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4 - Med > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is type 1 diabetes ? briefly

A

insulin deficiency form autoimmune destruction of insulin-secreting pancreatic beta cells

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2
Q

diabetes definition. what are the 3 values ?

A
  • Random plasma glucose > 11.1mol/L
  • Fasting plasma glucose > 7.0mmol/L
  • HbA1C > 48 mmol/mol
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3
Q

describe the C-peptide levels in T1DM patient ?

A

C-peptide levels are typically low in T1DM patients

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4
Q

what are the 4 ts of DM ?

A

toilet, thin, tired, thirsty

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5
Q

describe the features of T1DM and briefly what pathophys causes these symptoms ?

A

thirst, polyuria, weight loss, fatigue, blurred vision
- pee glucose out (glucose pulls water with it whoever it goes) => more dehydration
- hyperglycaemia => neuropathy, blurred vision, damaged blood vessels

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6
Q

what does complete lack of insulin in body cause ? long answer

A

body is in perceived starved state
- fat breakdown and formation of glycerol + FFA => oxidised to ketone bodes in liver => hyperglycaemia and rising ketone bodies
- glucose + ketones escape in urine => osmotic diarises => reduces circulating blood vol
- rising ketones cause vomiting

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7
Q

general mx of DKA ?

A
  • rehydration, insulin, replacement of electrolytes (K+)
  • then treat underlying cause
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8
Q

general Mx of T1DM ongoing ?

A

insulin deficiency so treatment aims to keep blood glucose as normal as possible
- calculate carb content of meal to calculate insulin dose
- insulin therapy tries to mimic normal physiology

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9
Q

describe basal bolus insulin therapy ?

A

normally low level insulin secreted by beta cells to balance effects of glucagon/cortisol (patient should take background dose)

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10
Q

describe insulin therapy in T2DM ?

A

basal insulin: inject once at night - adjust insulin dose themselves based on fasting glucose (but this does not cover exercise or meals)
- before sleep reduces chance of hypoglycaemia

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11
Q

when does ketogenesis normally occur ? why useful

A

when there is insufficient glucose supply + glycogen stores exhausted (prolonged fasting)
- ketones can cross BBB => brain can use as fuel

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12
Q

where does ketogenesis occur ?

A

liver takes fatty acids and converts them to ketones (water soluble fatty acids)

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13
Q

what blood gas is DKA ?

A

life-threatening metabolic acidosis (diabeteic ketoacidosis)

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14
Q

what is initial counter regulatory mechanism to the acidosis in DKA ?

A

initially kidney makes enough bicarb to contract ketones but eventually => ketoacidosis

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15
Q

what does the excessive hyperglycaemia in DKA cause ? effect on kidneys

A

hyperglycaemia overwhelms the kidney => glucose filtered into urine => draws water with it (osmotic diuresis) => polyuria => severe dehydration => excessive thirst (polydipsia)

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16
Q

describe insulins affect on K ? what happens with insulin started ?

A

insulin normally drives K into cells
- when insulin treatment started => increase K in cells => severe hypokalaemia => fatal arrhythmias

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17
Q

what are the different pathophysiological process going on in DKA ? (5)

A
  • hyperglycaemia
  • dehydration
  • ketosis
  • metabolic acidosis
  • K imbalance
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18
Q

DKA RF ? (2)

A
  • inappropriate/inadequate insulin therapy
  • infection
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19
Q

DKA Ix ? (4)

A
  • VBG
  • Blood ketones
  • capillary blood glucose
  • FBC
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20
Q

DKA Mx ?

A

FIGPICK
- Fluids
- Insulin
- glucose (fluids with dextrose infusion)
- Potassium replacement
- infections (treatment underlying trigger)
- Chart (fluid balance)
- Ketones

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21
Q

what values indicate impaired glucose tolerance ? (2)

A
  • fasting plasma < 7
  • OGTT 2 hr value 7.8<x<11.1
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22
Q

type 2 diabetes pathophysiology ?

A

repeated exposure to glucose + insulin => cells become resistant to insulin => more insulin required => pancreas becomes fatigued + damaged => produce less insulin => chronic hyperglycaemia => micro/macrovascular complications + infections
(insulin deficiency + resistance)

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23
Q

what is pre-diabetes ?

A

heading towards diabetes, is reversible
- high HbA1c, impaired fasting glucose, impaired glucose tolerance

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24
Q

what investigations would you do for diabetes presentaiton ? results ?

