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Year 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

WHO definitions of DM

A

reduction in insulin action sufficient to cause level of hyperglycaemia which will result in microvascular pathology:

plasma glucose concentration (mmol/L):
-fasting >7.0 (x2 or + symptoms)
OR
-2h post glucose load (or random glucose) >11.1
\+
-HbA1c > 48 mmol/mol
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2
Q

WHO definitions of impaired glucose tolerance (non diabetic hyperglycaemia)

A

blood glucose is raised above normal but not enough to cause microvascular damage:

plasma glucose concentration (mmol/L):
-fasting <7.0
OR 
-2h post glucose load  7.8-11.1
\+
-HbA1c 42-47 mmol/mol
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3
Q

what does HbA1c represent

A

glycosylated haemoglobin (over a period of 3 months)

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4
Q

which kind of fat drives insulin resistance

A

abdominal obesity (visceral fat)

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5
Q

risk factors in insulin resistance diabetes

A 
family history
ethnicity (black african, south asian)
age
social deprivation
diet composition
lack of exercise
overweight and obesity (visceral)
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6
Q

what is the twin cycle hypothesis in DMT2

A

pre existing insulin resistance: positive calori balance leads to:

liver cycle: increase liver fat –> resistance to insulin suppression of hepatic glucose production –> increase plasma glucose/ increase insulin secretion

pancreas cycle: increase liver fat –> increase VLDV triglyceride –> taken up by beta cells in pancreas: increase islet triglyceride–> decrease acute insulin response to food –> increase in plasma glucose

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7
Q

def polyphagia

A

excessive hunger or increased appetite

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8
Q

clinical presentation of diabetes

A
  • symptoms of hyperglycaemia (thirst, polyuria, polyphagia, tiredness, weight loss + subacute Candida infection )
  • hyperglycaemic emergency (diabetic ketoacidsis or HHS)
  • diabetic complications (neuropathy, retinopathy, nephropathy, ACS, Stoke, PVD, erectile dysfunction)
  • asymptomatic (present at cardiovascular disease review, NDH or gestational diabetes annual review, age related health check, other acute illness
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9
Q

different types of insulin

A

quick acting: route: subcutaneous injection/infusion, IV infusion

slow acting: route: subcutaneous injection only
(can have added chemical compounds added to slow the absorption i.e. isoprene, lente, soluble)

bi-phasic (mixes of QA and SA, ratio of 25/75 or 30/70)

(basal analogues)

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10
Q

what increases insulin sensitivity

A

reduced calorie intake increased islet function
weight loss
exercise

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11
Q

what are the different drugs for type 2 diabetes

A
  • reduce insulin resistance (biguanides i.e. metformin and thiazolidenediones i.e. pioglitazone)
  • increase beta cell activity (sulphonylureas i.e. gliclazide and meglitinides i.e. nateglinide)
  • increase GLP1 activity (DPP4 inhibitors i.e. sitagliptin and ingrains, GLP1 agonists i.e. exenatide)
  • slow glucose absorption (acarbose: alpha-glucosidase inhibitor)
  • enhance glucose excretion (SGL2 inhibitors ie dapagliflozin)
  • insulin supplementation
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12
Q

main side effects of diabetes drugs

A
  • weight gain (all drugs that increase beta cell activity: sulphonylureas, meglitinides and insulin)
  • hypoglycaemia (all drugs that increase beta cell activity: sulphonylureas, meglitinides and insulin)
  • GI symptoms ie diarrhoea, nausea, abdo discomfort (metformin, incretins, acarbose)
  • weight loss (metformin, incretins, SGLT2 inhibitors)
  • random i.e. osteoporosis (pioglitazone), UTI (SGLT2 inhibitors)
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13
Q

what you check in your annual tests for diabetes

A 
lipids
UACR (urine albumin:creatinine ratio)
eGFR
foot exam
refer to diabetic eye screening program
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14
Q

risk factors for microvascular diabetic complications

A

insulin resistance
genes
proportional to hyperglycaemia and hypertension

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15
Q

how does visual loss occur in diabetic eye disease

A
  • capillary leakage

- capillary occlusion

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16
Q

stages of chronic kidney disease (CKD)

A

stage 1: microproteinuria: kidney damage with normal/increased GFR (GFR>90)
stage 2: mic/macroproteinuria: kidney damage with mid reduction GFR (GFR 60-90)
stage 3: macroproteinuria: moderate reduction GFR (GFR 30-59)
stage 4: macroproteineuria: severe reduction GFR (GFR 15-29)
stage 5: macroprotinuria: kidney failure ESRF (GFR<15)

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17
Q

minimising blindness in diabetes (primary, secondary prevention and salvage therapy)

