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Medicine > Endo > Flashcards

Endo Flashcards

1
Q

Mx of Addison’s Disease?

A

Hydrocortisone + fludrocortisone

Management of intercurrent illness in addisons:

in simple terms the glucocorticoid dose should be doubled

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2
Q

common precipitating factors of DKA?

A

infection, missed insulin doses and myocardial infarction

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3
Q

features of DKA?

A

abdominal pain

polyuria, polydipsia, dehydration

Kussmaul respiration (deep hyperventilation)

Acetone-smelling breath (‘pear drops’ smell)

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4
Q

diagnostic criteria of DKA?

A

glucose > 11 mmol/l or known diabetes mellitus

pH < 7.3

bicarbonate < 15 mmol/l

ketones > 3 mmol/l or urine ketones ++ on dipstick

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5
Q

mx of DKA?

A

fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially.

insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 14 mmol/l an infusion of 5% dextrose should be started

correction of hypokalaemia (add KCl if K+<5.5)

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6
Q

MOA Sulfonylureas?

A

Sulfonylureas are oral hypoglycaemic drugs used in the management of type 2 diabetes mellitus. They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

Common adverse effects

hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide)

weight gain

Rarer adverse effects

syndrome of inappropriate ADH secretion

bone marrow suppression

liver damage (cholestatic)

peripheral neuropathy

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7
Q

diagnosis of phaeochromo?

A

Urine analysis of vanillymandelic acid (VMA) is often used (false positives may occur e.g. in patients eating vanilla ice cream!)

Blood testing for plasma metanephrine levels.

CT and MRI scanning are both used to localise the lesion.

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8
Q

mx of phaeo?

A
  1. alpha blockade
  2. +? beta blockade

Once medically optimised the phaeochromocytoma should be removed.

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9
Q

factors suggesting benign adrenal disease on CT?

A

Size less than 3cm

Homogeneous texture

Lipid rich tissue

Thin wall to lesion

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10
Q
A

Thyroid acropachy

seen in Graves disease

due to autoimmune reactions of the thyroid antibodies causing soft tissue swelling under the nail bed.

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11
Q

causes of primary hyperPTH?

A

80%: solitary adenoma

15%: hyperplasia

4%: multiple adenoma

1%: carcinoma

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12
Q

features of primary HyperPTH?

A

bones, stones, abdominal groans and psychic moans’

polydipsia, polyuria

peptic ulceration/constipation/pancreatitis

bone pain/fracture

renal stones

depression

hypertension

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13
Q

ix of primary hyperPTH?

A

raised calcium, low phosphate

PTH may be raised or normal (inappropriately normal)

technetium-MIBI subtraction scan

pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

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14
Q

tx of hyperPTH in pts not fit for surgery?

A

calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery

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15
Q

Impt adverse effects of Carbimazole?

A

carbimazole used in mx of hyperthyroidism

agranulocytosis:

If the patient develops any symptoms of an infection, particularly sore throat or fever then must seek urgent medical review and a FBC must be performed to check the neutrophil count.

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16
Q

what can be used as ‘rescue therapy’ for exacerbations of neuropathic pain

A

tramadol

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17
Q

mx of addisonian crisis?

A

hydrocortisone 100 mg im or iv

1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic

continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action

oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

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18
Q

meningococcal septicaemia -> hypoadrenalism

A

Waterhouse-Friderichsen syndrome

  • adrenal haemorrhage
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19
Q

Pt with hypothyroidism being treated.

What is the single most important blood test to assess her response to treatment?

A

TSH

As the majority of unaffected people have a TSH value 0.5-2.5 mU/l it is now thought preferable to aim for a TSH in this range

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20
Q

diagnosis of T2DM?

A

If the patient is symptomatic:

  • fasting glucose greater than or equal to 7.0 mmol/l
  • random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

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21
Q

definition of pre diabetes?