A
  • oral glucose tolerance tests: fasting plasma glucose, give 75g glucose drink, measure plasma glucose 2 hrs later
  • HbA1c: >48
  • random glucose >11
  • fasting glucose >7
  • OGTT 2 hr resut >11
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25
Q

T2DM Mx ?

A

dietary modification, exercise, weight loss, monitor complications (retinopathy, kidney disease, diabetic foot)
- drug therapy

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26
Q

describe overall T2DM drug therapy ?

A
  • first line: metformin
  • then add: sulphonlyurea, DPP4 inhibitor, SGLT2 inhibitor
  • third line: triple therapy with metformin + 2 secondary drugs
  • add insulin therapy
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27
Q

what HbA1c is dual therapy commenced for T2DM ?

A

> 58 mmol/mol

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28
Q

what are incretins ? what do they act on (2)

A

hormones secreted by intestiatnl endocrine cells that act on stomach to delay gastric emptying
- act on beta cells to increase insulin production
- act on liver to reduce glucagon release

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29
Q

what is HHS ? describe a bit. how different form DKA ?

A

hyperosmolar hyperglycaemia state
- serious complication of (mainly) T2DM involving hyperglycaemia, hyperosmolaltiy (high solute), vol depletion in the absence of significant ketoacidosis

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30
Q

what prevents HHS from becoming DKA ?

A

low level insulin suppresses lipolysis + ketogenesis => prevents DKA

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31
Q

what causes HHS ?

A

results from insulin deficiency and high conc of counter regulatory hormones (glucagon, cortisol, GH)
- blood sugar too high for too long => severe dehydration + confusion

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32
Q

HHS RF ?

A
  • infection
  • inadequate insulin
  • MI in diabetic patients
  • restricted water
    (occurs mostly in older people with T2DM, often initial presentaiton)
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33
Q

HHS Px ?

A

about 1 week Hx
- polyuria, polydyspisa, weakness, weight loss, tachycardia, hypotension, acute cognitive impairment

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34
Q

HHS Ix ? and results (6)

A
  • Blood glucose (high)
  • blood ketones (low)
  • VBG (mild acidosis)
  • serum osmolatliy (high)
  • FBC (leukocytosis)
  • electrolytes (low K)
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35
Q

HHS Mx ? (4)

A
  • IV fluids + K replacement
  • IV insulin
  • treat acute illness (infection)
  • thromboprophylaxis (LMWH)
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36
Q

when do you give the low dose IV insulin in HHS Mx ? why ?

A

must be adequately hydrated before insulin administration because insulin drives glucose into cell => water follows
- what little water remained IV => intracellular => circulatory failure => cardiac arrest

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37
Q

HHS treatment complications ? (2)

A
  • insulin related hypoglycaemia
  • treatment related hypokalaemia
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38
Q

name some compactions of established diabetes ?

A
  • vascular disease: chief cause of death
  • nephropathy
  • diabetic retinopathy
  • cataracts
  • diabetic foot
  • diabetic neuropathy
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39
Q

describe a bit about diabetic neuropathy ?

A

loss of pain sensation => increase mechanical stress => repeated joint injury
- symmetric sensory polyneuropathy (glove + stocking numbers, tingling + pain - worse at night)

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40
Q

what counts as hypoglycaemia ?

A

plasm glucose < 3mmol/L

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41
Q

which drugs are usually responsible for hypos in a known diabetic ?

A

insulin or sulphonylurea
(increased activity, missed meal, accidental/non-accidental overdose)

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42
Q

causes of hypos in a non-diabetic ?

A
  • pituitary insufficiency
  • Addisons disease (adrenal insufficiency)
  • insulinoma (islet cell tumour)
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43
Q

what is hyperthyroidism ?

A

increased production of thyroid hormone by thyroid gland

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44
Q

main causes of hyperthyroidism ? (3) most common

A
  • graves disease (most common)
  • toxic multi nodular goitre
  • iodine excess
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45
Q

complications of hyperthyroidism ? (5)

A
  • HF (cardiomyopathy)
  • angina
  • AF
  • bone mineral loss
  • thyroid storm
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46
Q

what is primary hyperthyroidism ? due to pathology where ? describe TSH, T3 and T4 levels

A

due to thyroid pathology, thyroid producing excessive quantities
- low TSH
- high T3/T4

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47
Q

what is secondary hyperthyroidism ? due to pathology where ? describe TSH, T3 and T4 levels

A

due to hypothalamic or pituitary pathology, thyroid makes excessive thyroid hormone as a result of over stimulation of TSH
- High TSH
- High T3/T4

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48
Q

features/presentation of hyperthyroidism ? (8)

A
  • anxiety, irritabilty
  • sweating, heat intolerance
  • weight loss
  • fatigue
  • frequent loose stolls
  • tachycardia
  • sexual dysfunction
  • oligomenorrhoea
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49
Q

what is the general Mx for hyperthyroidism ? (4) think complication

A
  • BB for initial sx mx (lower HR => reduce AF risk)
  • carbimazole
  • radioactive iodine
  • surgery
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50
Q

What is graves disease ?

