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Finals > Endo > Flashcards

Endo Flashcards

1
Q

Antibodies in thyroid glands

A
  • Anti-thyroid peroxidase Abs: autoimmune so Hashimito’s and Graves
  • Anti-thyroglobulin Abs: Graves, Hashimoto, cancer
  • TSH receptor Abs: bind to TSH and stimulate so Graves
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2
Q

Radioisotope findings in thyroid

A
  • diffuse: Graves
  • focal area: toxic multinodular goitre and adenomas
  • cold area: cancer
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3
Q

difference between primary and secondary hyperT

A
  • 1: thyroid gland behaving abnormally
  • 2: hypothal/pit behaving abnormally
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4
Q

most common cause of hyperthyroidism.

A

Graves

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5
Q

Toxic multinodular goitre

A
  • aka Plummer’s disease
  • nodules develop on the thyroid gland, which are unregulated by the thyroid axis and produce excessive thyroid hormones
  • most common in over 50 y/os
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6
Q

Reason for exopthalmos in Graves

A
  • TSH receptors behind the eye
  • Inflammation, swelling and hypertrophy of the tissue behind the eyeballs forces them forward
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7
Q

What is pretibial myxoedema

A
  • caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area).
  • Gives the skin a discoloured, waxy, oedematous appearance over this area
  • Specific to Grave’s: reaction to TSHR abs
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8
Q

causes of hyperthyroidism

A

GIST
- Graves
- Inflammation (thyroiditis)
- Solitary toxic thyroid nodule
- Toxic multinodular goitre

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9
Q

Causes of hypothyroidism

A
  • Hashimoto’s (developed)
  • Iodine deficiency (developing)
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10
Q

Causes of thyroiditis (hyperT then hypoT)

A
  • De Quervain’s thyroiditis
  • Hashimoto’s thyroiditis
  • Postpartum thyroiditis
  • Drug-induced thyroiditis
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11
Q

Features of hyperthyroidism

A
  • anxiety and tachycardia
  • sweating and heat intolerance
  • weight loss
  • Fatigue
  • Insomnia
  • Frequent loose stools
  • Sexual dysfunction
  • Brisk reflexes on examination
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12
Q

Graves’ disease specific features relating to the presence of TSH receptor antibodies

A
  • Diffuse goitre (without nodules), not painful
  • Eye disease, inc exophthalmos
  • Pretibial myxoedema
  • Thyroid acropachy (hand swelling and finger clubbing)
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13
Q

what is a Solitary Toxic Thyroid Nodule

A

usually benign adenoma
Mx- remove surgically

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14
Q

Phases of De Quervain’s thyroiditis

A
  1. Thyrotoxicosis (flu like sx)
  2. Hypothyroidism
  3. Return to normal
    painful goitre
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15
Q

Mx of De Quervain’s thyroiditis

A
  • NSAIDs for symptoms of pain and inflammation
  • Beta blockers for hyperthyroidism
  • Levothyroxine for hypothyroidism
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16
Q

what is a thyroid storm

A
  • rare presentation of hyperthyroidism aka thyrotoxic crisis
  • fever, tachycardia and delirium
  • can be life-threatening
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17
Q

Mx of thyroid storm

A
  • admission for monitoring
  • symptomatic treatment e.g. paracetamol
  • treatment underlying event
  • typically IV propranolol
  • anti-thyroid drugs: e.g. methimazole or propylthiouracil
  • Lugol’s iodine
  • dexamethasone - blocks conversion of T4 to T3
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18
Q

Mx of hyperthyroidism

A
  • Carbimazole (1st line)
  • Propylthiouracil
  • Radioactive iodine
  • Beta blockers
  • Surgery
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19
Q

How does carbimazole work

A
  • take for 12 to 18 months then continue on maintenance dose and either:
  • The carbimazole dose is titrated to maintain normal levels
  • A higher dose blocks all production, and levothyroxine is added
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20
Q

Risk of taking carbimazole

A

acute pancreatitis

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21
Q

How does propylthiouracil work

A
  • preferred if pt is pregnant
  • second-line drug
  • Used in a similarly to carbimazole
  • Small risk of severe liver reactions, including death
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22
Q

