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Passmed Specialty > ENDO 1 > Flashcards

ENDO 1 Flashcards

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1
Q

Presentation of DKA:

A

Abdominal pain
Kussmaul breathing
Polyuria
Polydipsia
Nausea and vomiting
Acetone breath
Dehydration
Hypotension
Altered consciousness

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2
Q

Presentation of HHS:

A

Elderly patient with T2DM

Over many days, insidious onset
Dehydration, polyuria, polydipsia
Lethargy
Nausea and vomiting
Consciousness altered
Focal neuro deficits
Hyperviscosity

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3
Q

Pathophysiology of T1DM:

A

Autoimmune destruction of pancreatic islet beta cells that produce insulin.

Absolute insulin deficiency.

Children / early adult life, tend to present in DKA or at least slightly unwell.

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4
Q

Pathophysiology of T2DM:

A

Defective insulin secretion
Failure of insulin sensitive tissue to respond

Relative insulin deficiency due to excess adipose tissue (not enough to go around the excess fatty tissue, leading to blood glucose increasing).

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5
Q

Thyroiditis vs Grave’s disease?

A

Thyroiditis - initially hyper then hypo in most cases:
More acute onset
Recent illness
Change in symptoms over weeks (Subacute thyroiditis)

Investigation: thyroid scintigraphy = globally reduced uptake of iodine-131

Graves:
Autoantibodies present e.g. TSH receptor antibodies (TRAb), TPO
Eye signs e.g. exopthalmos, ophthalmoplegia
Pretibial myxedema, thyroid acropachy with clubbing and soft tissue swelling hands and feet and periosteal new bone formation.

Thyroid scintigraphy = INCREASED uptake of radioactive iodine

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6
Q

Causes of raised prolactin (excess stimulation of the anterior pituitary):

A

Pituitary adenoma

Antipsychotics (dopamine antagonists that inhibit dopamine receptor; usually prolactin is inhibited by dopamine. More common in typical antipsychotics.)

Pregnancy
Oestrogens
Physiological - sleep, stress, exercise
Acromegaly (1/3 of patients)
PCOS
Primary hypothyroidism, due to TRH stimulating prolactin release.

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7
Q

Causes of primary gonadal failure:

A

Turner syndrome
CAH
Anorexia

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8
Q

ECG changes in hyperkalaemia:

A

Tented T waves occurs first

Loss of p waves
Broad QRS
Sinusoisal wave pattern
VF

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9
Q

Emergency treatment of hyperkalaemia.

A

Mild 5-5-5.9
Mod 6-6.5

Severe >=6.5, or ECG changes = emergency treatment:

IV calcium gluconate to stabilised myocardium, Insulin/dextrose infusion causes short term shift from ECF to ICF. +/- nebulised Salbutamol, temporary etc.

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10
Q

Causes and symptoms of hypocalcaemia:

A

Tetany; muscle twitching, cramping and spasm.
Perioral paraesthesia
Chronic = depression, cataracts
ECG = prolonged QT.
Trousseau’s sign
Chvostek’s sign

Vit D deficiency / osteomalacia
CKD
Hypoparathyroidism
Pseudohypoparathyroidism
Rhabdomyolysis initial stages
Magnesium deficiency (end organ PTH deficiency)
Massive blood transfusion
Acute pancreatitis

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11
Q

Causes and symptoms of hypercalcaemia:

A

Bones, stones, groans, psychic moans.
Corneal calcification.
Shortened QT on ECG
Hypertension
RENAL failure
Cancer
Hyperparathyroidism

  1. Primary hyperparathyroidism, most common cause in non-hospitalised patients.
  2. Malignancy, most common cause in hospital.
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12
Q

Treatment of hypocalcaemia vs hypercalcaemia:

A

Severe (carpopedal spasm, tetany, seizure, prolonged QT)= IV replacement , IV calcium gluconate 10ml 10% over 10 mins.

Hyper management: rehydration with normal saline, 3-4 litres per day. +/- bisphosphonates following rehydration.
Other options: calcitonin which has quicker effect than bis, steroids in sarcoidosis.