A

primary prevention: BM control, BP control

secondary prevention: early detection of sight threatening retinopathy (retinal screening), ALLC (anti VEGF), BM and BP control

salvage therapy: vitrectomy

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18
Q

minimising end stage kidney disease in diabetes (primary, secondary prevention and salvage therapy)

A

primary prevention: BM control

secondary prevention: early detection of minimal nephropathy (UACR, eGFR), intensive BP control (<120/75, ACEi, A2RB), BM and vascular risk factor control

salvage therapy: diet, epo, ca, vitD, bicarbonate, early AVF, early transplantation, dialysis

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19
Q

minimising amputation in diabetes (primary, secondary prevention and salvage therapy)

A

primary prevention: BM control, lifestyle (smoking, exercise, alcohol)

secondary prevention (early identification of ‘at risk’ feet, footwear protection programme, BM and vascular risk factor control

salvage therapy: prompt multidisciplinary high risk foot team, revascularisation, local amputation

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20
Q

minimising adverse pregnancy outcomes in diabetes (primary, secondary prevention and salvage therapy)

A

primary prevention: pre-pregnancy BM control/folate

secondary prevention: intense retinal and renal screening/management

salage therapy: anomaly screening, foeti-placental monitoring

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21
Q

What is the link between between diabetes an cardiovascular disease?

A

Metabolic syndrome
Lifestyles
Subclinical inflammation (raised CRP, TNF-alpha, IL6)

Lipid excess and hyperglycaemia are toxic to beta cells
More?

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22
Q

Abnormalities of insulin secretion and action DMT2

A

Insulin resistance: associated with central obesity and intracellular triglyceride accumulation in muscle and liver (often NAFLD)

Pathophysiology: Decreased beta cell mass and islet amyloid deposition (it is cosecreted with insulin)

Hypersécrétion of insulin (blood insulin levels are higher than normal)
Insulin insufficiency: Increase gluconeogenesis and reduced glucose uptake by peripheral tissues

More

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23
Q

where does the parathyroid hormone act upon?

A
  • kidneys (simulates tubules for increased reabsorption)
  • bones (stimulates osteoblasts to release RANKL which stimulates osteoclasts to reproduce)
  • gut (increase absorption of calcium)
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24
Q

what are the effects of hypercalcaemia?

A

NS:

  • anxiety
  • depresion
  • cognitive change
  • mantal changes
  • lethargy
  • coma

muscles (mainly gut smooth muscles)

  • weakness
  • cramping
  • nausea, vomiting
  • anorexia

heart: arrhythmias

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25
Q

treatment of hypercalcaemia

A

fluids and Lasix + treat underlying cause

bisphosphonates +/- calcitonin

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26
Q

pathophysiology of T1DM

A

beta cell destruction (early viral trigger)

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27
Q

pathophysiology of T2DM

A

insulin resistance and beta cell dysfunction

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28
Q

diabetic treatment goals

A
  • minimise treatment side effects (hypo, weight gain)
  • as near normal glucose as possible
  • cardiovascular risk management
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29
Q

def acromegaly

A

excess growth hormone

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30
Q

DKA clinical features

A
  • hyperventilation (metabolic acidosis)
  • vomiting (ketosis + hyperglycaemic gastric statis)
  • dehydration (osmosis diuresis + vomiting)
  • hypotension w/ warm peripheries (dehydration and vasodilation)
  • decreased conscious level (hypotension - CV shock)
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31
Q

DKA + HHS - metabolic characteristics

A
  • H20 deficiency
  • Na+, K+ deficiency
  • hyperglycaemia
  • metabolic acidosis (only in DKA)
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32
Q

DKA presenting test results

A
  • hyperglycaemia, glycosuria
  • ketoanaemia, ketonuria
  • highish Na+ and K+
  • raised urea and creatinine (muscle breakdown + hypotensive AKI)
  • lipid rated
  • leucocytosis
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33
Q

how to treat DKA/HHS

A

(prevention: never stop basal insulin)

  • fluid resuscitation (for hypovolaemic shock)
  • airway protection if comatose GCS<9 (aspiration pneumonitis)
  • careful IV fluids (cerebral oedema: once BP is fine, don’t replace all fluids)
  • monitor/replace K+ (for fatal arrhythmias)
  • prophylaxis LMWH (for PE)
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34
Q

symptoms/signs of severe hypoglycaemia

A
  • adrenergic symptoms (sweating, trembling, hunger)

- neuroglycopenia (parasthesia, blurred vision, confusion)