Potential side effect of carbimazole and PTU

A

agranulocytosis

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23
Q

How does radioactive iodine work

A
  • drink a single dose of radioactive iodine
  • emitted radiation destroys a proportion of the thyroid cells
  • Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine
  • Women must not be pregnant, breastfeeding and must not get pregnant within 6 months of tx
  • Men must not father children within 4 months of treatment
  • Limit contact with people after dose, particularly children and pregnant
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24
Q

How do BBs work in hyperthyroidism

A
  • block the adrenalin-related symptoms of hyperthyroidism.
  • Propranolol
  • control the symptoms e.g. palpatations
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25
Q

Surgical mx of hyperthyroidism

A
  • thyroidectomy
  • need levothyroxine
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26
Q

Complications of thyroid surgery

A

damage to parathyroid glands can result in hypocalcaemia –> QTc elongation on ECG

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27
Q

drug that can cause goitre and hypothyroidism

A

lithium

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28
Q

drug that can cause hypothyroidism and thyrotoxicosis

A

amiodarone

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29
Q

causes of secondary hypothyroidism

A

rarer
- Tumours (e.g., pituitary adenomas)
- Surgery to the pituitary
- Radiotherapy
- Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
- Trauma

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30
Q

presentation of hypothyroidism

A
  • Weight gain and fatigue
  • Dry skin, coarse hair and hair loss
  • Fluid retention
  • Heavy or irregular periods
  • Constipation
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31
Q

Mx of hypothyroidism

A

levothyroxine

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32
Q

What is myxoedema coma

A
  • Hypothermia and confusion
  • due to hypothyroidism
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33
Q

Mx of myxoedema coma

A
  • IV thyroxine
  • hydrocortisone
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34
Q

what is cushing’s syndrome

A
  • prolonged high levels of glucocorticoids in the body (cortisol)
  • hypokalaemic metabolic alkalosis
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35
Q

What is cushing’s disease

A

pituitary adenoma secreting excessive ACTH, which stimulates excessive cortisol release from the adrenal glands.
Not the only cause of Cushing’s syndrome

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36
Q

Causes of Cushing’s syndrome

A

CAPE
- Cushing’s disease
- Adrenal adenoma
- Paraneoplastic (ACTH released from a tumour outside of pituitary e.g. SCLC, carcinoid tumour)
- Exogenous steroids (dex, pred)

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37
Q

Features of Cushing’s

A
  • moon face
  • buffalo hump
  • abdominal striae
  • central obesity
  • proximal limb muscle wasting
  • easy bruising
  • hirsutism
  • hyperpigmentation (due to ACTH)
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38
Q

Conditions caused by Cushing’s

A
  • Hypertension
  • Cardiac hypertrophy
  • Type 2 diabetes
  • Dyslipidaemia
  • Osteoporosis
  • Adverse mental health
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39
Q

how does ACTH cause skin bronzing

A

stimulates melanocytes to produce melanin

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40
Q

how can you differentiate the cause of excess cortisol

A

Cushing’s disease and ectopic ACTH have excess ACTH so bronzing
Adrenal adenoma and exogenous don’t have it

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41
Q

Ix for Cushing’s

A
  • Overnight dexamethasone suppression test: should reduce cortisol, -veFB on CRH
  • 24hr urinary free cortisol
  • inferior pituitary
    petrosal sinus
    sampling
  • CT/PET to find ectopic source
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42
Q

Mx of Cushing’s syndrome

A
  • trans-sphenoidal surgery to remove pituitary adenoma
  • surgical removal of adrenal tumour
  • surgical removal of tumour producing ectopic ATC e.g. SCLC
  • bilateral adrenalectomy and then lifelong steroid replacement
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43
Q

key presenting feature of hyperaldosteronism

A

hypertension

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44
Q

where is renin produced

A

JG cell in afferent arterioles in kidney

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45
Q

where is ACE made

A

lungs

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46
Q

what is the effect of angiotensin II

A
  • stimulates release of aldosterone from adrenals
  • vasconstriction increasing BP
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47
Q

what is aldosterone and its effects

A

mineralocorticooid steroid acts on nephron to:
- increase sodium reabsorption
- increase potassium and hydrogen secretion