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13
Q

Symptoms associated with Cushing’s syndrome (high levels of glucocorticoid in the body):

A

Central obesity
Striae
Moon facies
Plethoric complexion
Buffalo hump
Proximal limb muscle wasting
Hirsutism
Easy bruising, poor skin healing
Hyperpigmentation of skin in Cushing disease only (high ACTH levels)

+ Hypertension, cardiac hypertrophy, T2DM, dyslipidaemia, osteoporosis and adverse mental health inc insomnia

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14
Q

Pathophysiology of acromegaly:

A

Excess growth hormone secondary to pituitary adenoma in over 95% of cases.

Minority caused by ectopic GHRH or GH production by other tumours e.g. pancreatic.

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15
Q

Causes and symptoms of adrenal insufficiency:

A

Addison’s = autoimmune destruction of adrenal glands, causing reduced cortisol and aldosterone.

Lethargy, weakness, anorexia, n&v, weight loss, salt craving.

Hyperpigmentation - primary Addison’s only

Vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia.

Crisis = collapse, shock, pyrexia.

Other causes:
(Primary) = TB, mets, meningococcal septicaemia, HIV, APS

(Secondary) = pituitary disorders

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16
Q

Causes and symptoms of hypopituitarism:

A

Causes:
Compression, pituitary apoplexy, Sheehan’s syndrome, hypothalamic tumours e.g. cranioph, trauma, radiation, also infiltrative causes e.g. sarcoidosis, haemochromatosis

LOW OF ALL THE HORMONES OF THE PITUITARY:
ACTH (tired, postural hypotension), GnRH (low fsh, lh, amenorrhoea, infertility, libido loss), GH (childhood = short stature), PROLACTIN (lactation problem), TSH (cold, constipation)

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17
Q

Diagnostic criteria for PCOS:

A

Rotterdam criteria; 2 of 3 present:

US evidence of cysts >=12, 2-9mm in size, uni or bilateral, one of both ovaries increased ovarian vol of >10cm3

Hyperandrogenism = hirsutism, infertility, acne, elevated total or free testosterone

Anovulation /amenorrhoea

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18
Q

Investigations in suspected PCOS and what they might show:

A

Pelvic US - multiple cysts

?Raised LH:FSH ratio, but not diagnostic
Testosterone normal or mildly elevated
Prolactin normal or mildly elevated
SHBG normal or low
Impaired glucose tolerance

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19
Q

Management of DKA. Is it different in children?

A

FLUID REPLACEMENT, isotonic saline even if acidotic. 5-8 litres deplete usually.

IV insulin infusion fixed rate. Continue long acting insulin, stop short acting insulin.

Once blood glucose <14, add 10% dextrose to the NaCl 0.9% regime.

Correct electrolytes, e.g. potassium

?Slower infusion in younger adults / children due to greater risk of cerebral oedema.

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20
Q

Management of HHS:

A

Fluid replacement; estimated losses between 100-220 ml/kg, IV NaCl 0.9%
0.5/1l / hour
Monitor potassium
Don’t give insulin unless blood sugars stop falling with fluids
VTE proph, older population and hyperviscosity

Vascular complciations can occur due to hyperviscosity e.g. MI and stroke.

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21
Q

Investigating thyroid function:

A

Thyroid examination

TFTs - serum TSH. T3 and T4

Auotantibodies

ESR and CRP

Doppler US

Thyroid scintigraphy and radio-uptake scan

Also ECG if irregular pulse was noted to rule out AF

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22
Q

Thyroid differentials and distinguishing factors (Grave’s, subacute, hashimoto’s, toxic multinodular goitre):

A

Grave’s disease - goitre, eye disease, autoantibodies esp TRAb, and also TPO. Scintigraphy high / increased uptake.

Subacute / De Quervain’s thyroiditis; preceding viral illness, presents with hyper, painful goitre and raised ESR, then euthyroid for 1-3 weeks, then hypo for a few months. Scintigraphy low uptake.

Hashimoto’s - chronic autoimmune, female, transient thyrotoxicosis at the start. Firm, non-tender goitre, anti TPO and Thyroglobulin antibodies. Associated with MALT lymphoma.

Toxic multinodular goitre - patchy uptake on scintigraphy. Goitre.

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23
Q

Risk factor for gestational diabetes:

A

Obesity BMI >30
Previous GD in pregnancy
Prev macrosomic baby >4.5kg
First degree relative GD
Family origin; South Asian, black caribbean and middle eastern

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24
Q

Cut off for gestational diabetes, and management:

Study These Flashcards
A

Fasting >=5.6
2hr post OGTT >=7.8

Fasting <7mmol, trial diet and exercise for 1-2 weeks.
Fasting >7, start insulin straight away, or if between 6.1 and 6.9 and evidence of e.g. macrosomia.

