetes

A
  • control of symptoms
    -prevention of acute emergencies, ketoacidosis
  • correct diagnosis
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22
Q

risk factors for T2DM

A

Lifestyle- obesity, lack of exercise, calorie and alcohol excess
- asian men
- HT
- ABOVE 40

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23
Q

SIGNS and symptoms of type2 diabetes

A

polydipsia
polyuria
glycosuria
central obesity
slower onset
blurred vision

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24
Q

3 step management process for diabetes

A

1- metformin - to inc insulin sensitivity
2- if HBA1C still high then dual therapy with dpp4, sulphonyl
3- if still high - triple therapy
then insulin

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25
Q

define DKA

A

Diabetic ketoacidosis

  • complete lack of insulin results in high ketone production and hyperglycaemia

medical emergency

glucose and ketones escape in urine but lead to osmotic diresis

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26
Q

Absence of insulin would cause

A

absence of insulin- uncontrolled catabolism,- unrestrained gluconeogenesis and decreased peripheral glucose uptake

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27
Q

signs of DKA

A

Pear drop breath due to ketones
hypotension
tachycardia

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28
Q

symptoms of DKA

A

Nausea+ vomitting
weight loss
very thirsty
confusion
lethargy
abdo pain

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29
Q

dka complications

A

cerebral oedema
adult resp distress syndrome
thromboembolism
aspiration pneumonia
death

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30
Q

treatment for DKA

A

replace fluid - 0.9 saline 3l for 3hrs
IV insulin- to stop ketones being made
restore electrolytes

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31
Q

how do sulphonylureas work

A
  • stimulate insulin release by binding to b-cell receptors
  • improve glycaemic control
    -can cause hypoglycaemia
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32
Q

what medication can cause osteoporosis, heart failure and weight gain

A

thiazolidinediones

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33
Q

ideal drug for type 2 diabetes would;

A

Reduce appetite and induce weight loss
Preserve -cells and insulin secretion
Increase insulin secretion at meal time
Inhibit counterregulatory hormones which increase blood glucose such as glucagon
Not increase the risk of hypoglycaemia during treatment

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34
Q

what do SGLT2 inhibitors do

A

-block the reabsorption of glucose in kidney in the Pct, increase glucose excretion and lowers blood glucose

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35
Q

define HHS

A

hyperosmolar hyperglycaemic state
marked hyperglycaemia
mild/ no ketosis

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36
Q

signs and symptoms of hhs

A

confusion and reduced mental state
lethargy
severe dehydration

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37
Q

investigations for HHS

A
  • random plasma glucose >11 mmol
    -urine dipstick- glucosuria
  • plasma osmolality -high
    U + E
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38
Q

pathophysiology of hhs

A

low insulin> increased gluconeogenesis

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39
Q

first line treatment for diabetes type 2

A

metformin

40
Q

How do ddp4 inhibitors work

A

Inhibit the release of glucagon
Can cause weight gain

41
Q

side effects of sglt2 inhibitors

A

-genital thrush
- inc risk of euglycaemic ketoacidosis

42
Q

what is shown with euglycaemic ketoacidosis

A

breakdown of fats with fasting
ketone levels rise
acidotic and nauesous
glucose levels are normal

43
Q

hypoglycaemia?

A

low blood sugar

44
Q

pathophysiological effects of hypoglycaemia

A

brain- cognitive dysfunction, seizures
heart- heart attack
msk- falls, fractures
circulation- inflammation, blood coagulation, endothelial dysfunction

45
Q

neuroglycopenia?

A

shortage of glucose in the brain resulting in alteration of neuronal function.

46
Q

neuroglycopenia symsptoms

A

-difficulty concentrating
- confusion
-weakness
-dizziness
-vision changes
-fatigue

47
Q

symptoms of hypoglycaemia

A
  • trembling
    -palpations
    -sweating
    -anxiety
    -hunger
48
Q

causes of hypoglycaemia

A

-long duration of diabetes
-tight glycaemic control
-old age
-drugs, alcohol
-sleeping
-increased physical activity

49
Q

to prevent hypoglycaemia in community

A
  • educate patients and caregivers on how to treat and recognise
    -instruct patients to report
50
Q

how to treat hypoglycaemia

A
  • recognise symptoms
    -confirm the need for treatment
    -treat with fast acting 15g carb to relieve symptoms
    -retest in 15 mins to ensure blood glucose
    -eat a long acting carb to prevent recurrence of symptoms
51
Q

Adv and dis of pre mixed insulin in diabetes

A
  • both basal and prandial components in a single prep
  • can cover insulin requirements for whole day

Dis
- requires consistent diet and exercise
- increase risk for nocturnal hypoglycaemia

52
Q

How would hypoglycaemia be avoided in the body

A

When glucose levels are low
Glucagon and adrenaline are released which allows for glycogenolysis

53
Q

Consequences of low blood sugar with diabetics

A

Altered thresholds, patient is unable to realise that levels are low
Glucose levels can go very low and they may pass out