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48
Q

What is Primary hyperaldosteronism

A
  • adrenal glands produce too much aldosterone
  • renin low because of high BP
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49
Q

causes of primary hperaldosteronism

A
  • Bilateral adrenal hyperplasia (most common)
  • An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)
  • Familial hyperaldosteronism (rare)
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50
Q

What is secondary hyperaldosteronism

A
  • excess renin stimulating excess aldosterone
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51
Q

causes of secondary hyperaldosteronism

A

renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:

  • Renal artery stenosis
  • Heart failure
  • Liver cirrhosis and ascites
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52
Q

Ix for hyperaldosteronism

A

aldosterone: renin
high aldosterone and low renin= primary (conn’s)
high aldosterone and high renin = secondary

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53
Q

effects of aldosterone

A
  • Raised blood pressure (hypertension)
  • Low potassium (hypokalaemia)
  • Blood gas analysis (alkalosis)
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54
Q

Mx of hyperaldosteronism

A
  • eplerenone
  • spironolactone
  • > 4cm surgical removal of adrenal adenoma
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55
Q

electrolyte imbalance in hyperaldosteronism (conn’s)

A

high Na
low K

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56
Q

what is adrenal insufficiency

A

adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone

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57
Q

Addison’s disease

A
  • adrenal glands have been damaged
  • reduced cortisol and aldosterone
  • primary adrenal insufficiency
  • MC cause if autoimmune
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58
Q

electrolyte imbalance in adrenal insufficiency

A

because low cortisol and aldosterone
- low Na
- high K
- low glucose

59
Q

what is secondary adrenal insufficiency

A

inadequate adrenocorticotropic hormone (ACTH) and a lack of stimulation of the adrenal glands, leading to low cortisol.
loss or damage to pituitary

60
Q

causes of secondary adrenal insufficiency

A
  • Tumours (e.g., pituitary adenomas)
  • Surgery to the pituitary
  • Radiotherapy
  • Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
  • Trauma
61
Q

What is tertiary adrenal insufficiency

A
  • Inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus
  • usually due to long term steroids
62
Q

Presentation of adrenal insufficiency

A
  • fatigue
  • Muscle weakness
  • Muscle cramps
  • Dizziness and fainting
  • Thirst and craving salt
  • Weight loss
  • Abdominal pain
  • Depression
  • Reduced libido
63
Q

Signs of adrenal insufficiency

A
  • bronze hyperpigmentation (low cortisol so ACTH stimulated, which stimulated melanocytes to produce melanin)
  • hypotension (postural)
64
Q

Ix for adrenal insufficiency

A
  • hyponatraemia
  • short SynACTHen test: ACTH can be measured directly. High in primary, low in secondary
65
Q

Mx of adrenal insufficiency

A
  • replace steroids with hydrocortisone for cortisol and fludrocortisone for aldosterone
  • medical alert tag
  • double dose during illness
66
Q

What is Addisonian crisis

A
  • severe adrenal insufficiency
  • Reduced consciousness
  • Hypotension
  • Hypoglycaemia
  • Hyponatraemia and hyperkalaemia
  • Can be triggered by infection etc.
67
Q

Mx of Addisonian crisis

A
  • IM or IV 100mg hydrocortisone
  • IV fluids
  • IV dextrose
68
Q

Ideal body glucose conc

A

4.4-6.1

69
Q

how to diagnose DKA

A
  • Hyperglycaemia >11
  • Ketonsis >3
  • Acidosis <7.3
70
Q

Mx of DKA

A
  1. IV fluids over 48hrs
  2. Insulin fixed rate infusion started after 1hr + 40mmol potassium as insulin drives it into cells
  3. dextrose when glucose <14
    can stop IV insulin and glucose when on subcut and no more ketones or acidosis and more alert and wanting to eat food
71
Q

complications during DKA mx

A
  • hypoglycaemia
  • cerebral oedema
  • hypokalaemia
  • pulmonary oedema
72
Q

autoantibodes in T1DM

A
  • Anti-islet cell antibodies
  • Anti-GAD antibodies
  • Anti-insulin antibodies
73
Q

long term complications of T1DM

A

Macrovascular
- CAD
- peripheral ischaemia
- stroke and hypertension

Microvascular
- peripheral neuropathy
- retinopathy
- kidney disease (nephropathy)