25
Types of secondary diabetes, and how to they differ from T1DM / T2DM?
Pancreatic diabetes e.g. pancreatitis and pancreatic cancer Cushing's syndrome Acromegaly Steroids
26
Investigations in suspected adrenal disease / Cushing syndrome:
Consider iatrogenic, ACTH dep and indep causes. HYPOKALAEMIC METABOLIC ALKALOSIS + impaired glucose tolerance. Ectopic ACTH e.g. secondary to small cell lung cancer = low potassium. Overnight low dose dex suppression test = first line. Patients WITH Cushing's will not have their morning cortisol spike suppressed. 24hr urinary free cortisol (2 measurements) Bedtime salivary cortisol (2 measurements) High dose dex suppression test, measuring cortisol and ACTH.
27
Pathophysiology of Addison's disease:
Autoimmune destruction of adrenals, causing reduced cortisol and aldosterone.
28
Management of a) Addison's disease + investigations b) Cushing's disease.
Addison's - short Synacthen test to measure plasma cortisol before and after synthetic ACTH. Also adrenal autoantibodies to 21-hydroxylase may be present. Also ?9am serum cortisol sample, if <100 definitely abnormal. Hydrocortisone in 2 or 3 divided doses, majority in first half of the day, and fludrocortisone (double hydrocort in illness, fludro same.) Cushing's - dependent on cause e.g. trans-sphenoidal removal if pit adenoma, surgical adrenal tumour or ectopic ACTH tumour e.g. lung. ?Remove both adrenals and life long replacement.
29
Difference between Cushing's disease and Cushing syndrome:
Cushing disease = pituitary adenoma secreting ACTH, stimulating excessive cortisol release from the adrenals. Cushing syndrome has other causes including prolonged courses of exogenous corticosteroids.
30
Causes of hyponatraemia, split into urinary sodium <20 and >20mmol, depending on volume status:
Water excess or sodium depletion. Take into context with urinary sodium and osmolality. https://handbook.ggcmedicines.org.uk/media/1099/195-hyponatraemia-flowchart-1-final-200717e.pdf
31
Causes of hypernatraemia:
Dehydration Excessive IV saline Diabetes insipidus Very careful when correcting, can lead to cerebral oedema; brain tissue can lose sodium and potassium rapidly, lowering of other things e.g. water goes slower. Should correct at 0.5mm/hour
32
What is serum osmolality?
Measure of the number of osmotically active particles in 1kg of serum. Can help differentiate between hypertonic, hypotonic (true) or osmolar hyponatraemia (pseudo due to e.g. lipids and paraproteins in blood)
33
What is the diagnostic criteria for PCOS called?
Rotterdam criteria
34
Explain insulin resistance in PCOS
Lack of response to insulin hormone, results in high blood sugar levels. Can present with acanthosis nigricans.
35
4 types of thyroid cancer:
Papillary , young females, good prognosis Follicular Medullary - parafollicular C cells, secrete calcitonin, MEN2 Anaplastic - hashimoto's thyroiditis
36
Discuss the cancers present in MEN 1 and MEN 2a/b.
MEN1 = 3Ps Parathyroid, Pituitary, Pancreas *(insulinoma, gastrinoma recurrent peptic ulceration) Most common presentation = hypercalcaemia. MEN2a = 2Ps + Medullary thyroid Parathyroid, Phaeo, RET oncogene. MEN2b = 1P = phaeo + medullary thyroid. Marfanoid body habitus, neuromas. RET oncogene
37
Function of the parathyroid gland / parathyroid hormone:
PTH is produced in response to low calcium and acts to raise it. Bones --> increase osteoclast activity, releasing calcium and phosphate, raising serum calcium and phosphate. Kidneys --> distal tubule (stimulate calcium reabsorption), proximal tubule (decreases phosphate reabsorption, more free calcium as less phosphate for it to bind to), stimulates kidney to convert vit d to active form calcitriol which acts to increase absorption from SI, kidneys and provides negative feedback
38
Symptoms of hyperparathyroidism.
80% of patients are asymptomatic. Bones stones abdominal groans, psychic moans Associated with hypertension
39
Symptoms of hypoparathyroidism, + investigation results and main cause.
Main symptoms of hypoparathyroidism are secondary to hypocalcaemia (see previous hypocalcaemia card). PTH reduced e.g. secondary to thyroid surgery. LOW CALCIUM, high phosphate. Treated with alfacalcidol.
40