54
Q

objectives if t2dm treatment other than glucose control

A

to reduce risk of cvd
chronic kidney disease
microvascualr complications

55
Q

microvascular complications linked to diabetes

A

diabetic retinopathy
nephropathy
severe non / proliferation
neuropathy
microalbuminuria

56
Q

hba1c target

A

7%

57
Q

presenting feautures of diabetes

A

thirst
polyuria- excess urine
weight loss and fatigue
hunger
blurred vision
vaginal candidiasis

58
Q

type 1 sugggestive features

A

onset in childhood/ normally sudden
lean body habitus
prone to DKA
high levels of islet autoantibodies

59
Q

what would happen if you stopped producing insulin

A

increased and uncontrolled fat metabolism, impair glucose uptake, FFA are transported into the liver

60
Q

three things you need for definitive diagnosis of DKA

A
  • HYPERGLYCAEMIA
    -RAISED PLASMA KETONES
    -METABOLIC ACIDOSIS
61
Q

what is the significance of ANTI- gad

A

the more anti gad you have the more likely you are to have type 1 diabetes

62
Q

type 2 suggestive feautures

A

usually presents in over 30’s
onset is gradual
FH is often positive
diet exercise and oral meds can control it

63
Q

3 main issue with neuropathy

A

pain
autonomic issues
insensitivity

64
Q

signs of vascular disease

A

diminished or absent pedal pulses
cold feet and toes
poor skin and nails
abscence of hair and nails

65
Q

most common cause of blindness in the working population

A

diabetic retinopathy

66
Q

risk factors of DR

A

long duration diabetes
poor glycaemic control
hypertensive
on insulin treatment
pregnancy

67
Q

hallmark of diabetic nephropathy

A

development of proteinuria
followed by progressive decline in renal function

68
Q

risk factors for diabetic nephropathy

A

poor bp control
poor bg control

69
Q

pathophysiology of diabetic nephropathy

A

glomerulus changes
increase ofr glomerular injury
filtration of proteins
diabetic nephropathy

70
Q

treatment of diabetic nephropathy

A

blood pressure control
glycemic control
ARB/ACEI
proteinuria control
cholestrol control

71
Q

leading cause of amputations

A

diabetic nephropathy

72
Q

what can cause excess protein in urea

A

exercise
infection
fever
congestive heart failure
marked hypertension
pregnancy

73
Q

specific values needed to diagnose diabetes

A

symptoms and random glucose of more than 11.1 mmol/l
fasting plasma glucose more than 7.0 mmol/l
hba1c of more than 48

74
Q

what is a normal glucose level

A

between 4-7 mmol/l

75
Q

biochemical values of DKA

A

glucose around 50mmol/l
high K+
hco3- less than 15mmol
urea and creatinine raised

76
Q

what is MODY

A

maturity onset diabetes of the young
diagnosed at <25y

77
Q

which genes have been found to have mutations that cause MODY

A

HNF1A
HNF4A

78
Q

how would you treat MODY3

A

with sulphonylurea
often do not need insulin

79
Q

what would make you think MODY instead of type 1 diabetes

A

if a parent is affected
absecence of islet autoantibodies

80
Q

what would c peptide tell you about mody and type 1

A

MODY the patient would have normal levels of c peptide meaning they can produce their own insulin

T1- low levels of c peptide

81
Q

what physical signs would indicate permanent neonatal diabetes

A

small babies
epilepsy
muscle weakness ( floppy baby )

82
Q

most common cause of chronic pancreatitis

A

alcohol

83
Q

cushings syndrome ?

A

Body produces excess cortisol
increased insulin resistance , reduced glucose uptake into peripheral tissues

84
Q

what occurs in pheochromocytoma

A

excess production of adrenaline
increased gluconeogenesis
decreased glucose uptake

85
Q

which group of drugs increase insulin resistance the most

A

steroids

86
Q

macrovascular complications of DM

A

-coronary artery disease
-peripheral ischemia
-stroke
-ht

87
Q

microvascular complications of DM

A

-peripheral neuropathy
- retinopathy
- kidney disease

88
Q

infection related complications of DM

A
  • UTI
  • pneumonia
    -skin and soft tissue infection
    -fungal infection
89
Q

Sglt2 inhibitors cause a side effect of ….

A

Glycosuria

90
Q

Common examples of sglt2 Inhibitors

A

Dapaglifozin
Cinaglifozin
Empaglifozin

91
Q

What are dpp4 inhibitors

A

They work to inhibit the dpp4 enzyme

92
Q

Pathiphysiology of dpp4 inhibitors

A

Glp1 aids in
Decrease in gastric emptying
Increase insulin release, decrease glucagon
Decreases appetite
Inhibits allow this to occur

93
Q

Common example of dpp4 inhibitor

A

Sitagliptib

94
Q

What medication commonly causes hypoglycaemia

A

Gliclazide

95
Q

What medication can cause UTI in women

A

Sglt2

96
Q

When managing dka what electrolyte should be managed closely

A

Potassium

endocrinology (6 decks)

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