FINALS - Passmed > Endo > Flashcards

Endo Flashcards

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1
Q

subacute thyroiditis (de qervain) typical presentation, MC cause, investigation + Mx

A
  • tender goitre, hyperthyroidism and raised ESR
  • MC triggered by viral illness
  • Ix: thyroid scintigraphy [Technetium thyroid scan]: globally reduced uptake of iodine-131.
  • Mx: self limiting, most pts don’t need treatment. thyroid pain can be managed with aspirin or NSAIDs and severe cases may require CSX
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2
Q

What are the symptoms of hyperkalemia?

A
  • Muscle weakness
  • Muscle cramps
  • Paraesthesia
  • Palpitations
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3
Q

What are the ECG changes associated with hyperkalemia?

A
  • Flat P waves
  • PR interval prolongation
  • Short QT interval
  • Broad QRS
  • Tented T waves
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4
Q

What is the immediate treatment for cardiac membrane protection in hyperkalemia?

A

10ml of 10% IV calcium gluconate or calcium chloride

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5
Q

What is the role of insulin/dextrose infusion in hyperkalemia?

A

Causes an intracellular shift of potassium

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6
Q

What are the key causes of hyponatremia?

A
  • Nausea and vomiting
  • Headache
  • Lethargy
  • Weakness
  • Muscle aches
  • Confusion
  • Ataxia
  • Decreased consciousness
  • Seizures
  • Respiratory arrest
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7
Q

What is the management for acute hyponatremia presentation?

A

Saline 3% is administered

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8
Q

What is the management for chronic hyponatremia?

A

Saline 0.9% administered slowly

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9
Q

What can occur if saline is administered too quickly in chronic hyponatremia?

A

Cerebral edema and central pontine myelinolysis

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10
Q

What investigations are useful in diagnosing a cause for hyponatremia?

A
  • Serum and urine osmolarity
  • TFTs for hypothyroidism
  • Early morning cortisol levels for adrenal insufficiency
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11
Q

What is the pathophysiology of hyperkalemia in chronic kidney disease?

A

Reduced glomerular filtration rate (<15 ml/min/1.73 m²) and oliguria lead to decreased renal excretion of potassium.

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12
Q

What complications can arise from hyperkalemia?

A

Cardiac arrhythmia and/or arrest

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13
Q

parathyroid physiology

A

chief cells of the parathyroid glands detect hypocalcaemia –> increased PTH output.
PTH raises the calcium by acting on:
- Increasing osteoclast activity in bones (reabsorbing calcium from bones).
- Increasing calcium reabsorption in the kidneys (less calcium is lost in urine).
- Increasing vitamin D activity, resulting in increased calcium absorption in the intestines.

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14
Q

Causes of hyperparathyroidism

A

1: MC = parathyroid adenoma –> excessive PTH release –> hypercalcaemia symptoms – treated by surgical removal
2: caused by parathyroid hyperplasia. Usually secondary to CKD or vitamin D deficiency. Hyperplasia resolves if underlying cause is treated.
3: caused by persistent parathyroid hyperplasia, even after treating the underlying cause. Treated surgically by removal

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15
Q

hyperparathyroidism investigations

A
  • serum calcium raised
  • low PO4
  • inappropriately normal PTH or elevated PTH
  • x-ray/ DEXA scan: pepper pot skull, osteitis fibrosa cystica
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16
Q

Cushing’s syndrome Vs Cushing’s disease?

A

Cushing’s disease = pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), which stimulates excessive cortisol release from the adrenal glands

Cushing’s syndrome = features of prolonged high levels of glucocorticoids in the body.

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17
Q

Causes of Cushing’s syndrome

A

C–Cushing’s disease (a pituitary adenoma releasing excessiveACTH)
A–Adrenal adenoma (anadrenal tumoursecreting excesscortisol)
P–Paraneoplastic syndrome [MC in small cell lung cancer]
E–Exogenous steroids (patients taking long-term corticosteroids

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18
Q

what dermatological presentation can help narrow down the cause of Cushing’s syndrome?

A

hyperpigmentation
* ACTH excess stimulates melanocytes into producing more melanin –> hyperpigmentation.
* this is T4 seen in conditions of ACTH excess - adrenal insufficiency or pituitary adenoma