A

primary hyperthyroidism
- autoimmune condition where RSH antibodies cause primary hyperthyroidism

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51
Q

what are TSh antibodies ? with what condition are they associated ? what do they cause ?

A

graves disease
- They are abnormal antibodies produced by immune system that mimic TSH => stimulate thyroid receptors => hyperthyroidism (+thyroid hypertrophy + hyperplasia)

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52
Q

what % of ppl with graves disease present with eye disease ? what is the biggest RF for this ?

A

thyroid eye disease seen in 25-50% of ppl with graves disease
- smoking is biggest RF

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53
Q

Mx of graves related eye disease ?

A

Stop smoking !
- if severe disease: high dose steroids (IV Methylpred)

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54
Q

Graves disease oe (4)

A
  • exophthalmos
  • pretibial myxoedema
  • diffuse goitre
  • acropathy
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55
Q

describe these ? associated with what condition ?
- exophthalmos
- pretibial myxoedema
- acropathy

A

graves disease
- exophthalmos: budging of eyes due to inflam, swelling and hypertrophy)
- pretibial myxoedema: skin reaction to TSH receptor Ab => mucin deposits => discolouration)
- acropathy: swelling of hands, clubbing of fingers

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56
Q

what Ix for graves disease ? what would they show ?

A

primary hyperthyroidism
- TFT: low TSH, high T3/4
- TSH receptor Ab (+ve)

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57
Q

patient present with thyroid nodules. what is first line Ix ?

A

US
(and check TSH)

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58
Q

graves disease Mx ?

A
  • prolonged antithyroid drug therapy (carbimazole - normal thyroid function after 4-8 weeks, then titrate down)
  • BB initially
  • OR radioactive iodine + Pred OR thyroid surgery + levothyroxine
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59
Q

causes of diffuse goitre ? (3)

A
  • iodine deficiency
  • de quervains
  • autoimmune (graves, hashimotos)
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60
Q

causes of nodular goitre ? (1)

A
  • multi nodular goitre (patients are usually euthyroid)
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61
Q

what is De Quervains thyroiditis ? another name ? describe it ?

A

subacute granulomatous thyroiditis
- temporary inflame of third gland characterised by triphasic course
- presume to be viral

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62
Q

which thyroid disease has triphasic course ? describe the phases

A

De Quervains thyroiditis
- transient thyrotoxicosis (due to thyroid follicular damage)
- hypo phase (as TSH levels fall due to -ve feedback)
- euthyroidism

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63
Q

De Quervains thyroiditis presentation ?

A
  • initial thyrotoxic phase: thyroid pain, high T3/4, systemic illness like flu
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64
Q

De Quervains thyroiditis Ix and results ?

A
  • thyroid US
  • low TSH
  • high T3/4
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65
Q

De Quervains thyroiditis mx ?

A

sorts itself out so just supportive care with NSAIDS (thyroid pain), BB (for tachycardia) + levothyroxine (for sx of hypothyroidism)

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66
Q

what is thyroid storm ? another name ?

A

thyrotoxicosis/thyroid storm
- life threatening condition associated with un or underrated hyperthyroidism

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67
Q

thyrotoxicosis/thyroid storm px ?

A
  • tachycardia cardia
  • High BP
  • high body temp
  • High RR
  • agitation
  • confusion
  • goitrethyrotoxicosis/thyroid storm
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68
Q

thyrotoxicosis/thyroid storm Mx ?

A

do not wait for Ix results if urgent tx needed, confirm with technetium uptake if possible
- high dose antithyroid drugs (carbimazole)
- corticosteroids (prednisolone)
- BB blockers
- supportive care
if left untreated => high mortality rate

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69
Q

what is most common thyroid cancer aetiology ?

A

papillary most common (60%)

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70
Q

how does thyroid cancer most commonly present ?

A

asymptomatic thyroid nodule detected by palpation or US in a woman in her 30s or 40s
- uncommon: hoarseness, dysnpoea, dysphagia

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71
Q

how is thyroid cancer diagnosis made ?

