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Endocrinology > Diabetes Revision > Flashcards

Diabetes Revision Flashcards

(107 cards)

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1
Q

what are the 4 roles of insulin

A

facilitation of glucose transport into cells (via GLUT4)

stimulation of glycogenesis

inhibition of glycogenolysis

inhibition of gluconeogenesis

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2
Q

what effect does insulin have on fatty acids

A

encourages entry of fatty acids into adipose tissue

promotes chemical reactions that use fatty acids for triglyceride synthesis

inhibits lipolysis

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3
Q

what is insulins effect on amino acids

A

promotes uptake bu muscles and other tissues

stimulates protein synthesis

inhibits the degradation of proteins

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4
Q

what other than blood glucose can trigger the release of insulin

A

GI hormones (glucose dependent insulinotrophic peptide) stimulate release in anticipation of food being ingested

elevated blood amino acids

parasympathetic nervous system stimulates pancreas to secrete insulin (sympathetic decreases secretion e.g. adrenaline)

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5
Q

do babies of mother with diabetes have low birth weight

A

no tend to be higher than (have usual length)

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6
Q

what birth defect is seen in babies from diabetic mothers

A

spina bifida, anencephaly, caudal regression
abnormalities of the great vessels
increased fat and skeletal growth and organomegaly

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7
Q

what are the chances of a child developing diabetes if one parent or sibling has it

A

5-6%

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8
Q

diabetes is teratogenic, when is the risk highest

A

in the first 8 weeks

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9
Q

why does hyperglycaemia affect the foetus so much

A

as glucose can cross placenta but insulin cant

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10
Q

is metformin safe in pregnancy

A

yes

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11
Q

what are diabetic mothers at increased of during pregnancy

A

still birth and pre eclampsia

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12
Q

what vitamin should diabetic mothers take in pregnancy

A

folic acid

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13
Q

what four hormones increase blood glucose

A

glucagon, adrenaline, cortisol, growth hormone

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14
Q

what causes the release of adrenaline

A

sympathetic stimulation of the adrenal gland

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15
Q

how does adrenaline increase blood glucose

A

inhibits secretion of insulin, increases synthesis of glucose by inhibiting uptake

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16
Q

how does growth hormone increase blood glucose

A

stimulated in response to hypoglycaemia, stress, exercise, deep sleep

decreases glucose uptake, increases protein synthesis

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17
Q

why do tissues rely on fat metabolism in type 1DM

A

as glucose cant enter the cells

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18
Q

what type of diabetes is there amyloid deposition within islets

A

non insulin dependent diabetes (type 2)

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19
Q

what type of diabetes in insulinitis seen in

A

type 1- beta cell destruction

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20
Q

what are the diagnostic criteria for diabetes

A

Fasting plasma glucose >= 7.0 mmol/L

And/or a plasma glucose 2 hours after a 75g oral glucose load OR a random glucose >= 11.1 mmol/L

(one +ve test + symptoms= diagnosis or 2 + tests
Other terms:
Impaired glucose tolerance: 2 hour glucose between 7.0 and 11.1 mmol/L
Impaired fasting glucose: Fasting glucose between 6.0 and 7.0 mmol/L

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21
Q

what is gestational diabetes

A

diabetes that develops in pregnancy- resolves post natally

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22
Q

what is secondary diabetes

A

occurs secondary to other pathology (e.g. endocrinopathies- cushings, acromegaly. haemachromatosis, post pancreatitis, cystic fibrosis)

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23
Q

what is monogenic diabetes

A

due to mutation in gene regulating insulin secretion or action e.g.
maturity onset diabetes of the young