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35
Q

treatment of severe hypoglycaemia

A
  • able to cooperate: lucozade
  • conscious but unable to cooperate: glucogel (buccal)
  • comatose: glucagon (sc, im, iv), IV glucose AVOID (venotoxic)
36
Q

clinical diagnosis of T1DM

A
  • hyperglycaemia (random glucose > 11mmol/L)
  • polyuria
  • polydipsia
  • weight loss
  • excessive tiredness
37
Q

causes of thyrotoxicosis

A
  • Grave’s disease
  • multi nodular goitre
  • solitary toxic nodules
  • drugs (interferon, amiodorone)
38
Q

what is Graves disease

pathophysiology

A

autoimmune process resulting in a stimulating ab to TSH receptor

39
Q

symptoms and signs of thyrotoxicosis

A
  • weight loss
  • good appetite
  • tachycardia
  • AF
  • sweating
  • heat intolerance
  • irritability
  • mood swings
  • frequent bowel action
  • increase goitre
  • lid retraction, lid lag
  • exothalamus of the eye/proptosis
  • peri orbital oedema
40
Q

what are the clinical features only found in Grave’s disease

A
  • thyroid acropachy
  • exopthalmos
  • pretibial myxoedema
  • ophthalmoplegia
41
Q

what is the treatment for thyrooxicosis

A
  • beta adrenergic blockers
  • antithyroid drugs (carbimazole, propylthiouracil)
  • radioactive iodine
  • surgery
42
Q

side effects of antithyroid drugs?

A 
rash, itching
arthralgia
nausea, vomiting
mild leucopenia
agranulocytosis
43
Q

clinical difference between euthyroid state and mild hypothyroidism

A
  • hoarse or deep voice
  • myalgia and muscle weakness
  • cold intolerance
  • constipation
44
Q

what is the pathophysiology of Hashimoto’s thyrotoiditis

A

T cell infiltration and thyroid tissue destruction : ab to TPO and thyroglobulin

45
Q

clinical features of hypothyroidism

A 
weight gain 
lethargy 
cold intolerance 
cool dry skin 
dry brittle hair, nail changes
constipation, heavy periods 
muscle cramps
46
Q

test of sub-clinical hypothyroidism

A

raised TSH, still maintained T3/T4

47
Q

treatment of hypothyroidism in elderly patients

A

if IHD: should be started on low dose (25microg) and then increased every 4 weeks

48
Q

red flag symptoms for thyroid cancer

A
  • nodule
  • dysphagia
  • neck pain
  • hoarseness
  • personal history of radiation to neck
  • FH of thyroid cancer
49
Q

main histological types of thyroid carcinomas

A 
papillary carcinoma
follicular carcinoma
anaplastic carcinoma
lymphoma
medullary cell carcinoma

(papillary and follicular carcinoma derived from follicular epithelial and good prognosis)

50
Q

thyroid cancer treatment

A
  • surgery (total thyroidectomy or lobectomy)
  • post-operative radioactive iodine treatment
  • thyroid hormone suppression (to suppress TSH so tumour growth is not stimulated)
51
Q

what is a goitre?

A

enlarged thyroid

52
Q

diffuse goitre: sign of what conditions?

A

Grave’s disease
Hypothyroidism (Hashimoto’s)
Colloid goitre (euthyroid)
Iodine deficiency; drugs (lithium)

53
Q

nodular goitre: sign of what conditions?

A

multi nodular goitre
solidary nodular
cysts

54
Q

FNA and cytology- diagnostic grading

A

Thy1: non diagnostic (inadequate cellularity): do test again
Thy2: benign (usually colloid nodules)
Thy3: indeterminate (“follicular lesion”: could be adenoma or carcinoma)
Thy4: suspicion of malignancy
Thy5: diagnostic of malignancy

55
Q

what is postpartum thyroiditis

A

transient following pregnancy
can cause hyper, hypo or both
up to 12 months post birth BUT usually between 3-4 months post birth
associated with T1DM and TPO ab

56
Q

pathophysiology of sheehan syndrome

A

pituitary infarction following postpartum haemorrhage leading to hypothyroidism

57
Q

which drug can induce both hypo and hyperthyroidism

A

amiodorone

58
Q

low T4

high TSH

A

primary hypothyroidism

59
Q

high T4

low TSH

A

primary hyperthyroidism

60
Q

low TSH

low T4

A

TSH deficiency (secondary hypo)

61
Q

high TSH

normal T4

A

subclinical hypothyroidism

OR poor compliance with thyroxine

62
Q

what treatment for hypertension in diabetes

A
  1. ACEi/ARB
    • Ca channel blocker/diuretic
    • ca channel blocker/diuretic
63
Q

BMI weight classes

A 
heathy weigh: 18.5-24.9
overweight: 25-29.9
obesity I: 30-34.9
obesity II: 35-39.9
obesity III: 40+
64
Q

when do you consider referring an obese patient to specialist series (for their obesity)

A
  • underlying causes of obesity needs assessing
  • complex disease states and/or needs that can’t be managed in tier 2
  • conventional treatment unsuccessful
  • drug treatment being considered for BMI>50
  • specialist intervention may be needed (i.e. low calorie diet)
  • surgery being considered
65
Q

what drug treatment for obesity, and at what point should you consider it? How long should you use it for?