A

fine needle aspiration

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72
Q

thyroid cancer treatment ?

A
  • total thyroidectomy + radioactive iodine ablation + TSH suppression (levothyroxine)
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73
Q

what is hypothyroidism ?

A

inadequate output of thyroid hormones by thyroid gland

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74
Q

name causes of primary hypothyroidism ? (4) main cause

A
  • autoimmune (primary atrophic hypo, hashimotos - most common)
  • post thyroidectomy
  • drug induced (treatment of hyper can cause hypo - carbimazole, radioactive iodine, surgery)
  • iodine deficiency
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75
Q

name cause of secondary hypothyroidism

A

hypopituitarism (v rare)

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76
Q

hypothyroidism presentaiton ? (9)

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair, hair loss
  • fluid retention (oedema, ascites)
  • heavy or irregular periods
  • constipation
  • goitre
  • eyelid oedema
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77
Q

hypothyroidism RF ? (6)

A
  • female
  • meddle age
  • iodine deficiency
  • treatment for thyroid disease
  • FHx of autoimmune thyroiditis
  • amiodarone use
78
Q

hypothyroidism Ix and results ? primary and secondary ?

A

thyroid hormones abnormally low:
- primary (absence/dysfucntion of thyroid): High TSH, low T3/4
- secondary (pituitary/hypothalammic dysfunction): Los TSH, Low T3/4

79
Q

hypothyroidism Mx ?

A

replace thyroid hormone with oral levothyroxine (synthetic T4 which is metabolised to T3 in body)
- titrate until normal TSH levels

80
Q

hypothyroidism pregnancy associated complications

A
  • eclampsia
  • anaemia
  • prematurity
  • low birth weight
81
Q

what is hashimotos thyroiditis ?

A

primary autoimmune hypothyroidism
- caused by autoimmune inflam of thyroid gland
- initially causes goitre => thyroid gland atrophy

82
Q

hashimotos thyroiditis associated with what antibody ?

A

anti-TPO and antithyoglobulin Ab

83
Q

hashimotos thyroiditis pathophys ?

A

immune system makes Ab that attack thyroid gland => large WBC build up in thyroid => thyroid damage => can’t amen sufficient thyroid hormones

84
Q

hashimotos thyroiditis Ix ? and results (3)

A

autoimmune primary hypothyroidism
- high TSH
- low T3/4
- thyroid peroxidase Ab (+ve)

85
Q

hashimotos thyroiditis Mx ?

A

levothyroxine

86
Q

what produces parathyroid hormone ? in response to what ?

A

chief cells in the parathyroid glands produce parathyroid hormone in response to hypocalcamiea

87
Q

what does PTH affect ?

A

acts to raise blood calcium
- increase osteoclast activity
- increase calcium absorption form gut (increase activity of Vit D)
- increase calcium reabsorption form kidneys

88
Q

hyperparathyroidism presentation ?

A
  • renal stones
  • painful bones (+fractures)
  • abdominal moans (constipation, N+V)
  • psychiatric groans (depression)
89
Q

primary hyperparathyroidism. caused by what ? describe the PTH and Ca levels

A

(usually solitary adenoma) caused by uncontrolled PTH produced by tumour of parathyroid gland
- PTH high
- Calcium low

90
Q

solitary adenoma mx ? what type of hyperparathyroidism is it ?

A

primary hyperparathyroidism
- treatment: surgical removal of tumour

91
Q

secondary hyperparathyroidism. caused by what ? describe the PTH and Ca levels ?

A

(low vit D of CKD) => reduced Ca absorption from intestine, kidneys and bones => hypocalcaemia => high PTH => parathyroid hyperplasia
- PTH high
- Ca low or normal

92
Q

tertiary hyperparathyroidism. caused by what ? describe the PTH and Ca levels ?

A

when secondary continues for long rime => parathyroid gland hyperplasia => increase baseline PTH => when corrected, parathyroid gland overactive => hypercalcaemia
- PTH high
- Ca High

93
Q

what is hypoparathyroidism ? aetiology ? describe Ca and Pi levels

A

relative or absolute deficiency of PTH => low serum Ca + high serum phosphate
- mostly post surgical

94
Q

what ECG change may be seen in hypoparathyroidism

A

prolonged QT interval (low serum Ca)

95
Q

hypoparathyroidism Mx ?

A

IV Ca + magnesium sulphate (if low Mg)

96
Q

hypercalacaemia signs and symptoms ? (4)

A

bones, shoes, grounds, psychic moans

97
Q

hypercalacaemia causes ?