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19
Q

list investigations for Cushing’s syndrome

A

1st line screening tests

  • 24 hour urinary free cortisol
  • Late-night salivary cortisol: Cortisol levels normally drop late at night; however, this diurnal variation is lost in Cushing’s syndrome. Therefore, elevated late-night salivary cortisol levels are indicative of the condition
  • overnight low dose dexamethasone suppression test

localisation/ other tests

  • high dose dexamethasone suppression test - differentiates pituitary from ectopic causes of Cushing’s syndrome.
  • ACTH blood levels - assess ACTH in/dependence.
  • CT abdomen for adrenal tumours
  • CT chest for small cell lung cancer
  • Full blood count may show a high white blood cell count
  • U&Es may show low potassium if an adrenal adenoma is also secreting aldosterone
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20
Q

summarise the dexamethasone suppression test

A
  • Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)
  • Low-dose 48-hour test (used in suspected Cushing’s syndrome)
    High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome) Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)
  • Low-dose 48-hour test (used in suspected Cushing’s syndrome)
    High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)
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21
Q

what is Nelson’s syndrome

A
  • Nelson’s syndrome involves the development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback.
  • It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones.
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22
Q

treatment of Cushing’s syndrome

A

treat the underlying cause:

  • Cushing’s disease – pit. Adenoma: trans-sphenoidal resection to remove adenoma
  • Ectopic ACTH source or adrenal carcinoma: treat the underlying cancer OR use adrenal steroid inhibitors: Ketoconazole + metyrapone
  • Iatrogenic: review medication and try weaning if possible – must reduce slowly to avoid adrenal crisis
  • Adrenal tumour: tumour resection or adrenalectomy.
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23
Q

what is pseudo-cushing’s

causes and presentation

Study These Flashcards
A

Cushingoid signs and symptoms + abnormal cortisol levels BUT no HPA pathology associated.

  • caused by: alcoholism, depression or stress disorders.

Clinical presentation:

  • The patient may present with obesity, hypertension and glucose intolerance
  • but lacks other classical features of Cushing’s syndrome such as moon face, central obesity or purple striae.
24
Q

how do you differentiate between Cushing’s and pseudo-cushing’s

Study These Flashcards
A

An insulin stress test is used to differentiate between true Cushing’s and pseudo-Cushing’s.

