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Phase 1c > Diabetes and Pituitary > Flashcards

Diabetes and Pituitary Flashcards

1
Q

How does Diabetes Mellitus type 1 cause hyperglycaemia

A

pancreatic islet beta cells destroyed (autoimmune response)
ABSOLUTE insulin insufficiency leading to lipolysis and ketogenesis

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2
Q

how does diabetes mellitus type 2 cause hyperglycaemia

A

reduced peripheral sensitivity to insulin
reduced insulin production (over time)

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3
Q

which alleles are associated with type 1 diabetes

A

HLA DR3/4 (hoes in la diabetic aRound 3/4)

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4
Q

risk factors for t2d

A

obesity, HTN, inactivity, disturbed lipids

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5
Q

typical patient profile T1DM

A

<20 yrs
FH autoimmune
presents with polyuria and polydipsia
presents with weight loss and fatigue

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6
Q

DKA symptoms and signs

A

nausea and vomiting
abdo pain
kussmaul breathing (deep hyperventilation)
sweet-smelling breath (ketonaemia)

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7
Q

typical patient profile T2DM

A

> 40 yrs
often asymptomatic
polyuria, polydipsia
RF: obesity, hypertension, south asian/ afro-carribean
examination: acathosis nigricans, symptoms of micro/macrovascular complications of T2DM

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8
Q

How is a diagnosis of DM made

A

symptomatic + 1 test
asymptomatic + 2 different tests on two different days

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9
Q

tests specific for T1DM

A

urine dip for glucose and ketones
specific antibodies are useful to distinguish between T1 and T2 but not necessary for T1 diagnosis
Anti-GAD (80%) and islet cell antibodies (ICA) (70-80%)

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10
Q

tests for type 1 and 2

A

n= normal, d= diabetes, prediabetes is between

random glucose (n <11.1, d=>11.1)
fasting glucose (n <5.5, d=> 7.0)
2hr post prandial glucose (n< 7.8, d =>11.1)
HbA1c (n <42 [6%], d=> 48 [6.5%]

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11
Q

HbA1c should not be used in

A

children or young ppl
pt suspected of having T1DM
pt with symptoms of diabetes <2 months
pt at high risk and acutely ill
pt taking meds that cause rapid glucose rise (steroids, antipsychotics)
pt with acute pancreatic damage including pancreatic surgery
presence of factors that influence HbA1c

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12
Q

Management of T1DM

A

insulin
personalised to pt
monitored daily using capillary glucose and over time using HbA1c (3mo)
basal-bolus regime = long acting (subcut insulin glargine o.d) + short acting (subcut insulin lispro and aspart pre-meal)

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13
Q

T2D management summary

A

lifestyle mods
glycaemic control
lipid management
bp management
antiplatelets

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14
Q

lifestyle mods T2DM management

A

diet
exercise
education

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15
Q

glycaemic control T2DM management

A

If HbA1c > 48 on lifestyle modification start metformin
if HbA1c >58 metformin + another drug (DPP-4i, pioglitazone, sulfonylurea and sglt-2i)
if HbA1c still >58:
metformin + sulfonylurea + (DPP-4i or pioglitazone)
metformin + sglt-2i + (pioglitazone or sulfonylurea)
insulin based treatment

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16
Q

BP management T2DM

A

all BP management starts with ACEi/ARB rather than CCB even if patient is black or over age 55

step 1: ACEi or ARB (ARB preferred for black pts)
step 2: add CCB or thiazide
step 3: ACEi/ARB + CCB + thiazide
check potassium, consult specialist
step 4: if K<4.5, add spironolactone. of K>4.5, add b-blocker

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17
Q

lipid management T2DM

A

atorvastatin 20 mg o.d if 10-year cardiovascular event risk =>10%
atorvastatin 80 mg o.d if IHD/CVD/PAD

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18
Q

antiplatelet management (T2DM)

A

Aspirin 75mg for patients with IHD/CVD/CVD

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19
Q

A 65yr old man present to his GP for bp check. ambulatory bp constantly above 140/90. PMH shows gout and T2DM for which he takes metformin and allopurinol. He is black

which is the most appropriate drug

A: Amlodipine
B: Bendroflumethiazide
C: Irbesartan
D: Ramipril
E: Spironolactone

A

The correct answer is irbesartan. This medication is an angiotensin II receptor blocker (A2RB).
It is used to manage hypertension in diabetic patients, as it has a renoprotective effect.Black African and Afro-Caribbean patients are prescribed calcium channel blockers first-line for hypertension.
However, as the patient is diabetic, ACE inhibitors/A2RBs are preferred due to their renoprotective effect. In black African and Afro-Caribbean patients, A2RBs are preferred over ACE inhibitors.