A

HbA1c 42-47

or fasting glucose 6.1-6.9

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22
Q

when is HbA1c not reliable?

A

misleading HbA1c results can be caused by increased red cell turnover (see below)

Conditions where HbA1c may not be used for diagnosis:

haemoglobinopathies

haemolytic anaemia

untreated iron deficiency anaemia

suspected gestational diabetes

children

HIV

chronic kidney disease

people taking medication that may cause hyperglycaemia (for example corticosteroids)

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23
Q

impaired fasting glucose?

A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

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24
Q

impaired glucose tolerance?

A

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

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25
Q

diabetic complications?

A

macrovascular (ischaemic heart disease, stroke) and microvascular (eye, nerve and kidney damage) complications.

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26
Q

pathophysiology of T1DM?

A

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
This results in an absolute deficiency of insulin resulting in raised glucose levels

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27
Q

pathophysiology of T2DM?

A

caused by a relative deficiency of insulin due to an excess of adipose tissue. In simple terms there isn’t enough insulin to ‘go around’ all the excess fatty tissue, leading to blood glucose creeping up.

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28
Q

other causes of diabetes?

A

chronic pancreatitis

haemochromatosis.

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29
Q

principles of managing diabetes?

A

drug therapy to normalise blood glucose levels

monitoring for and treating any complications related to diabetes

modifying any other risk factors for other conditions such as cardiovascular disease

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30
Q

main side effects of metformin?

A

Gastrointestinal upset
Lactic acidosis*

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31
Q

metformin and eGFR?

A

Cannot be used in patients with an eGFR of < 30 ml/min

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32
Q

what may reduce risk of developing thyroid eye disease in graves disease pts?

A

stop smoking

prednisolone

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33
Q

acute illness, a normal TSH and low T3 and T4 levels

A

sick euthyroid syndrome

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34
Q

blood pressure targets in T2DM?

A

no organ damage: < 140 / 80

end-organ damage: < 130 / 80

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35
Q

risk factor modification in T2DM?

A

Blood pressure

target is < 140/80 mmHg (or < 130/80 mmHg if end-organ damage is present)

ACE inhibitors are first-line

Lipids

following the 2014 NICE lipid modification guidelines only patients with a 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin. The first-line statin of choice is atorvastatin 20mg on

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36
Q

features of hyperaldosteronism?

A

hypertension

hypokalaemia (e.g. muscle weakness). This is a classical feature in exams but studies suggest this is seen in only 10-40% of patients

alkalosis

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37
Q

ix of hyperaldosteronism?

A

high aldosterone: renin ratio

high-resolution CT abdomen and adrenal vein sampling : to differentiate between unil and bilat sources of aldosterone excess

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38
Q

mx of bilateral adrenocortical hyperplasia?

A

spironolactone

  • aldosterone antagonist
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39
Q

mx of adrenal adenoma causing hyperaldosteronism?

A

surgery

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40
Q

most common type of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (90%)

(responsible for biosynthesis of aldosterone + cortisol)

-> Increased plasma 17-hydroxyprogesterone levels

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41
Q

pathophysiology of hyperosmolar hyperglycaemic state (HHS)?

A
  1. ) Severe hyperglycaemia
  2. ) Dehydration and renal failure
  3. ) Mild/absent ketonuria

Hyperglycaemia -> osmotic diuresis with associated loss of Na and K

Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg)-> hyperviscosity of blood.

Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.

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42
Q

features of HHS?

A

General: fatigue, lethargy, nausea and vomiting

Neurological: altered level of consciousness, headaches, papilloedema, weakness

Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

Cardiovascular: dehydration, hypotension, tachycardia

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43
Q

diagnosis of HHS?

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)

Note: A precise definition of HHS does not exist

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44
Q

Goals of mx of HHS?

A
  1. Normalise the osmolality (gradually)
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)
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45
Q

1st line mx of HHS?