  • UTI, candidiasis, pneumonia
74
Q

HbA1c targets in T2DM

A
  • 48 for new T2
  • 48 for Lifestyle + metformin
  • 53mmol/mol for any drug that may cause hypoglycaemia (sulfonylurea)
  • 53 for pt requiring more than one antidiabetic medication
75
Q

Mx of T2DM flowchart

A
  1. metformin ( and add SGLT2 if CVD risk)
  2. sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
  3. triple therapy or insulin therapy
  4. switch one of triple therapy to GLP1 (BMI >35)
76
Q

example of SGLT2 inihibitor

A

flozins (dapaglaflozin)
wee out sugar

77
Q

example of DPP4 inhibitor

A

gliptins (sitagliptin)
cause headaches

78
Q

example of sulfonylureas

A

amides/ides (gliclazide)
can cause weight gain

79
Q

when is pioglitazone contradindicated

A

in heart failure

80
Q

side effects of metformin

A
  • GI sx (try modified release)
  • lactic acidosis secondary to AKI
81
Q

what is Hyperosmolar Hyperglycemic State

A
  • rare but potentially fatal complication of T2DM
  • hyperosmolality (water loss leads to very concentrated blood)
  • high sugar levels (hyperglycaemia)
  • absence of ketones
82
Q

presentation of HHS

A
  • polyuria
  • polydipsia
  • weight loss
  • dehydration
  • tachycardia
  • hypotension
  • confusion
83
Q

Mx of HHS

A

IV fluids
senior escalation
careful monitoring

84
Q

options for mx of diabetic neuropathy

A
  • Amitriptyline – TCA
  • Duloxetine – SNRI (don’t use if eGFR<30)
  • Gabapentin –anticonvulsant
  • Pregabalin – anticonvulsant
85
Q

what is acromegaly

A

excess growth hormone from pituitary

86
Q

presentation of acromegaly

A

SOL in pituitary- headache and bitemporal hemianopia
- frontal bossing
- coarse sweaty skin
- large nose, hands, feet, jaw
- macroglossia
- Hypertension, T2DM, hypertrophic heart, arthritis
- bilateral carpal tunnel syndrome

87
Q

Ix for Acromegaly

A
  • OGTT (glucose should suppress GH normally)
  • Insulin like growth factor (first line)
  • MRI pituitary
88
Q

Findings in acromegaly

A
  • high glucose, calcium, phosphate
  • high GH and prolactin
89
Q

Mx of acromegaly

A
  • trans-sphenoidal surgery
  • pituitary radiotherapy
  • Pegvisomant: GH antagonist
  • Octreotide: stop GH release
  • Dopamine agonists (cabergoline, bromocriptine)
  • somatostatin
90
Q

role of PTH

A

raise blood calcium by:
- increase osteoclast activity
- increase calcium reabsorption in kidneys
- activate vit D, increasing Ca absorption in intestines

91
Q

Sx of hypercalcaemia

A

stones, bones, groans and moans
- kidney stones
- painful bones
- abdo groans
- psych moans

92
Q

what is primary hyperparathyroidism

A
  • uncontrolled PTH by tumour in PT gland
  • Depression, nausea, constipation, bone pain due to high Ca2+
  • raised ca, low phosphate
  • pepperpot skull on XR
    Mx- remove tumour or cinacalcet if co-morbidities
93
Q

what is secondary hyperparathyroidism

A
  • insufficient vit D or CKD reduces Ca absorption in intestines.
  • So PT glands excrete more PTH
  • Ca is low or normal, PTH is high
    Mx: correct vit D deficiency or renal transplant
94
Q

What is tertiary hyperparathyroidism

A
  • when secondary happens for too long causing unregulated PTH.
  • Pt glands hyperplasia causes increase PTH
  • so high Ca
95
Q