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20
Q

Complications for DM

A

Acute metabolic:
hypoglycaemia
DKA
hyperosmolar hyperglycaemic state

Long term microvascular:
retinopathy
neuropathy
nephropathy

long term macrovascular:
ischaemic heart disease
cerebrovascular disease
peripheral artery disease

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21
Q

plasma glucose hypoglycaemia

A

<3.6 mmol/L

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22
Q

cause of hypoglycaemia

A

inappropriate insulin regime
missed meals
drugs (sulfonylureas, SGLT-2 inhibitors etc)

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23
Q

signs of hypoglycaemia

A

tachycardia
tremor
sweating
pallor
anxiety
drowsiness
confusion
altered behaviour (aggression)
coma

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24
Q

Treatment of hypoglycaemia

A

give sugar
conscious - oral glucose and complex carb
impaired consciousness - IM glucagon 1mg
IV 10% dextrose infusion if glucagon fails to improve symptoms

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25
Q

A 20yr old man with T1DM brought into A+E following a seizure after a heavy night out yday. Injected insulin this morning but fell back asleep before eating. Drowsy in ambulance but now cannot be roused. Ambulance staff performed cap glucose which was 1.8 mmol

what is most urgent step in the management of this pt

A: IV insulin
B: IM glucagon
C: IL 0.9% saline
D: feed sugary foods
E: 500 mL 50% IV dextrose

A

This patient is experiencing severe hypoglycaemia with neuroglycopaenic effects of seizures and reduced consciousness

B: administration of IM glucagon 1mg is the initial management for hypoglycaemic patients with reduced consciousness. It will stimulate the liver to convert glycogen to glucose and release this into the blood therefore increase hepatic glucose output and increasing blood sugar levels. If this does not bring glucose >4mmol/L after 10 mins, IV dextrose at 10% or 20% should be administered

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26
Q

Is DKA more common T1 or T2

A

T1

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27
Q

DKA triad

A

hyperglycaemia, ketonaemia and metabolic acidosis

high levels of glucose cause polyuria which causes dehydration (treat with IV fluids)
high levels of ketones (treat with insulin) is highly acidic which leads to enzyme dysfunction resulting in coma and death

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28
Q

DKA treatment

A

rehydrate with IV fluids and reduce ketones with insulin

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29
Q

hyperosmolar hyperglycaemic state is more common in which type of diabetes

A

t2dm

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30
Q

difference in pathophysiology is DKA and HHS

A

DKA- absolute lack of insulin and increased stress hormones causing hyperglycaemia, ketonaemia and metabolic acidosis

HHS- hyperglycaemia but no ketonaemia as still some insulin to suppress ketogenesis

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31
Q

difference in causes dka and hhs

A

both- infection, other acute illness and non-adherence to diabetes meds

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32
Q

signs and symptoms DKA and HHS

A

dka- collapse/confusion, abdo pain, nausea, vomiting, kussmaul breathing, dehydration

hhs- same minus abdo pain

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33
Q

Ix results for DKA and HHS

A

dka: ketones > 3mmol/L, pH < 7.3, plasma glucose > 11

hhs: ketones <3mmol/L, pH normal, plasma glucose > 30

34
Q

Mx for dka and hhs

A

fluids started first (normal saline) + potassium chloride (is k+ < 5.5)
IV insulin after fluids and only when K+ not <3.5
include dextrose if fluids falls < 14
treat underlying cause

35
Q

13 yr old boy presents to a+e with generalised abdo pain. nauseous and vomited 4 times. progressively getting drowsier. groans when you palpate his abdomen

what is the most appropriate initial management option?