A

Fluid replacement

(IV 0.9% NaCl)

*If serum osmolarity is not declining despite positive balance with 0.9% NaCl, then the fluid should be switched to 0.45% NaCl solution which is more hypotonic relative to the HHS patients serum osmolarity

aim of treatment should be to replace approx 50% of estimated fluid loss within the first 12h and the remainder in the following 12h

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46
Q

key parameter to monitor while treating HHS?

A

osmolality (+Na and glucose)

Guidelines suggest that serum osmolarity, sodium and glucose levels should be plotted on a graph to permit appreciation of the rate of change. They should be plotted hourly initially.

A safe rate of fall of plasma glucose of 4-6 mmol/hr is recommended.

rate of fall of plasma Na should not > 10 mmol/L in 24h.

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47
Q

is insulin required in HHS?

A

NO

unless

significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L)

ie. mixed DKA/HHS picture

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48
Q

diagnostic ix of addisons?

A

short synACTHen test

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49
Q

1st line tx of acromegaly?

A

trans-sphenoidal hypophysectomy is 1st line for majority

dopamine agonist (bromocriptine) and somatostatin analogue (octreotide) used as medical adjuncts

or radiotx

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50
Q

in mx of DKA, what rate should insulin be set up at?

A

started at 0.1 unit/kg/hr.

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51
Q

what may cause HbA1c levels to be higher than expected?

A

due to increased red blood cell lifespan

e.g

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

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52
Q

what medication is best to add to metformin in pt who is obese T2DM?

A

DPP-4 inhibitors are useful in T2DM patients who are obese

e.g. sitagliptin

Sitagliptin works by essentially increasing satiety and the insulin response to high-glucose content foods and so is more helpful in patients who overeat.

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53
Q

best choice for 2nd drug to add to metformin in T2DM pt who is non-obese?

A

sulfonylurea such as gliclazide or glibenclamide

  • most effective at reducing blood glucose
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54
Q

drug causes of gynaecomastia?

A

spironolactone (most common drug cause)

cimetidine

digoxin

cannabis

finasteride

gonadorelin analogues e.g. Goserelin, buserelin

oestrogens, anabolic steroids

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55
Q

ix of suspected pituitary adenoma?

A

a pituitary blood profile (including: GH, prolactin, ACTH, FH, LSH and TFTs)

formal visual field testing

MRI brain with contrast

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56
Q

diagnostic ix of acromegaly?

A

oral glucose tolerance (OGTT) with serial GH measurements.

in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia

in acromegaly there is no suppression of GH

may also demonstrate impaired glucose tolerance which is associated with acromegaly

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57
Q

what ix is used to differentiate T1DM from other types of diabetes?

A

C-peptide

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58
Q

when do u decide to add another drug to metformin or a third drug?

A

HbA1c>58

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59
Q

tx of choice for toxic multinodular goitre?

A

radioiodine

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60
Q

what is the first line insulin regimen for T1DM pts?

A

first-line insulin regime should be a basal–bolus using twice‑daily insulin detemir

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61
Q

MEN1?

A

3 Ps

Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

MEN1 gene

auto dom

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62
Q

MEN2a?

A

2 Ps 1 M

Parathyroid (60%)
Phaeochromocytoma

Medullary thyroid ca

RET oncogene

auto dom

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63
Q

MEN 2b?

A

1 P, 3 Ms

Phaeochromocytoma

Medullary thyroid cancer

Marfanoid

Multiple neuromas

RET oncogene

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64
Q

diabetic foot disease occurs due to?

A

neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin

peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia

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65
Q

how are diabetics screened for diabetic foot disease?

A

screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse

screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

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66
Q

tertiary hyperPTH?

A

Ca high, PTH high

occurs following a prolonged period of secondary hyperparathyroidism, which is a high PTH with a low calcium - the parathyroid glands begin to function autonomously having undergone hyperplastic/adenomatous change.

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67
Q

how to differentiate primary from secondary adrenal insufficiency?