25
signs of hypocalcaemia
- Chvostek's sign = tapping over parotid (CN7) causes facial muscles to twitch - Trousseau's sign = wrist flexion, finger abduction and spasming often occurs after 2 minutes of cuff inflation above systolic pressure - tetany: muscle twitching, cramping and spasm - perioral paraesthesia - if chronic: depression, cataracts - ***ECG: prolonged QT interval***
26
treatment for hypoparathyroidism
alfacalcidol
27
MC cause of hyperparathyroidism
Primary hyperparathyroidism is most commonly due to a solitary adenoma
28
Klinefelter's syndrome cause and features
Klinefelter's syndrome is associated with karyotype 47, XXY. Features: often taller than average lack of secondary sexual characteristics small, firm testes infertile gynaecomastia - increased incidence of breast cancer elevated gonadotrophin levels but low testosterone
29
non-functioning pituitary adenoma sx
- hypopituitarism - [fatigue, weakness, weight changes, low blood pressure, and decreased libido. Key signs include cold intolerance, infertility, headache, and in children, growth failure. Common symptoms are linked to specific deficiencies in ACTH, TSH, GH, and FSH/LH] - pressure effects: visual field defects [e.g. bitemporal hemianopia], headaches, hearing difficulties.
30
Signs of severe DKA
- Blood ketones > 6.0 mmol/L - Bicarbonate level < 5.0 mmol/L - Venous/arterial pH < 7.0 - Hypokalaemia on admission (< 3.5 mmol/L) - GCS < 12 or abnormal AVPU scale - Oxygen saturation < 92% on air (assuming normal baseline respiratory function) - Systolic BP < 90 mmHg - Pulse > 100 or < 60 bpm - Anion gap > 16 [(Na+ + K+) - (Cl- + HCO3-)]
31
pathophysiology of DKA
- Reduced / no levels of insulin --> ↓ glucose uptake in cells --> metabolism of lipids for alternative energy source in liver --> release of FFAs in liver -->↑ ketogenesis in liver[FFA’s --> ketones] and acidosis as they are acidic. - ↑ glucose and ketones in the blood --> osmotic diuresis as both are excreted via urine. They pull more water and electrolytes into the urine --> volume depletion, hypotension, and renal impairment if not promptly managed. - Acidosis caused by ketones -->Kussmaul breathing in an attempt to raise the pH by breathing off CO2 - Reduced glucose reaching brain cells -->↓ consciousness
32
Dx criteria for DKA
- Glucose >11 mmol/L - HCO3 <15 mmol/L - pH <7.30 - Ketonaemia (≥3 mmol/l) or 2+ ketones on dipstick
33
high risk patient groups in DKA
- elderly - pregnant - adolescent/ young adult - 18-25 - co-mordities: renal failure + heart failure.
34
complications of DKA
- Cardiovascular: - VTE due to dehydration, immobility, and a hypercoagulable state. - Arrhythmias due to electrolyte imbalance esp. hyperkalaemia. - Cerebral oedema - rapid fluid admin [especially in kids] - Acute respiratory distress syndrome - AKI – due to dehydration usually transient - Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia - Pulmonary oedema - Rhabdomyolysis - Pancreatitis - GI bleeding
35
normal blood glucose in an adult and a child
* >4 * >2.5
36
diabetic sick day rules
When glucose has been above 15 mmol/L for more than 2 hours: * Check blood glucose level every 2-4 hours * Check ketone level 2-4 hourly * Drink at least 100mls fluid every hour (gradually-sips) * Give additional doses of insulin every 2 hours according to usual management plan * 10% of total daily dose of insulin if ketones 1.5-3 mmol/L * 20% of total daily dose of insulin if ketones >3 mmol/L * If vomiting, unable to keep fluids down or ketone levels rising -> A+E (10% or 20% of total daily dose)
37
if a pt on a fixed dose of insulin has a hypo, how do you adjust their dose moving forwards
If on fixed dose insulin, simple rule is to cut preceding dose of insulin by 20% + refer to diabetic nurse
38
osmolalitty eqn
[2 x Na] + blood glucose + urea= osmolality
39
All patients with diabetes who are treated with insulin must notify the DVLA. For the DVLA to license an insulin-treated individual with a Group 1 licence, they must meet all the following criteria:
* Adequate hypoglycaemia awareness * No more than 1 episode of severe hypoglycaemia while awake in the preceding 12 months AND the most recent episode occurred more than 3 months ago * Practises appropriate glucose monitoring * Not regarded as a likely risk to the public while driving * Meets the visual standards for acuity and visual field * Under regular review
40
2 main causes of hypercalcaemia
1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients 2. Malignancy: the commonest cause in hospitalised patients. This may be due to a number of processes, including; * PTHrP [Parathyroid hormone-related protein] from the tumour e.g. squamous cell lung cancer * bone metastases * myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
41
HHS vs DKA - clinical findings
* HHS has no acidosis/significant ketosis, * the history is longer and * the glucose is often significantly raised eg >30mmol/L
42
HHS diagnostic criteria
There are no precise diagnostic criteria but the following are typically seen: * hypovolaemia * *Clinical features are commonly secondary to hypovolaemia and include fatigue, lethargy, altered consciousness, hypotension and tachycardia* * hyperglycaemia (blood sugar > 30mmol/L) * a serum osmolality > 320mosmol/kg. [calculated as 2 x [Na] + glucose ] /// * no significant hyperketonaemia (<3 mmol/L) * no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)
43
HHS pathophysiology
* **basically : hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion** * In HHS, extreme hyperglycaemia (>30 mmol/L) raises plasma osmolality above 320 mOsm/kg. * This hyperosmolar state causes water to shift from intracellular to extracellular compartments, leading to cellular dehydration, particularly in brain cells, which can cause neurological symptoms such as confusion or coma
44
HHS CFs
polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion
45
HHS Mx + complications
* **early senior involvement** 1. fluids 2. insulin - only if glucose stops falling with fluids 3. VTE prophylaxis because of hyperviscosity of blood due to hyperosmolality. [t4 key complications = stroke and MI]
46
The first line insulin regime in children with type 1 diabetes is
a multiple daily injection basal-bolus insulin regimen
47
acromegaly Ix
1. Serum IGF-1 2. OGTT to confirm dx if IGF-1 raised
48
typical bloods of hyperaldosteronism
raised sodium low potassium
49
MC causes of primary hyperaldosteronism
1. bilateral idiopathic adrenal hyperplasia = MC 2. Conn's syndrome= adrenal adenoma 3. unilateral hyperplasia 4. familial hyperaldosteronism 5. adrenal carcinoma
50
hyperaldosteronism Ix + Mx
**Ix** * 1st line = renin:aldosterone ratio ==> high aldosterone levels alongside low renin levels * gold = high res- CT abdo - looking for adrenal hyperplasia or adenoma * if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia **Mx** * adrenal adenoma: surgery (laparoscopic adrenalectomy) * bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
51
hyponatraemia, hyperkalaemia, and hypoglycaemia
adrenal crisis or Addisonian crisis [synonyms]
52
adrenal crisis typical triad
hyponatraemia, hyperkalaemia, and hypoglycaemia
53
Thyrotoxicosis with tender goitre =
subacute (De Quervain's) thyroiditis Mx = NSAIDs or aspirin in more severe cases steroids are used, particularly if hypothyroidism develops
54
effect on LH and FSH: 1. anorexia: 1. premature ovarian failure/insufficiency 1. Hypogonadotrophic hypogonadism 1. PCOS 1. pregnancy
1. low LH + FSH 2. high LH + FSH 3. low LH + FSH 4. Normal or mildly ↑ LH + normal/low FSH 5. low LH + FSH
55
hypertension with hypokalaemia and mild alkalosis MC cause
hyperaldosteronism MC cause = bilateral adrenal hyperplasia
56
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