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24
Q

what are the chances of getting type 1 diabetes if your parent or twin has it

A

parent 25%
MZ twins 35%
siblings 6%

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25
what are the chances of getting type 2 diabetes if your parent or twin has it
MZ twins 80-90% DZ twins 30-40% sibling 3/4x risk of normal population if both parents have it then 70-80%
26
what type of diabetes is more genetic
type 2 (polygenic)
27
what would you expect insulin concentrations to be in a T1DM patient
low to none | some retain small amounts of insulin secretion
28
what would you expect insulin concentrations to be in a T2DM patient
normal to high
29
what antibodies are tested in T1DM/ young T2DM
GAD and IA-2
30
what HbA1c should T2DM aim for
53
31
what might precipitate T2DM presentation
infectino
32
what are the features of secondary diabetes
cushingoid bronze pigmentation (haemachromatosis) acanthosis
33
what should you ask for in PMH in T1DM
pancreatitis, autoimmune conditions, heavy alcohol consumption
34
what is the relationship between diabetes and corticosteroids
increase blood sugar
35
how do you calculate plasma osmolarity
2 x (plasma Na+ + plasma K+) + plasma urea + plasma glucose
36
what is the purpose of the anion gap
evalutaes metabolic acidosis (high= metabolic acidosis)
37
what is the anion gap formula
= (Na+ + K+) - (Cl- + HCO3-)
38
what has more microvascular complications T2 or T2 DM
Type 2
39
what causes the temporary blurry vision seen in diabetes
high blood sugar causes lens of eye to swell or blurry/ double vision in hypos
40
what can cause hypos in T1DM controlled with insulin
too much insulin, exercise not enough carb intake, alcohol., insulin, vomiting/ illness, coeliac, addisons (cortisol deficient), pituitary disease (reduce ACTH reduce cortisol)
41
even when not eating why when ill might T1DM need more insulin
as stress hormones released when ill will increase blood glucose
42
what is addisons
a primary renal disease
43
why are patients with pituitary disease are greater risk of hypos
as also release GH
44
what is the prevelance of coeliac in normal population and in diabetics
1 in 100 in pop | 1 in 20 in diabetics
45
what can reduce HbA1c
conditions that increase cell turnover
46
what can cause DKA
infection, surgical abdomen, silent MI
47
what is the management for DKA
ABC HX and exam for cause cardiac monitor + other monitoring if required IV fluids IV insulin (no bolus) watch K+, replace aggressively to prevent hypokalaemia and cardiac arrest
48
what is the relationship between insulin and potassium
insulin drives K+ into the cells and blood K can drop
49
should eggs be avoided if you have high cholesterol
no
50
what are the treatment steps for T2DM
1- metformin ``` 2- metformin + SGLT 2 metformin + GLP-1 metformin + DDP-4 inhibitor metformin + TZD metformin + insulin ``` (metformin - SGLT 2 - GLP- 1)
51
what shouldnt be given with TZDs
GLP-1 analogues and DPP-4 inhibitors
52
what does GLP-1 do
is secreted when food ingested- increases insulin secretion
53
what does DPP-4 do
breaks down GLP-1
54
when should metformin be avoided
patient with renal failure or lactic acidosis
55
what are the main side effects of SUs
hypos (especially in elderly as renal function decreases with age), weight gain, stimulates appetite
56
what do TZDs
promote fatty acid uptake and adipogenesis
57
should people with fatty liver disease be given TZD
yes reduce lipid content in the liver and act as insulin sensitisers
58
who should you not get TZDS to
elderly slim females, heart failurem osteoporosis, bladder cancer
59
what acts faster gliclazide or metformin
gliclazide 2-3 days | metformin 2-3 weeks
60
why do you not give fix mix insulin to young people
does not allow flexibility of meals
61
what do you recommend doing for T1DM ill patients
keep giving insulin, check BG and ketones, get carbs in the patient
62
what do you recommend a T1DM wanting to do exercise
eat before or reduce insulin dose
63
what does increased body Na predispose to
hypertension
64
what does the AGE pathway interfere with
proteoglycans, basement membranes, enzyme activity, cellular receptors, increases nucleic acid damage
65
what is the relevance of microalbuminuria
shows presence of albumin in urine, suggestive of diabetic nephropathy or hypertension
66
how do you manage micoralbuminuria
tackle hypertension if present - ace inhibitors
67
what bad effects might tight glycaemic control cause
hypos, weight gain, worsen vascular complications (ischaemia)
68
what are the stages of retinal grading
none, background, moderate, severe, proliferative
69
what is metabolic syndrome
glucose intolerance, impaired glucose tolerance or DM and/or insulin intolerance along with any two of: - impaired glucose regulation/ diabetes - insulin resistance - raised arterial BP - raised plasma triglycerides and/or low HDL - central obesity - microalbuminuria
70
how is insulin resistance linked to T2DM