A

skin hyperpigmentation

primary: problem in the adrenal. decreased feedback -> high ACTH from pit.

POMC -> ACTH + MSH (melanocyte stimulating hormone)

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68
Q

Tests to confirm Cushing’s syndrome?

A

overnight dexamethasone suppression test (most sensitive)

24 hr urinary free cortisol

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69
Q

endocrine parameters reduced in stress response?

A

Insulin

Testosterone

Oestrogen

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70
Q

definition of diabetes mellitus?

A

multisystem disorder due to absolute or relative lack of endogenous insulin -> high blood glucose levels -> metabolic and vascular complications

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71
Q

T1DM vs T2DM?

A

T1DM: autoimmune destruction of B cells -> absolute insulin deficiency

usually starts in adolescents

presents w polyuria/ dipsia, weight loss, DKA

anti-islet, anti-glutamic acid decarboxylase Abs

T2DM: insulin resistance and B-cell dysfunction -> relative insulin deficiency

usually older pts

presents w polyuria, dipsia, complications, weight gain

high genetic concordance: 80% in Monozygotic twins

assoc w obesity, high caloric intake, alcohol excess

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72
Q

secondary causes of diabetes mellitus?

A

drugs: steroids, atypical neuroleptics, anti-HIV
pancreatic: chronic pancreatitis, panc ca, CF, haemochromatosis

Endo: Phaeo, cushings, Acromegaly

Other: glycogen storage diseases

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73
Q

what is metabolic syndrome?

A

central obesity (increased waist circumference) and 2 of:

high triglycerides,

low HDL

HTN

Hyperglycaemia: DM, IGT, IFG

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74
Q

Mx of diabetes mellitus?

A

MDT: GP, endocrinologist, surgeons, specialist nurses, dieticians, chiropodists

Monitoring: 4Cs glycaemic control, Complications, competency, coping

Lifestyle modification:

diet, exercise, smoking cessation, reduce alcohol

Medications: Statins (regardless of lipids), Anti-hypertensives (e.g. ACEi), aspirin (primary prevention due to raised CVD risk)

Glycaemic Control medications: oral hypoglycaemics/ insulin

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75
Q

what to monitor in DM patients?

A

glucose Control:

  • record of complications: DKA, HONK, hypos
  • Cap blood glucose
  • HbA1c
  • BP, lipids

Complications:

macrovascular- pulses, BP, cardiac auscultation

Micro: fundoscopy, Albumin:Cr, U+Es, sensory testing + foot exam

competency:

  • w insulin injections
  • check injection sites
  • BM monitoring

coping:

  • psychosocial: depression
  • occupation
  • home life
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76
Q

statins in diabetics?

A

give all DM pts statins if >40 regardless of lipids level for primary prevention

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77
Q

BP target for DM pts?

A

<130/80

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78
Q

what anti-hypertensive class is best for DM?

A

ACEi

(BB may mask hypos, thiazides may increase [glucose])

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79
Q

Aspirin in diabetics?

A

aspirin is used for pirmary prevention if >50 or <50 w other CV RFs

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80
Q

1st line oral hypoglycaemic medication for DM?

A

Metformin

(if HbA1c> target after lifestyle changes)

SE: nausea, diarrhoea, abdo pain, lcatic acidosis

CI: eGFR<30, tissue hypoxia (sepsis, MI), morning before GA and iodinated contrast media

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81
Q

principles w insulin administration?

A

ensure pt education about

  • self adjustment w exercise and calories
  • titrate dose
  • family member can abort hypos w sugary drinks of Glucogel

finger prick BM after meal informs re short-acting insulin dose (for that last meal)

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82
Q

insulin requirements in illness?

A

generally increase even if food intake decreases

maintain calories e.g. milk

check BMs >4hrly and test for ketonuria

increase insulin dose if glucose rising

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83
Q

side effects of insulin?

A

hypoglycaemia

lipohypertrophy

  • rotate injection sites

weight gain in T2DM

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84
Q

Diabetic complications?

