Endo general Flashcards

1
Q

What are the symptoms of hyperthyroidism?

A

Cardio- palpitations, SOB
Metabolic- weight loss
Psychiatric- anxiety, agitation
Neuro- tremors, shakes
GI- diarrhoea, increased appetite
Skin- sweating, heat intolerance

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2
Q

What are the signs of hyperthyroidism?

A

Cardio- tachycardia, flow murmur, AF, hypertension
Psychiatric- anxiety, agitation
Neuro- hyperreflexia, tremor
Skin- Pre-tibial myxedema, onycholysis
Ocular- exophthalmous, stare
Neck- goitre, tender, nodules

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3
Q

What distinguishes Graves disease from other causes of hyperthyroidism?

A
  • Ocular involvement only present in graves disease (except the stare/lid retraction from sympathetic activation)
  • Pre-tibial myxedema specific to graves disease
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4
Q

What is the enzyme deficiency in typical congenital adrenal hyperplasia? What is tested for at birth

A

21 hydroxylase deficiency

17 hydroxyprogesterone (OHP) is tested for at birth as will be a very high levels in the blood

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5
Q

What are the classes of hyponatraemia and how are they differentiated?

A
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6
Q

What is psuedohyponatraemia? How is hyponatraemia investigated?

A
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7
Q

What are the different classes of hypernatraemia?

A
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8
Q

What is the alternate calculation for the Delta Gap?

A

Na - Cl - 36

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9
Q

What is an alternate method of determining if there is an A-a gradient without performing the calculation?

A

PaO2 should be at least 4x the Fi02
ie 0.21 x 4 = 88 (lower limit of normal Pa02 at sea level)

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10
Q

When calculating the anion gap should the measured or corrected Na+ be used?

A

The measured Na+ is used for the anion gap calculation

The corrected Na+ is only used in determining the presence of dehydration and pseudohyponatraemia

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11
Q

How is water deficit estimated using Na+ value?

A

Fluid deficit = (Weight x 0.6) x ([measured Na+/140] - 1)

ie for a 100kg male with Na+ 170

100 x 0.6 = 60
170/140 = 1.2
60 x (1.2-1) = 12L deficit

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12
Q

What is an alternate method for determining the PA02 other than Fi02 x 713?

A

%Fi02 x 7
ie 0.21 = 21%
21x 7 = 147, 0.21 x 713 = 149
50 x 7 = 350, 0.50 x 713 = 356

A good rough approximation, add slightly more if want complete accuracy but not needed for determing if A-a gradient present

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13
Q

What is the maximum rate of correction for hypernatraemia?

A

Usually use 5% dextrose to correct hypernatraemia, unless severe intercurrent hypovolaemia/shock

Aim to correct Na+ no more than 10-12mmol/L per 24hr period

Most cases are presumed to be chronic (>48hrs), acute usually in context of salt poisoning or diabetes insipidus with exacerbation (ie surgery) and should be screened for

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14
Q

What does an elevated anion gap in the absence of acidosis suggest?

A

A raised anion gap >20, and especially >30 suggests a high change of a masked HAGMA being present

If a metabolic alkalosis is found suggest looking at the anion gap and delta gap to see if concurrent HAGMA

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15
Q

What are the main differentials for a triple base disturbance

A

Salicylate toxicity
CNS infections (ie causing SIADH)
Pneumonia/Lung tumour with hyponatraemia

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16
Q

What is the morbidity and mortality of DKA?

A
  • Cerebral oedema has a 70% mortality rate
  • DKA is responsible for 70% of diabetes deaths in kids <10
  • Overall mortality for DKA is 5-15%
  • DKA during pregnancy has a foetal death rate of 50%

Risk factors for cerebral odema
- <5yo
- First presentation
- Long history poor control
- Corrected sodium >160

17
Q

What are the endpoints of hypertonic saline?

A
  • When the patient is asymptomatic (ie no seizures)
  • When the Na+ has risen by 20mmol
  • When the serum Na+ is >125

Serum sodium shouldn’t rise more than 10mmol/24hrs and 25mmols/48hrs

18
Q

What are the diagnostic criteria for SIADH?

A
  • Urine osmolality >100mmol/Kg and Urine sodium >20mmol/ml
  • Normal or unchanged cardiac, hepatic, renal, thyroid and adrenal function
  • Absence of extracellular volume depletetion
  • Hypotonic hyponatraemia
19
Q

What are the risk factors for hypernatraemia?

A
  • Extremes of age
  • Diabetes
  • Hypertonic infusions
  • Tube feeding
  • Osmotic diuretics
  • Lactulose
  • Polyuria disorders
  • Altered mental status
  • Mechanical ventilation
20
Q

What are the causes of hypocalcaemia and issues around treatment?