A

orlistat, only if:

  • BMI>28 w/ risk factors
  • BMI>30
  • continue therapy beyond 3 months only if person has lost >5% of initial body weight
  • naltrexone-buproprion
66
Q

when can you consider bariatric surgery for obesity treatment?

A
  • BMI>40, or 35>BMI>40 + other significant disease that could be improved if they lost weight
  • all non surgical measures have been tried and not achieved
  • will/has received intensive management in tier 3 services
  • fit for anaesthesia and surged
  • commits to long term follow up
67
Q

what are the main actions of stimulated glucocorticoids

A 
gluconeogenesis
glycogen deposits 
protein catabolism 
fat deposits 
sodium retention 
potassium loss 
free water clearance
uric acid production 
circulating neutrophils
68
Q

what are the main effects when glucocorticoids are inhibited

A 
protein synthesis 
host respond to infection 
lymphocyte transformation 
delayed hypersensitivity 
circulating lymphocytes and neutrophils
69
Q

causes of cushing syndrome

A
  • pituitary dependent (Cushing’s disease)
  • ectopic ACTH producing tumours
  • adrenal carcinoma/adenoma
  • exogenous steroids
70
Q

symptoms of cushion’s syndrome?

A
  • change of appearance
  • weight gain (central)
  • hair growth/acne
  • think skin/easy bruising
  • depression
  • psychosis
  • insomnia
  • muscular weakness
  • back pain
  • amenorrhoae/gomenorrhoea
  • poor libido
  • growth arrest in children
  • polyuria/polydipsia
71
Q

signs in Cushing’s syndrome?

A
  • moon face
  • hypertension
  • buffalo hump
  • central obesity
  • depression/psychosis
  • glycosuria
  • oedema
  • hirsutism
  • acne
  • bruising
  • poor wound healing
  • skin infection
  • striae
  • pigmentation
  • osteoporosis
  • proximal muscle wasting
72
Q

diagnosis of cushion’s syndrome

A
  • 48h low dose dexamethasone tests (suppress cortisol production normally but no in Cushing’s disease or tumours)
  • 24h urinary free cortisol measurement
73
Q

adrenal gland blood supply

A
  • superior suprarenal artery (from inferior phrenic)
  • middle suprarenal artery (abdominal aorta)
  • inferior suprarenal artery (renal artery)
74
Q

venous drainage of adrenal gland

A

right suprarenal vein –> inf vena cava

left suprarenal vein –> left renal vein

75
Q

when is serum cortisol the lowest

A

evenings

76
Q

how do you define adrenal crisis

A

adrenal insufficient (low levels of cortisol) sick patient, hypotension, hyponatraemia

77
Q

Causes of primary hypoadrenalism

A 
Autoimmune disease 
TB 
Surgical removal
Haemorrhage/ infarction 
Infiltration (malignant destruction/amyloid)
Schilder’s disease
78
Q

Symptômes of Addison’s disease

A 
Weight loss
Malaise
Weakness
Fever
Anorexia
Nausea/vomiting 
Diarrhoea/constipation
Dépression 
Confusion 
Myalgia
Syncope (postural hypotension)
79
Q

Signs of Addison’s disease

A 
Loss of weight 
General wasting 
Pigmentation 
Postural hypotension 
Loss of body hair
Dehydration
hyponatraemia, hyperkalaemia and azotaemia
80
Q

what is addison’s disease?

A

destruction of entire adrenal cortex (corticosteroids, mineralicorticoids and sex steroids are reduced)

81
Q

how does aldosterone affect potassium, sodium, bicarb, H20 and BP

A

promotes sodium reabsorption and potassium excretion in the kidney
promotes regeneration of bicarb
H20: increase reabsorption
BP: increase BP

82
Q

what are the hormones produced by the pituitary?

A

anterior: GnRH, GHRH, somatostatin, dopamine, TRH, CRH
posterior: vasopressin, oxytocin

83
Q

what conditions result from pituitary deficiencies/excess

A 
prolactinoma
acromegaly
cushion's disease
Nelson syndrome
non functional tumours
craniopharngioma
84
Q

types of diabetes insipidus

A
  • cranial DI: too little vasopressin produced by the kidney
  • nephrotic DI: kidney become insensitive to vasopressin and does not make aquaporin channels to reabsorb H20 from collecting duct
85
Q

how do you diagnose diabetes insipidus

A

water restriction test and measure Na (would be hypernatraemic)

86
Q

embryological layers of the medulla

A

cortex: mesoderm
medulla: neuroectoderm

87
Q

treatment of Cushing’s syndrome

A

surgery

drugs: metyrapone, ketoconazole

Year 3 (7 decks)

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