Biochemical / hormonal results in primary vs secondary vs tertiary hyperparathyroidism:
PTH elevated in all (obviously) Primary Calcium high Phosphate low Urine calcium:creatinine >0.01 Solitary adenoma 80% Secondary Calcium low or normal Phosphate high Vitamin D low Hyperplasia due to low calcium in CHRONIC RENAL FAILURE Tertiary Calcium normal or high Phosphate decreased or normal Vit D normal or decreased ALP elevated Hyperplasia due to correction of underlying renal disease e.g. transplant, all 4 glands.
41
Biochemical / hormonal results in hypoparathyroidism:
PTH reduced Low calcium High phosphate Treat with alfacalcidol
42
What is monogenic diabetes?
MODY most common form. AD inheritance, impairment in insulin secretion but NOT insulin action. Not driven by lifestyle factors. MODY3 is most common.
43
Presentation of monogenic diabetes / MODY:
Younger patients Mild, non-ketotic hyperglycaemia, persistent, asymptomatic Only DKA if severe illness. Normal weight No signs of insulin resistance <25
44
Klinefelter's causes hypogonadism. What is the chromosomal abnormality present, and what are the clinical features?
47XXY Taller than average Lack of secondary sexual characteristics Small, firm testes Infertility Gynaecomastia alongside increased incidence of breast cancer Gonadotrophin levels raised but LOW testosterone
45
What does a phaeochromocytoma secrete, and which genetic syndromes may it be associated with?
Catecholamines Von Hippel Lindau MEN II Neurofibromatosis
46
3 10%s of phaeochromocytoma, what are they?
10% bilateral 10% extra-adrenal (adjacent to aortic bifurcation) 10% malignant
47
Clinical features of a phaeochromocytoma, and the main clinical test:
HYPERTENSION tachycardia, palpitations headaches sweating anxiety 24 urinary metanephrines 97% sensitivity
48
Surgery is the definitive management of a phaeochromocytoma, however they must first be stabilised with medical management to reduce anaesthesia and surgical risks. What medical management is indicated?
Alpha blockers first e.g. phenoxybenzamine Beta blockers e.g. propranolol Prevents haemodynamic instability in surgery.
49
Why are urinary metanephrines the test of choice compared to serum catecholamine or adrenaline level, and compared to urinary catecholamines?
Serum catecholamine or adrenaline fluctuates a lot and only has a very short half life. Metanephrines have longer half life and more stable levels.
50
Imaging to look for a phaeochromocytoma?
CT or MRI
51
What is Conn's syndrome?
Primary hyperaldosteronism caused by an adrenal adenoma.
52
What is the most common cause of primary hyperaldosteronism?
Bilateral idiopathic adrenal hyperplasia
53
Discuss the normal function of aldosterone including where it is secreted from and where it exerts it's action, and what triggers it's release.
Aldosterone = mineralocorticoid secreted from adrenal gland. It increases sodium reabsorption, and potassium secretion from the distal tubule (SAVES SALT). Increases hydrogen secretion from the collecting ducts. More fluid is retained in the body, increases intravascular volume and BP.
54
3 other causes of primary hyperaldosteronism.
Unilateral hyperplasia Familial hyperplasia Adrenal carcinoma
55
Clinical features of primary hyperaldosteronism:
HYPERTENSION and hypokalaemia (muscle weakness, more common with adrenal adenomas). Metabolic alkalosis (aldosterone increases hydrogen secretion from collecting ducts).
56
Indications for suspicion of primary hyperaldosteronism, and first line investigation?
Hypertension with hypokalaemia Hypertension resistant to treatment Plasma aldosterone/renin ratio = HIGH ALDOSTERONE with LOW RENIN
57
Positive plasma aldosterone / renin ratio shows high aldosterone levels alongside low renin; why does this happen, and what further investigations are warranted?
Renin is low due to negative feedback on the JG cells due to the high sodium. High resolution CT abdomen and adrenal vein sampling (unilateral vs bilateral sources of aldosterone excess)
58
Management of an adrenal adenoma vs. bilateral adrenocortical hyperplasia:
Adrenal adenoma = laparoscopic adrenalectomy Bilateral adrenal hyperplasia = aldosterone antagonist e.g. spironolactone

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