A

Hyperglycaemia: DKA, HONK

hypoglycaemia

infection

Macrovascular: MI, CVA

Microvascular

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85
Q

what macrovascular complications are assoc w DM?

A

MI: may be silent due to autonomic neuropathy

CVA

PVD: claudication, foot ulcers

tx: manage CV risk factors.

anti-hypertensives to reduce BP, statins for lipids,

stop smoking, HbA1c control

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86
Q

prevention of macrovascular complications in DM?

A

Good glycaemic control (HbA1c <6%) prevents both macro and microvasc complications

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87
Q

what are the microvascular complications assoc w DM?

A

kidney failure

retinopathy

Peripheral + autonomic neuropathy -> diabetic feet

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88
Q

what are diabetic feet due to?

A
  1. Ischaemia

Peripheral arterial disease

critical toes, absent pulses

ulcers: painful, punched out, foot margins
2. Peripheral neuropathy
- > loss of protective sensation
- > Charcot’s joints, pes cavus, claw toes

injury or infection over pressure points

ulcers: painless, punched out, pressure points e.g. metatarsal heads, calcaneum

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89
Q

arterial vs neuropathic ulcers?

A

arterial:

painful, punched out, foot margins, deep

neuropathic:

pressure points (Metatarsal heads, calcaneum), painless, punched out

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90
Q

Mx of diabetic feet?

A

conservative:

daily foot inspection w mirror

comfortable/ therapeutic shoes

regular chiropody

medical:

tx infection: benpen+ fluclox +/- metronidazole

surgical:

abscess or deep infection/ spreading cellulitis, gangrene, suppurative arthritis

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91
Q

features of diabetic nephropathy?

A

hyperglycaemia -> nephron loss and glomerulosclerosis (Kimmelstiel-Wilson lesions)

features:

microalbuminuria: urine albumin:Cr ratio >30mg/mM

if present -> ACEi/ ARB

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92
Q

what kind of diabetic nephropathy does one see?

A

nephron loss

glomerulosclerosis (kimmelstiel-wilson lesions)

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93
Q

pathogenesis of diabetic retinopathy?

A

microvascular disease -> retinal ischaemia -> raised VEGF -> new vessel formation

-> intra ocular haemorrhage and possible vessel detachment w profound global sight loss

and

localised damage to the macula/ fovea of the eye w loss of central visual acuity

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94
Q

presentation of diabetic retinopathy?

A

retinopathy and maculopathy

cataracts

new vessels on iris -> glaucoma

CN palsies

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95
Q

classification of diabetic retinopathy?

A

Background retinopathy:

  • dots: microaneurysms
  • blot haemorrhages
  • hard exudates

Pre-proliferative retinopathy:

  • cotton wool spots (retinal infarcts)
  • venous bleeding
  • haemorrhages

Proliferative Retinopathy:

  • new vessels
  • pre-retinal or vitreous haemorrhage
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96
Q

Diabetic maculopathy?

A

decreased visual acuity

hard excudates within one disc width of macula

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97
Q

mx of diabetic retinopathy?

A

laser photocoagulation

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98
Q

Ix of diabetic retinopathy?

A

fluorescein angiography

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99
Q

what types of neuropathies are seen in DM?

A

ischaemia: loss of vasa nervorum
metabolic: glycosylation, Reactive O2 species

symmetric sensory polyneuropathy

  • glove and stocking -> loss of all modalities
  • absent ankle jerks
  • numbness, tingling, pain

mononeuropathy/ mononeuritis multiplex

e.g. CN3/6 palsies

Femoral Neuropathy

  • painful asymmetric weakness and wasting of quads w loss of knee jerks

autonomic neuropathy

  • postural hypotension
  • urinary retention
  • gastroparesis -> early satiety, bloating
  • erectile dysfunction
  • diarrhoea

diabetic amyotrophy:

  • weakness + excruciating pain in thigh, hip, butt
  • absent reflexes
  • usually unilateral
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100
Q

mx of peripheral neuropathy due to DM?