A

most commonly malignancy (bone mets, myeloma or primary hyperparathyroidism (parathyroid demos most common)
- vit D intoxication
- tertiary hyperparathyroidism

98
Q

what is malignancy associated hypercalcaemia ?

A

most common metabolic abnormality in cancer patients (+ poor prognostic factor)
- causes: PTH-related protein produced by the tumour, local osteolysis

99
Q

malignancy associated hypercalcaemia mx ?

A
  • aggressive rehydration
  • bisphosphonates
  • continue mx of underlying cause: chemo for cancer
100
Q

hypocalcaemia may be an artefact of what ?

A

may be artefact of hypoalbuminaemia

101
Q

hypocalcaemia px ?

A

campus, perioral numbness
- if severe: seizures - spasms

102
Q

hypocalcaemia causes ?

A
  • CKD
  • hypoparathyroidism
  • hypomagnesaemia
  • vit d deficiency
103
Q

hypocalcaemia mx ?

A

calcium supplement, with daily plasma Ca2+ checks

104
Q

what is cushings syndrome ?

A

manifestation of pathological hypercortisolism from any cause
- glucocorticoid excess + loss of normal HPA axis + loss of circadian rhythm of cortisol release

105
Q

what is cushings disease ?

A

pituitary adenoma secretes excessive ACTH => cushings syndrome
- bilateral adrenal hyperplasia

106
Q

causes of cushings syndrome ? (4)

A

CAPE
- cushings disease
- adrenal adenoma
- paraneoplastic
- exogenous
(can be ACTH dependant or independent)

107
Q

features of cushings syndrome ? (5)

A
  • round in middle/central obesity
  • thin limbs, proximal limb muscle wasting
  • moon face
  • abdominal straie
  • menstrual abnormailites
108
Q

some other signs of cushings syndrome ?

A

high stress hormone causes:
- hypertension
- cardiac hypertrophy
- hyperglycaemia (+DM)
- depression + insomnia
- osteoporosis

109
Q
A
110
Q

Dexamethasone suppression test (DST): what result would indicate cushings syndrome ?

A

low dose: when cortisol level not suppressed => cushings syndrome

111
Q

Dexamethasone suppression test (DST): what would these results indicate on high dose (after already abnormal low dose test)
- Cortisol suppressed ?
- High cortisol + low ACTH ?
- high cortisol + high ACTH ?

A

high dose (after already abnormal low dose test): cortisol suppressed => cushings disease
- cortisol high + ACTH low => adrenal adenoma
- high cortisol + high ACTH => ectopic ACTH

112
Q

if cause of cushings syndrome is adrenal adenoma, what electrolytes might be impacted ?

A

low potassium if aldosterone also secreted by adrenal adenoma

113
Q

what is Addisons disease ?

A

primary adrenal insufficiency
- lean, tanned, tired, tearful

114
Q

what is adrenal insufficiency ?

A

where adrenals don’t produce enough steroid hormones (particularly cortisol and aldosterone)

115
Q

describe primary adrenal insufficiency ? cause ?

A

Addisons disease
- adrenal glands damaged and adrenal cortex destruction => low aldosterone + low cortisol secretion
(usually autoimmune)

116
Q

how does aldosterone affect Na + K ? so how they be affected in adrenal insufficiency ?

A

increased aldosterone => Na absorption + K excretion
- so Addisons: hyponatraemia, hyperkalaemia

117
Q

describe the train findings in addisonian crisis ?

A
  • hyponatraemia
  • hyperkalaemia
  • hypoglycaemia
    ( low mineralocorticoid => low Na + high K)
    (low glucose due to low cortisol)
118
Q

describe secondary adrenal insufficiency ? causes ? (4)

A

inadequate ACTH => low cortisol
- due to surgical removal of pituitary tumour, infection, loss of blood flow to pituitary, radiotherapy)

119
Q

describe tertiary adrenal insufficiency ? causes

A

inadequate CRH
(due to long term oral steroids => hypothalamic suppression)

120
Q

signs and symptoms of adrenal insufficiency ?

A

(lean, tanned, tired, tearful)
- fatigue, nausea, cramps, abdo pain, reduced libido

121
Q

what causes the “tanned” symptom of Addisons

A

bronze hyperpigmentation
- ACTH => increased melanin from melanocytes

122
Q

what investigations for adrenal insufficiency ?

A
  • U+E (hyponatraemia, hyperkalaemia)
  • early morning cortisol
  • ACTH (high in primary, low in secondary)
  • short synacthen test (diagnostic)
123
Q

describe the short synacthen test ? to diagnose what ?