A. fixed rate insulin infusion
B. variable-rate insulin infusion
C. 10 U actrapid STAT
D. 10 ml 10% calcium gluconate
E. IL IV 5% dextrose

A

A. DKA treatment is IV fluids, fixed-rate insulin infusion

36
Q

background retinopathy: findings and management

A

blot and dot haemorrhages/ hard exudates

mx: improve glycaemic control

37
Q

pre-proliferative retinopathy: findings and management

A

background retinopathy findings + cotton wool spots
mx: pan-retinal laser photocoagulation

38
Q

proliferative retinopathy: signs and management

A

non-proliferative + new vessels on disk (neovascularisation)
neovascularisation is often associated with retinal detachment and vitreous haemorrhage which leads to vision loss
mx: pan-retinal laser photocoagulation

39
Q

maculopathy retinopathy: signs and management

A

hard exudates happens to be near macula
mx: intravitreal VEGF (vascular endothelial growth factor) inhibitors

40
Q

nephropathy signs, ix and mx

A

signs: oedema, polyuria, lethargy, hypertension

ix: 1st line urinalysis. increased ACR = microalbuminuria
gold standard - renal biopsy showing Kimmelstiel Wilson nodules

mx- ACEi/ARB (renoprotective)
- improve glycaemic control

41
Q

what do you find in peripheral neuropathy

A

glove and stocking distribution
loss of sensation esp feet
monofilament on lower limb exam
loss of ankle jerk/vibration sense/fractures (Charcot’s joint)

42
Q

what do you find in mononeuropathy

A

sudden motor loss usually eg wrist drop, foot drop, 3rd nerve palsy

43
Q

what do you find with autonomic neuropathy

A

difficulty swallowing, delayed gastric emptying, bladder dysfunction
postural hypotension
cardiac autonomic supply

44
Q

mx of neuropathy

A

glycaemic control
if painful use neuropathic pain agent (duloxetine, pregabalin, gabapentin)

45
Q

what is diabetes insipidus

A

inadequate secretion or sensitivity to vasopressin (ADH)
hypotonic polyuria

46
Q

2 types of diabetes insipidus

A

cranial - lack of vasopressin release from posterior pituitary

nephrogenic - collecting ducts insensitive to vasopressin

47
Q

causes of cranial and nephrogenic DI

A

cranial: pituitary tumour/surgery, traumatic brain injury, infection (meningitis), sarcoidosis/TB, subarachnoid haemorrhage
nephrogenic: lithium therapy, electrolyte imbalance (high Ca, low K), idiopathic, ureteric obstruction, inherited (AVPV2 gene)

48
Q

control of osmolality following water deprivation

A

water deprivation
increased serum osmolality
osmoreceptors stimulated
posterior pituitary releases vasopressin (ADH)
increased water reabsorption from renal collecting ducts
reduced urine volume, increased urine osmolality and reduced serum osmolality

49
Q

presentation for DI

A

polyuria (incl nocturia)
polydipsia
dehydration: tachycardia/reduced tissue turgor, dry mucous membranes
signs of the cause (eg bitemporal hemianopia)

50
Q

Ix for DI

A

U+Es (Ca/K for cause, Na (rarely raised), increased urea)
glucose to exclude DM
plasma osmolality = high
urine osmolality = low (>700 excludes DI)

51
Q

diagnostic test for types of DI

A

water deprivation test

water restricted fr 8 hrs
plasma and urine osmolality measured every hour
after 8 hrs give desmopressin and measure urine osmolality

52
Q

management of DI

A

treat the cause
cranial: intranasal desmopressin (should not drink large amounts of water on this med)
nephrogenic: thiazide diuretic, low salt/protein diet

53
Q

SIADH Ix

A

serum Na low
urine Osm high
urine Na high

54
Q

causes of SIADH

A

CNS: Subarachnoid haemorrhage, tumour, TB
pulmonary: pneumonia, bronchiectasis
malignancy: small cell lung cancer
drugs: carbamazepine, SSRI
idiopathic

55
Q

management for mild SIADH

A

treat cause
immediate fluid restrict for hyponatraemia
if ineffective: oral demeclocycline, IV vaptan