What is SIADH

A
  • increased release of ADH from posterior pituitary
  • increases water reabsorption –>dilute blood–>hyponatraemia
  • euovolaemic hyponatraemia
  • high urine osmolality and high urine sodium
96
Q

presentation of SIADH

A
  • headache
  • fatigue
  • muscle ache and cramps
  • confusion
  • severe hypoNa= seizure and reduced GCS
97
Q

causes of SIADH

A
  • Post-operative after major surgery (1)
  • Lung infection, particularly atypical pneumonia and lung abscesses
  • Brain pathologies, e.g. head injury, stroke, intracranial haemorrhage or meningitis
  • Medications (SSRIs (2) and carbamazepine)
  • Malignancy, particularly small cell lung cancer (3)
  • HIV
98
Q

how to diagnose SIADH

A
  • exclude other causes
  • very high urine osmo and low serum osmo
99
Q

Mx of SIADH

A
  • admit if symptomatic or severe
  • treat underlying cause
  • fluid restrict
  • Vasopressin receptor antagonist (tolvaptan)
100
Q

What is osmotic demyelination syndrome

A
  • AKA central pontine myelinolysis
  • correcting severe hypoNa too quickly
101
Q

What is diabetes insipidus

A
  • lack of ADH (cranial)
  • lack of response to ADH (nephrogrenic)
    kidneys unable to reabsorb water and concentrate urine
102
Q

What is primary polydipsia

A

normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria). This is not diabetes insipidus.

103
Q

Nephrogenic DI

A
  • kidneys do not respond too ADH
    Causes
  • idiopathic
  • Medications, particularly lithium
  • Genetic mutations in the ADH receptor gene
  • Hypercalcaemia
  • Hypokalaemia
  • Kidney diseases (e.g PCKD)
104
Q

What is cranial DI

A
  • hypothalamus does not produce ADH for the pituitary gland to secrete

Causes
- idiopathic
- brain tumours, injury or surgery
- meningitis or encephalitis
- Genetic mutations in the ADH gene
- Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)

105
Q

Presentation of diabetes insipidus

A
  • Polyuria (> 3L urine per day)
  • Polydipsia
  • Dehydration
  • Postural hypotension
106
Q

Ix of diabetes insipidus

A
  1. Serum glucose (to exclude diabetes mellitus)
  2. Serum K+ (exclude hypokalaemia)
  3. Serum Ca (exclude hypercalcaemia)
  4. Plasma and urine osmolality
  5. (diagnostic): 8-hour water deprivation test
107
Q

Water deprivation test findings

A

measure urine osmolality post deprivation.
Give desmopressin (synthetic ADH)

  • primary polydipsia: deprivation increases urine osmolality- no desmopressin needed
  • Cranial DI, osmolality high after giving desmopressin as kidneys can respond to ADH
  • Nephrogenic DI: urine osmolality before and after desmopressin
108
Q

Mx of Diabetes insipidus

A
  • treat underlying cause (e.g. lithium)
  • desmopressin for cranial DI

Nephrogenic
- access to plenty of water
- high dose desmopressin
- thiazide diuretics
- NSAIDs

109
Q

what is a phaeochromacytoma

A

tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline)

110
Q

where is adrenalin produced

A

chromaffin cells in the medulla of the adrenal glands

111
Q

genetic disorders associated with phaeochromacytoma

A
  • Multiple endocrine neoplasia type 2 (MEN 2)
  • Neurofibromatosis type 1
  • Von Hippel-Lindau disease
112
Q

Presentation of phaeochromacytoma

A

fluctuating sx due to adrenaline production
- anxiety, sweating
- headache, palpitations
- tremor
- hypertension
- tachycardia

113
Q

Ix for phaeochromacytoma

A
  • Plasma free metanephrines
  • 24-hour urine catecholamines
  • 24hr urine metanephrines 1st line
114
Q

Mx of Phaeochromacytoma

A
  1. Alpha blockade (phenoxybenzamine or doxazosin)
  2. Beta blockade
  3. Cut out- surgery when BP is well controlled
115
Q

Type of multiple endocrine Neoplasia

A

Men 1
Men 2a
Men 2b

116
Q

MEN1

A

3P’s
- pituitary
- pancreatic (insulinoma)
- parathyroid (hyperparathyroidism)

117
Q

MEN2a

A

2P’s 1M
- parathyroid
- phaeochromacytoma
- medullary thyroid

118
Q

MEN 2b

A

1P 2M’s
- phaeochromacytoma
- Medullary thyroid,
-Mucocutaneous neuromas
(& Marfanoid)

119
Q

serum osmolality formula

A

serum osmolality = (2 x Na+) + glucose + urea.