A

paracetamol for pain

or Neuropathic pain meds: gabapentin, amitriptyliine

101
Q

diagnosis of femoral neuropathy/ amyotrophy from DM?

A

nerve conduction and EMG

102
Q

mx of autonomic dysfunction in DM?

A

postural hypotension: fludrocortisone

diarrhoea: codeine phosphate

103
Q

pathogenesis of DKA?

A

ketogenesis: low insulin -> decreased glucose utilisation + increased fat B-oxidation

increased generation of ketone bodies (acidic)

dehydration: severe hyperglycaemia (osmotic diuresis) + high ketones -> vomiting

Acidosis

104
Q

diagnosis of DKA?

A

cap ketones: ≥ 3mM (≥ 2+ on dipstick)

Acidosis: pH <7.3 (Severe if pH<7.1)

Hyperglycaemia: ≥11.1 mM or known DM

105
Q

IX of DKA?

A

capillary blood glucose and ketones

Urine: ketones and glucose, MCS

VBG: acidosis + high K

Bloods: FBC, U+E, Glucose, cultures

CXR: evidence of infeciton

106
Q

what is Klinefelter’s Syndrome?

A

47 XXY

  • often taller than average
  • lack of secondary sexual characteristics
  • small firm testes
  • infertile
  • gynaecomastia (increased incidence of breast CA)
  • elevated gonadotrophin levels

diagnosis by chromosomal analysis

107
Q

complications of DKA?

A

cerebral oedema: excess fluid administration

-> commonest cause of mortality

aspiration pneumonia

hypoK

HypoPO4 -> resp and skeletal muscle weakness

thromboembolism

arrhythmias

108
Q

mx of DKA v simply?

A

GRIP

gastric aspiration

Rehydration

Insulin infusion (+ dextrose later)

Potassium replacement

109
Q

electrolyte abnormalities u may also see in DKA?

A

hypoNa

  • osmolar compensation for hyperglycaemia

amylase often raised (up to 10x)

excretion of ketones -> loss of potential bicarb-> hyperchloraemia metabolic acidosis after tx

110
Q

once glucose is normalised in DKA, why still administer insulin?

A

glucose decreases faster than ketones and iinsulin is necessary to get rid of the ketones

111
Q

Mx of DKA?

A

A-> E approach

**CALL FOR SENIOR HELP (Always)

Fluids: 0.9% NS via large bore cannula 1L stat if SBP<90, 1L over 1h if SBP>90

then 1L over next 2h/2h/4h/4h/6h

switch to 10% dex 1L /8h when glucose <14mM

K+ replacement: <5.5

3.5-5.5 -> 40mmol/L

<3.5mM -> consult senior for review

Insulin infusion:

Actrapid 0.1u/kg/h IVI (6u if no weight, max 15u)

112
Q

mx of DKA after acute mx of fluids/ insulin/ K+?

A

urinary catheter: aim 0.5ml/kg/h

NGT if vomiting or reduced GCS

thromboprophylaxis w LMWH

refer to specialist Diabetes team

find and treat precipitating factors

113
Q

what to monitor during DKA tx?

A

hourly cap glucose and ketones

VBG @ 60 min, 2h and then 2 hrly

plasma electrolytes 4hrly

114
Q

complications of hyperosmolar non-ketotic coma?

A

occlusive events are common: DVT, stroke

  • give LMWH
115
Q

Mx of hyperosmolar non-ketotic coma?

A

rehydrate w 0.9% NS over 48h

  • may need ~9L

wait 1h before starting insulin

  • may not be needed
  • start low to avoid rapid changes in osmolality (ie 1-3 u/hr)

look for precipitant: MI, infection, bowel infarct

116
Q

what is Whipples Triad for defining Hypoglycaemia?