56
Q

normal serum sodium

A

135-145 mEg/L

57
Q

hypovolaemic hyponatraemia causes and management

A

causes: diarrhoea, vomiting, diuretics

management: IV fluids

58
Q

euvolaemic hyponatraemia causes and management

A

causes: SIADH, hypothyroidism, adrenal insufficiency

1.TFTS - if normal then
2) do a shorty synacthen test to look for adrenal insufficiency
3) if normal look for cause, eg drug history, breast exam, CXR to look for lung pathology, brain scan

59
Q

hypervolaemic hyponatraemia causes and Mx

A

causes: liver failure, renal failure, heart failure

Mx: fluid restrict

60
Q

what to do in case of urinary sodium <20

A

if very severe hyponatraemia (seizures, reduced consciousness), give slow hypertonic saline (too fast can cause central pontine myelinolysis)

61
Q

sodium levels for hypernatraemia

A

serum Na > 145 mEg/L

62
Q

causes of hypernatraemia

A

unreplaced water loss
- GI losses, sweat loss
- renal losses: osmotic diuresis (eg HHS), diabetes insipidus

sodium overload (rare)
- Cushing’s, primary aldosteronism, iatrogenic (hypertonic saline)

63
Q

hypernatraemia presentation

A

lethargy
irritability
thirst
signs of dehydration
confusion
coma
fits

64
Q

management of hypernatraemia

A

correct water deficit - 5% dextrose
correct ECF volume depletion - 0.9% saline
measure Na+ every 4-6hrs

65
Q

types of pituitary adenoma

A

non-functional
-do not release hormones
-test visual fields
- brain MRI with contrast

functional
- acromegaly (GH secreting)
- prolactinoma (prolactin secreting)
- Cushing’s disease (ACTH secreting)

pituitary adenomas of either type can compress other parts of the pituitary gland (hypopituitarism)

can compress optic chiasm causing bitemporal hemianopia

66
Q

what are the causes of hyperprolactinaemia

A

physiology:
-pregnancy
-breast feeding

pathological:
-prolactinoma
-other pituitary adenoma (stalk compression)
-primary hypothyroidism

67
Q

presentation of men with hyperprolactinaemia

A

loss of libido, erectile dysfunction, infertility, galactorrhoea (uncommon)

mass effect of tumour: headaches/visual field defect

68
Q

presentation of women with hyperprolactinaemia

A

galactorrhoea, secondary amenorrhoea/oligomenorrhoea, loss of libido, infertility

mass effect of tumour: headaches/visual field defect

69
Q

how does hyperprolactinaemia affect GnRH

A

high prolactin suppresses GnRH pulsatility

70
Q

Ix for hyperprolactinaemia

A

pregnancy tests (exclude physiological hyperprolactinaemia)
TFTs
Basal serum prolactin
MRI preferred imaging

71
Q

Prolactinoma management

A

1st line- Dopamine receptor (D2) agonists eg bromocriptine, cabergoline > reduce prolactin secretion and tumour size

2nd line- Surgery

72
Q

when to suspects T2DM in adult

A

if they present with persistent hyperglycaemia plus clinical features eg polydipsia, polyuria, blurred vision, unexplained weight loss, recurrent infections, tiredness, acanthosis nigricans

73
Q

what is persistent hyperglycaemia defined as

A

HbA1c of 48 mmol/mol (6.5%) or more
fasting glucose of 7.0+
random plasma glucose pf 11.1mmol/L or more in presence of clinical features

74
Q

how is t2dm diagnosed

A

symptomatic: one abnormal HbA1c or plasma glucose result

asymptomatic: repeat testing

75
Q

metformin use has increased risk of which vitamin deficiency

A

b12

76
Q

which drug class to offer diabetic patients with cvs disease

A

SGLT-2 inhibitor

77
Q

what class of drug are gliclazide, glimepiride, glipizide and tolbutamide

A

sulfonylureas
associated with hypoglycaemia, weight gain

78
Q

what class of drugs are alogliptin, linagliptin, sitagliptin, saxagliptin and vildagliptin

A

DPP-4 inhibitors

79
Q

what class of drugs are canagliflozin, dapagliflozin, empagkiflozin and ertygliflozin

A

SGLT2 inhibitor
promote weight loss, improve cardiovascular outcomes

80
Q

what class of drugs are dulaglutide, exenatide, liraglutide, lixisenatide and semaglutide

A

GLP-1
should be reserved for combination therapy when other options failed

Phase 1c (13 decks)

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