120
Q

side effects of steroids

A

proximal myopathy

121
Q

what can interfere with levothyroxine absorption

A

iron and calcium carbonate, take 4hrs apart

122
Q

MODY features

A

Many types
onset by 25
if HNF1A subtype- give low dose sulfonylureas

123
Q

When is metformin contraindicated

A

when GFR <30

124
Q

sign of insulinoma

A

Whipple’s triad
1. Hypoglycaemia with fasting or exercise
2. reversal of symptoms with glucose
3. recorded low BMs at the time of sx

125
Q

what is Hashimoto’s associated with the development of

A

MALT lymphoma

126
Q

most common complication of thyroid eye disease

A

exposure keratopathy

127
Q

other complications of thyroid eye disease

A
  • optic neuropathy: emergency
  • Strabismus and diplopia
128
Q

Features of thyroid eye disease

A
  • exophthalmos
  • conjunctival oedema
  • optic disc swelling
  • ophthalmoplegia
  • inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
129
Q

Mx of thyroid eye disease

A
  • smoking cessation
  • topical lubricants may be needed to help prevent corneal inflammation caused by exposure
  • steroids
  • radiotherapy
  • surgery
130
Q

Over-replacement with thyroxine increases the risk of

A

osteoporosis
hyperthyroidism: due to over treatment
worsening of angina
atrial fibrillation

131
Q

MODY inheritance pattern

A

AD

132
Q

Types of thyroid cancer

A
  • papillary 70% excellent prognosis
  • follicular 20%
  • medullary 5% Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2
  • anaplastic 1% Not responsive to treatment, can cause pressure symptoms
  • lymphoma rare Associated with Hashimoto’s thyroiditis
133
Q

What is congenital adrenal hyperplasia

A

group of autosomal recessive disorders that impair adrenal steroid biosynthesis
- 21-hydroxylase deficiency (90%)
leading to cortisol deficiency and excess androgen production
- 11-beta hydroxylase deficiency (5%)
results in hypertension due to excess deoxycorticosterone
- 17-hydroxylase deficiency (very rare)
leads to mineralocorticoid excess with low androgen and estrogen levels

134
Q

side effects of SGLT-2 inhibitors

A
  • UTIs
  • genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
  • normoglycaemic ketoacidosis
  • risk of lower-limb amputation
135
Q

Klinefelters

A
  • high LH and FSH
  • low testosterone
  • 47 XXY
  • taller than average
  • lack of secondary sexual characteristics
  • small, firm testes
  • infertile
  • gynaecomastia
136
Q

Impaired fasting glucose

A

6.1-6.9

137
Q

Kallman’s syndrome

A
  • LH & FSH low-normal and testosterone is low
  • anosmia
  • ‘delayed puberty’
  • hypogonadism, cryptorchidism
138
Q

PTH and PTHrP in malignancy

A

In hypercalcaemia secondary to malignancy, PTH is low, although PTHrP may be raised

139
Q

Mx of gastrperesis due to diabetes

A

metoclopramide

140
Q

how do steroids affect neutrophils

A

neutrophilia

141
Q

Diabetic med associated with an increased risk of bladder cancer

A

Thiazolidinediones (pioglitazones)

142
Q

what med needs to be stopped in a diabetic patient w renal impairment before CT

A

metformin, can induce contrast nephropathy (treat with lots of IV fluids prior)x

143
Q

diabetic medications that can be taken on day of surgery

A
  • DPP4i gliptins
  • GLP 1 tides

Finals (26 decks)

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