A

help diagnosis Addisons
- given synacthen (artificial ACTH) => if cortisol level fails to rise => primary insufficiency (Addisons)

124
Q

Addisons Mx ? (2)

A

replacement with steroids titrated to signs, symptoms + electrolytes
- hydrocortisone (glucocorticoid to replace cortisol)
- Fludrocortisone (mineralocorticoid to replace aldosterone)

125
Q

what is addisonian crisis ?

A

acute presentaiton of severe Addisons, life threatening

126
Q

addisonian crisis presentation ? (6)

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponaetraemia
  • hyperkalaemia
  • very unwell
127
Q

addisonian crisis Mx ? (4)

A

don’t wait for investigations as is life threatening
- parenteral steroids (IV hydrocortisone)
- IV fluid resuscitation
- correct hypoglycaemia
- monitor fluid + electrolyte balance

128
Q

how does excess aldosterone affect sodium, water and renin ?

A

increase sodium
water retention
reduce renin release

129
Q

how does aldosterone affect electrolyte levels in the kidneys ? state where each is affected

A
  • increase Na reabsorption in distal tubule
  • increase K secretion in distal tubule
  • increase H+ secretion in collecting ducts
130
Q

what is primary hyperaldosteroneism ? name the causes ? main cause ?

A

adrenal gland produce too much aldosterone (=> reduce renin)
- adrenal adenoma (conns syndrome -2/3)
- bilateral adrenal hyperplasia (1/3)

131
Q

what is secondary hyperaldosteronism ? name the causes/aetiology

A

excessive renin => stimulate adrenals to secrete increased aldosterone
- aetiology: when BP in is disproportionately lower (renal artery stenosis, renal artery obstruction, HF)

132
Q

how does conns disease present ?

A

(hyperaldosteronism)
- hypertension
- lethargy
- mood disturbance

133
Q

describe the aldosterone and renin levels in primary and secondary hyperaldosteronism ?

A

1: High A, Low R
2: high A, High R

(also low K for both)

134
Q

hyperaldosteronism disease Mx ?

A

hyperaldonsteronism
- aldosterone antagonist (spironolactone)
- treat underlying causes: conns (laparoscopic adrenalectomy), renal artery stenosis (percutaneous renal artery angioplasty)

135
Q

patient presents with hypertension with hypokalaemia - what should you consider ?

A

conns disease

136
Q

in which circumstance should you consider conns as a reason for HTN ? (3)

A
  • hypertension with hypokalaemia
  • refractory HTN (despite > 3 antihypertensives)
  • HTN occurring before 40 yrs of age (especially in women)
137
Q

what is phaechromocytoma ?

A

catecholamine producing tumour
- a tumour of the chromatin cells that secrets unregulated + excessive Ad

138
Q

where is adrenaline produced ?

A

adrenaline is produced by chromatin cells (in the adrenal medulla)
(retroperitoneal organ)

139
Q

what does Ad stimulate ?

A

hormone and NT that stimulates SNS
- fight or flight
- increase arousal
- increase muscle tone
- increase HR
- increase BP

140
Q

describe the hormone secretion pattern in pheochromocytoma ?

A

Ad secreted in bursts => periods of worse symptoms and then settled

141
Q

pheochromocytoma important Hx point ?

A

25% are familial so important to ask about FHx

142
Q

pheochromocytoma px ? classic triad ? what precipitates sx ?

A

(fluctuate with rise + fall of Ad)
- anxiety
- sweating
- panic attacks
- headaches
- hypertension (can be v high)
- arrhythmias
classic triad: episodic headaches, sweating and tachycardia (patient feel as if about to die)
- precipitated by straining, stress, abdo pressure

143
Q

pheochromocytoma dx ?

A
  • 24 hr urine catecholamines
  • plasma free metanephrine (high) - gold standard
144
Q

pheochromocytoma mx ? (3)

A
  • alpha blockers (phenoxybenzamine)
  • BB (propanolol)
  • adrenalectomy
    (if malignant: chemo or radiotherapy)
145
Q

pheochromocytoma complicaiton ?

A

can progress to stroke, cardiogenic shock

146
Q

causes of hirsutism ? (4)

A
  • familial
  • idiopathic
  • increase androgen secretion by ovary (PCOS, ovarian cancer)
  • adrenal gland (late onset CAH, adrenal cancer, steroids)
147
Q

what is the physiology that causes an erection

A

neuronal release of NO => hyperpolarizes + relaxes vascular + smooth muscle => engorgment

148
Q

causes of erectile dysfunction (impotence) ? (3)

A
  • smoking
  • alcohol
  • diabetes (reduce NO + autonomic neuropathy)
149
Q

erectile dysfunction mx ?