A

Low plasma glucose <3mM

symptoms consistent w hypoglycaemia

relief of symptoms by glucose administration

117
Q

symptoms of hypoglycaemia?

A

autonomic: 2.5-3

sweating, anxiety, hunger, tremor, palpitations

neuroglycopaenic: <2.5

confusion, drowsiness, seizures, personality change, coma

118
Q

causes of hypoglycaemia?

A

exogenous drugs: insulin, gliclazide

pituitary insufficiency

liver failure

addisons

islet cell tumour (insulinomas)

119
Q

Hypoglycaemia + high insulin?

A

drugs: high C-peptide -> sulfonylurea

normal c-peptide -> Insulin

insulinoma

120
Q

hypoglycaemia + low insulin + no ketones?

cause

A

non-pancreatic neoplasms e.g. fibrosarcomas

insulin receptor Abs e.g. Hodgkins

121
Q

hypoglycaemia + low insulin + high ketones?

A

Alcohol binge w no food

pituitary insufficiency

addisons

122
Q

what is Nelson’s syndrome?

A

following bilateral adrenalectomy -> rapid enlargement of a pituitary corticotroph adenoma (ATH producing adenoma)

due to lack of cortison’s negative feedback

presents as: bitemporal hemianopia (mass effect), hyperpigmentation

123
Q

what is an insulinoma?

A

benign B-cell tumour usually seen w MEN1

presents w fasting/ exercise-induced hypoglycaemia

124
Q

Ix of insulinoma?

A

hypoglycaemia + high insulin

exogenous insulin does not suppress c peptide

MRI, EUS pancreas

125
Q

mx of insulinoma?

A

excision

126
Q

Mx of hypoglycaemia if pt is alert and orientated?

A

oral carbohydrates

rapid acting: lucozade

long acting: sandwich, next meal

127
Q

mx of hypoglycaemia in pt drowsy/ confused but swallow intact?

A

Glucogel/ hypostop

(buccal carb)

consider IV access

128
Q

mx of hypoglycaemia in pt if unconscious or concerned about swallow?

A

IV dextrose 100ml 20%

or IM Glucagon (esp if no access)

129
Q

problems with IM glucagon?

A

wont work in drunks + short duration of effect (20 min)

insulin release may -> rebound hypoglycaemia

130
Q

symptoms of thyrotoxicosis?

A

hot, sweating

weight loss

diarrhoea

tremor

palpitations

oligomenorrhoea +/- infertility

131
Q

signs of hyperthyroidism/

A

hands:

fast irregular pulse, fine tremor, warm/ moist skin, palmar erythema

face:

thin hair

lid lag

lid retraction

neck:

goitre

Graves specific:

  • Exophthalmos, ophthalmoplegia
  • pretibial myxoedema
  • thyroid acropachy
132
Q

Ix of hyperthyroidism?

A

TFTs: low TSH, high T4/3

Abs: TSH receptor, Thyroid Peroxidase

High Ca, LFTs

Radionuclide isotope scan

Visual fields, acuity, movements

133
Q

features of Graves disease?

A

diffuse goitre w increased iodine uptake

ophthalmopathy

pretibial myxoedema

triggers: stress, infection, childbirth

Assoc w T1DM, vitiligo, Addisons

134
Q

What is Plummer’s Disease?

A

toxic multinodular goitre

iodine scan shows hot nodules

135
Q

causes of hyperthyroidism?

A

Graves

Toxic multinodular goitre

thyroid adenoma

toxic phase of de Quervains thyroiditis

drugs: thyroxine, amiodarone

136
Q

mx of thyrotoxicosis?

A

medical:

symptomatic - BB e.g. propranolol

anti-thyroid - carbimazole (inhibits TPO) or propylthiouracil

radiological: radio iodine
surgical: thyroidectomy

137
Q

in Graves disease, how long do you tx pts with carbimazole?