is a predisposing factor
71
what is acromegaly and its link to diabetes
condition caused by excess GH, GH can also cause insulin resistance
72
what is cushings link to diabetes
excess cortisol can inhibit the uptake of glucose in the muscles- hyperglycaemia and insulin resistance
73
what names do SUs end in
ide (tolbutamide)
74
how do SUs work
action dependent on beta cell function (no use in T1DM), depolarise beta cells stimulating the release of insulin
75
what is the risk in SUs
hypos
76
what drug has an additive effect when used with SUs
biguanides (metformin)
77
what impedes the effectiveness of SUs
corticosteroids, thiazide diuretics
78
how does metformin cause weight loss
suppresses appetite | reduced absorption of glucose from the gut
79
how does glucose work
reduced absorption of glucose from the gut facilitates non insulin dependent entry of glucose into tissues inhibits liver gluconeogenesis enhances anaerobic glycolysis
80
what is the most serious side effect of metformin
lactic acidosis
81
what are the less serious side effects of metformin
nausea, vomiting, diarrhoea, metallic taste in the mouth
82
who should not get metformin
patients with: - renal failure - alcoholism - cirrhosis - chronic lung disease - cardiac failure - serious current illness - mitochondrial myopathy
83
what are glitazones
thiazolidinediones (TZDs)
84
how do TZDs work
bind to receptors within the cell nucleus and affect gene expression decreasing insulin resistance
85
what is the only glitazone licensed in the UK
pioglitazone
86
how do GLP-1 analogues work
mimic the actions GLP-1 which: - increases secretion of glucagon - decreases secretion of glucagon - increases insulin sensitivity in the peripheral tissues
87
how do DDP-4s work
inhibit DDP which inhibit GLP-1
88
what are the possible side effects of insulin
hypos hypers (overcompensation in response to slight hypo after dose- somogyi effect) reactions at injection site insulin resistance
89
what is the poyol/ aldose-reductase pathway
series of biochemical reactions which occur in the presence of raised intracellular glucose (esp in insulin dependent tissues) attempt to reduce glucose level in insulin dependent tissues that cannot regulate influx of glucose (insulin allows movement of glucose into the cell)
90
when does the poyol pathway become active
when there is very high intracellular glucose
91
what is the enzyme in the poyol pathway
aldose reductase
92
what is the role of aldose reductase
coverts glucose into sorbitol (sugar alcohol) | not all glucose is converted- some go into methylglyoxal and acetol (glycating sugars)
93
what does sorbitol do
exerts osmotic pressure on the cell (too large to diffuse out) which can cause damage to the cell so sorbitol dehydrogenase converts the sorbitol into fructose which diffuses out
94
what is AGE
advanced gylcation end products these are synthesised in the aldose reductase pathway- can cause damage to cells formed by glycating sugars and excess glucose binding to proteins
95
why is proteinuria done in diabetes
shows kidney damage either due to hypertension (diabetics more likely to get) or nephropathy
96
describe the process of nephropathy
the kidneys hypertrophy due to increased glomerular filtration rate- causes the afferent arteriole to dilate which leads to increased intraglomerular pressure = shearing forces which cause glomerular sclerosis (thickening of basement membrane and disruption of protein cross links) = kidney is no longer an effective filter
97
what is increased creatine a sign of in diabetes
renal failure
98
what pathway is responsible for the vascular complicationsin T2DM
poyol pathway (sorbitol-aldose-reductase pathway)
99
why is hypertension predisposed in diabetes
vasodilator effect of insulin blunted in diabetes action of insulin which increase BP- sodium and water reabsorption BMI of diabetic patients
100
patients with nephropathy should target their BP to be what
less than 130/80
101
how much more common is HPX in diabetics
2x normal population
102
what size monofilament for foot exams
10 g
103
how many areas are examined with monofilament on the feet
10 together
104
how does hyperglycaemic neuropathy present and resolve
discomfort in lower legs regain glycaemic control
105
when does acute painful neuropathy occur
rapid weight loss and poor glycaemic control (severe burning and contact sensitivity)
106
what causes retinopathy
capillary microangiopathy- proteins of vessel wall get more glycosylated, membrane thickens and becomes MORE permeable, increased transduction of protein which has a fibrous response with the retina damaging the retinas neural network small vessels also dilate causing micro-aneurysms also thrombosis of some capillaries - promotes neoangiogenesis which also damages the retinae
107
where do neuropathic food ulcers most commonly occur
high pressure areas e.g. metatarsal heads, big toe

Endocrinology (46 decks)

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