A
  • treat cause
  • counselling
  • oral phosphodiesterase inhibitors (sildenafil) (relax smooth muscle => improve arterial flow)
150
Q

in hypopituitarism, in what order are the hormones affected ?

A

reduced secretion of AP hormones
- GH, FSH/LH, TSH, ACTH, Prolactin

151
Q

what are the 3 causes of hypopituitarism ?

A
  • hypothalamus (Kallman - isolated GnRH deficiency)
  • pituitary stalk: trauma, surgery, craniopharyngioma
  • pituitary: tumour, irradiation, ischaemia (Sheehans, pituitary apoplexy)
152
Q

what is the aetiology of most pituitary tumours ?

A

almost always benign adenomas

153
Q

what are the 3 ways the pituitary tumours causes symptoms

A
  • tumour cause pressure on local structure (optic nerve => visual field defect - bilateral temporal hemianopia), headache)
  • pressure on normal pituitary
  • functioning tumour (producing hormones)
154
Q

pituitary Ix ?

A

MRI
- screening tests: IGF-1, ACTH, cortisol, TFTs, LH/FSH, short synacthen test

155
Q

pituitary tumour tx ?

A

hormone replacement (steroids before levothyroxine as thyroxin may precipitate adrenal crisis)
- surgery trans-sphenoidal

156
Q

What is galactorrhea ?

A

breast milk production no associated with pregnancy or breastfeeding

157
Q

what does increased prolactin cause ?

A

high prolactin => reduced GnRH => reduced LH/FSH => hypogonadism (menstrual irregularities, reduced libido ED), infertility, osteoporosis

158
Q

during pregnancy what stops milk production ?

A

oestrogen and progesterone inhibit prolactin secretion

159
Q

causes of hyperprolactinaemia ?

A
  • idiopathic
  • prolactinoma (adenoma)
  • hypothyroidism
  • meds (dopamine antagonists) - most common
160
Q

what are prolactinomas ?

A

tumours of pituitary gland that secrete excessive prolactin
- can be micro or macro (present with headaches and bitemporal hemianopia)

161
Q

prolacitnoma Mx ? depend on what ?

A

depends on size (pituitary MRI)
- dopamine agonists (cabergoline) to treat symptoms
- transphenoidal surgical removal of pituitary tumour

162
Q

what is acromegaly ? most common cause ?

A

clinical manifestation of excessive GH (produced from AP)
- usually caused by unregulated GH production form pituitary adenoma (99%)
- can be secondary to cancer (lung) that secretes ectopic GHRH or GH

163
Q

acromegaly px ?

A
  • space occupying (headache, visual field defect)
  • overgrowth of tissues secondary to GH (prominent brow, large nose + tongue and hands and feet, protruding jaw, arthritis)
  • organ dysfunction (hypertrophic heart, HTN, T2DM)
164
Q

acromegaly Ix ? (3)

A

random GH level is not useful as fluctuates alot
- IGF-1
- oral glucose tolerance test (increased glucose should suppress GH)
- MRI of brain

165
Q

acromegaly Mx ?

A
  • trans-sphenoidal surgical removal of pituitary tumour
  • if ectopic cause: pegnisomant (GH antagonist), octreotide (somatostatin analogue), cabergoline (dopamine agonists)
166
Q

acromegaly complications ?

A

associated with increased morbidity + premature mortality
- impaired glucose tolerance (may present with ketoacidosis)

167
Q

What is Diabetes insipidus (DI) ? what hormone involved and where ?

A

lack of ADH of lack of response to ADH
- ADH acts on collecting ducts in kidneys => reabsorb more water form urin
- DI prevents kidney s from being able to concentrate urine => polyuria, polydipsia and formation of inappropriately hypotonic (dilute) urine

168
Q

describe nephrogenic DI ? caused by ?

A

collecting ducts don’t respond to ADH (caused by lithium, genetic predisposition, intrinsic kidney disease, electrolyte imbalances)

169
Q

describe cranial DI ? causes ?

A

when hypothalamus does not produce ADH for pituitary to secrete
(idiopathic (50%), brain tumour, head injury, infection (meningitis/encephalitis/TB) brain surgery)

170
Q

DI Ix ?