A
  • Hypoparathyroidism (1)
  • Factitious (hypoalbuminaemia, EDTA tube malfunction)
  • Hypomagnesaemia
  • Pseudohypoparahyroidism
  • Low Vit D
  • Acute pancreatitis
  • Hyperphosphataemia
  • Hungry bone syndrome (post thyroid and parathyroidectomy)
  • Drugs ie furosemide

Treatment issues
- Alkalosis exacerbates hypocalcaemia so any metabolic acidosis must be corrected after calcium is replaced
- Sodibic and phosphate both cause calcium crystal formation and shouldn’t be used concurrently

21
Q

What are the symptoms and signs of hypercalcaemia? What is the treatment?

A

Clinical
- Short QT interval
- Prolonged PR and QRS
- Altered conscious state
- GI upset/abdominal pain
- Thirst

Treatment
- Pamidronate 60mg IV
- Frusemide IV
- IV rehydration
- RRT
- Definitive surgery

22
Q

What are the causes of hypercalcaemia?

A
  • Malignancy (breast, lung and cervix most common)
  • Hydrochlorothiazide use
  • Vitamin A + D toxicity
  • Sarcoidosis
  • Adrenal insufficiency
  • Phaeochromocytoma
  • High albumin/spurious
  • Hyperparathyroidism
  • Rhabdo
  • Lithium toxicity
23
Q

What are the main causes of adrenal insufficiency?

A
  • Addisons disease
  • Bilateral adrenal haemorrhage (Waterhouse Friedrichsen syndrome ie from meningococcal sepsis)
  • Infections ie Tuberculosis, HIV
  • Ketoconazole
  • Malignancies
  • Iron toxicity
  • Autoimmune (ie sarcoidosis)
24
Q

What are the causes of and clinical effects seen in Addisonian crisis?

A

Clinical
- NAGMA
- Hyponatraemia hyperkalaemia
- Skin pigmentation
- Hypotension
- GI upset/pain

Causes
- Major surgery/anaesthesia
- AMI
- Hypoglycaemia
- Major trauma
- Drugs (morphine, chlorpromazine)
- Pscyhiatric illness

25
Q

What are the features of pheochromocytoma?

A

Tests
- Urine metanephrines and catecholamine
- MRI/PET (octreotide scintigraphy)
- Clonidine suppression test

Clinical
- PAROXYSMAL catecholamine surges
- Panic attacks
- Hypertensive/vasoconstrictive crises ie APO, ICH, AMI
- Strong association with thyroid carcinoma

Treatment
- Alpha = Phentolamine
- Beta = b-blocker of choice, but give this after controlling the alpha (unopposed alpha syndrome)
- IV fluids

26
Q

What are the symptoms and causes of Wernicke’s Encephalopathy?

A

Pathology
- Thiamine is co-factor in synthesis of ATP from glucose, lack of thiamine leads to cell starvation

Causes
- Malnutrition (reduced uptake) ie anorexia, weird diets, starvation, hyperemesis gravidarum
- Liver disease (reduced storage)
- Alcoholism (impaired uptake(
- Hypercatabolic states (ie extensive malignancy, terminal HIV)
- Dialysis (increased clearance)
- Often brought on by sudden increase in glucose intake when thiamine depleted (ie refeeding)

Clinical
- Ophthalmoplegia particularly CN VI
- nystagmus
- Altered mental status
- Ataxia
- Polyneuropathy worse in legs
- Heart failure (wet beri beri)
- Hypothermia from hypothalamus damage

27
Q

What are the electrolyte abnormalities associated with hyperventilation?

A

Hypocalcaemia
Hypokalaemia
Hypophosphataemia

all lower in the setting of hypocarbic respiratory alkalosis

28
Q

What is the Strong Ion difference and how is it calculated?

A

The difference between the number of cations and anions in the plasma
- Na/K/Ca/Mg - Cl/lactate/Urate

Simplified SID
- Na - Cl
- Should equal 42

If >42 then there is a chloride deficit and metabolic alkalosis
If <42 then there is a chloride excess and a hyperchloraemic acidosis (ie NAGMA)

29
Q

What are the differentials for elevated ketones?

A
  • DKA
  • Alcoholic ketoacidosis
  • Starvation ketosis
  • Pregnancy
  • Metabolic deficiencies (usually children/neonates)
30
Q

What are the causes of hypokalaemia?

A

Drugs
- Insulin
- Beta adrenergics
- Diuretics (frusemide)
- Potassium binders

Endocrine
- Period hypokalaemia paralysis
- Alkalosis
- Hyperaldosteronism (Conns)
- Hyperthyroidism
- Cushings, DKA

GI
- Upper and lower GI losses
- Vomiting and diarrhoea
- Mucous secreting tumours
- Zollinger-Ellison syndrome

Renal
- RTA 1 and 2
- Barters
- Over dialysis

31
Q

What are the typical doses of different replacement therapies for potassiun?

A
  • Slow/Span K = 8mmol
  • Chlorvescent = 14mmol
  • 10mmol IV in 100mls of 0.29% Saline
  • 30mmols IV in 1000mls of 0.9% Saline