A
  • U+E (high Na), low urine osmolality, high serum osmolality
  • water deprivation test
171
Q

describe the water deprivation test ? to test for what ?

A

cranial vs nephrogenic DI
- avoid fluid for 8 hrs, urine osmolality measured, synthetic ADH (desmopressin), 8 hrs later urine osmolatly checked again
- CDI (low urine osmo first, then high after desmo)
- NDI (low uric osmo first, remain low after desmo)

172
Q

DI Mx ?

A

treat underlying cause, oral IV fluids
- CDI (desmopressin)

173
Q

DI complication ?

A

both can present with hypernatraemia (med emergency)

174
Q

what is SIADH ? explain a bit/pathophys

A

syndrome of inappropriate anti diuretic hormone
- inappropriately large amounts of ADH as result of posterior pituitary secreting too much ADH (or small cell lung cancer)
- excessive ADH => excessive water reabsorption in collecting ducts => dilute Na in blood => hyponatraemia (+ not usually fluid overload) =

175
Q

what type of sodium imbalance does SIADH cause ?

A
  • excessive ADH => excessive water reabsorption in collecting ducts => dilute Na in blood => hyponatraemia (+ not usually fluid overload) => euvolaemic hyponatraemia
  • patients have high urine osmolality and high urine sodium
176
Q

SIADH sx ?

A

relate to hyponatraemia: fatigue, headache, muscle aches, cramps, confusion
- severe hyponat: seizures + reduced consciousness

177
Q

SIADH aetiology ?

A
  • post op
  • infection (lung pneumonia)
  • head injury
  • medication (amiodarone)
  • malignancy (small cell lung cancer)
178
Q

how is SIADH Dx ?

A

diagnosis of exclusion: low serum Na, low serum osmolality, low serum urea, high urine osmolality, high urine sodium
- negative shorty synacthen test
- CXR to look for pneumonia, lung abscess, lung cancer
- if no clear cause then suspect malignancy

179
Q

SIADH Mx ?

A

treat underlying cause, stop causative medication, correct Na slowly to prevent central pontine myelinolysis
- IV hypertonic saline + fluid restriction, tolcaptan (ADH receptor blockers) b

180
Q

what level counts as hyperkalaemia ? main complications ?

A

it is high serum potassium: plasma K+> 6.5 mmol/L (potential emergency)
- main complications: cardiac arrhythmias (VF) which can be fatal (cardiac arrest)

181
Q

cause of hyperkalaemia ?

A
  • AKI
  • CKD (stages 4-5)
  • rhabdomyolysis
  • adrenal insufficiency (Addisons)
  • medication (aldosterone antagonists (spiro), ACEI, ARB, NSAID
182
Q

ECG signs of hyperkalaemia ?

A
  • tall peaked T waves
  • flattened of absent P waves
  • broad GRS
183
Q

hyperkalaemia Mx ?

A

stop the medication, change diet
- insulin + dextrose infection (drives carbs into cell - takes K with it)
- and calcium gluconate (stabilises cardiac cells, reduce risk of arrhythmia)
- nebulised salbutamol: temporarily drives K into cells

184
Q

what counts as hypokalaemia

A

plasma K+< 2.5 mmol/L

185
Q

hypokalaemia causes ?

A

cause by increased K excretion or increased K moving into cells (=> less in blood)
- insuline: can be caused by insulin overdose in T1DM

186
Q

hypokalaemia presentation ?

A
  • severe muscle weakness or paralysis
  • cardiac arrhythmias (palpitations)
  • cramps
187
Q

hypokalaemia ECG changes ?

A

bradycardia
ST depression

188
Q

hypokalaemia Mx ?

A

oral potassium (oral K+ supplment)
- if severe: consider IV K+ continuously
NEVER five K+ as a fast stat bolus dose !!

189
Q

what counts as hypothermia ? typical patient ?

A

core (rectal temp) < 35 degrees
- most patients are elderly and do not complain of or feel cold so have to tried to warm up
- in the young: usually from cold exposure (near drowning) or secondary to impaired consciousness (following excessive alcohol or drugs)

190
Q

hypothermia px ?

A

if shivering then hypothermia is mild, if not shivering despite <35 then is severe
- sx: confusion, agitation, reduced GCS, coma, bradycardia, hypotension

191
Q

hypothermia Mx ?

A

(if heat too quickly => peripheral vasodilation + shock)
ABCDE approach
- slowly reward: aim for 1/2 degree per hr
- remove wet clothing, warm IV, cardiac monitoring

do not declare anyone dead until warm + dead.

4 - Med (12 decks)

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