A

for 12-18 mos then withdraw

50% relapse -> surgery or radioI

138
Q

contraindications to radioiodine mx of hyperthyroidism?

A

pregnancy

lactation

139
Q

complications of thyroidectomy?

A

recurrent laryngeal n damage -> hoarseness

hypoPTH

hypothyroidism

140
Q

features of thyroid storm?

A

high temp

agitation, confusion, coma

tachycardia, AF

acute abdomen

HF

141
Q

precipitants of a thyroid storm?

A

recent thyroid sx or radioI

infection

MI

trauma

142
Q

Mx of thyroid storm?

A

Resus, A->E, call senior help

  1. fluid resus + NGT
  2. Bloods: TFTs + cultures if infection suspected
  3. Propranolol PO/IV
  4. Digoxin may be needed
  5. Carbimazole then Lugol’s Iodine 4h later to inhibit thyroid
  6. Hydrocortisone
  7. tx cause
143
Q

symptoms of hypothyroidism?

A

cold intolerance

weight gain

lethargy

constipation

menorrhagia

low mood

144
Q

signs of hypothyroidism?

A

cold hands

bradycardic

slow relaxing reflexes

dry hair and skin

puffy face

goitre

myopathy, neuropathy

ascites

myxoedema -> subcut tissue swelling in severe hypothyroidism, typically around eyes and dorsum of hand

145
Q

causes of hypothyroidism?

A

primary: atrophic thyroiditis, Hashimotos thyroiditis, post-partum, post-deQuervains, iodine deficiency (commonest worldwide), drugs- carbimazole, amiodarone, lithium
congenital: thyroid agenesis

post surgical: thyroidectomy, radioiodine

146
Q

Atrophic thyroiditis vs Hashimoto’s thyroiditis?

A

Atrophic:

thyroid abs +ve: anti-TPO, anti-TSH

lymphocytic infiltrate -> atrophy (no goitre)

Hashimotos:

TPO +ve, anti thyroglobulin +ve

atrophy + regen -> goitre

147
Q

mx of hypothyroidism?

A

levothyroxine

  • titrate to normalise TSH

check for other autoimmune disease e.g. Addisons

148
Q

features of Acromegaly?

A

Symptoms: amenorrhoea, headache, snoring, sweating, arthralgia, carpal tunnel

Face: coarse facial appearance, large tongue, prognathism (jaw protrudes), interdental spaces, prominent supraorbital ridges, big ears

Hands: spade-like hands, thenar wasting (carpal tunnel)

Other: increase in shoe size, excessive sweating and oily skin

features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia

raised prolactin in 1/3 of cases → galactorrhoea

6% of patients have MEN-1

149
Q

complications of acromegaly?

A

hypertension

diabetes (>10%) or impaired glucose tolerance

cardiomyopathy, LVH, increased risk IHD/ stroke

colorectal cancer

150
Q

features of myxoedema coma?

A

hypothyroid +

hypothermia

hypoglycaemia

heart failure: bradycardia + low BP

coma and seizures

151
Q

Mx of myxoedema coma?

A

Correct any hypoglycaemia

T3/T4 IV slowly

Hydrocortisone 100mg IV

tx hypothermia and HF

152
Q

mx of thyroid cyst?

A

aspiration or excision

153
Q

mx of de quervains thyroiditis?

A

pain relief -> nsaids

Self limiting: conservative approach

154
Q

what is Riedel’s thyroiditis?

A

dense fibrosis that replaces normalthyroid parenchyma

mass effects

hard fixed thyroid mass

assoc w retroperitoneal fibrosis

mx: conservative

155
Q

ix of cerebral oedema if suspected?

A

CT head

156
Q

indications for thyroid surgery?

A

pressure symptoms

relapse hyperthyroidism

cosmetic

carcinoma

157
Q

what to do pre-op in thyroid surgery?

A

render euthyroid w antithyroid drugs

  • start 10d prior to surgery as they increase vascularity

check for phaeo preop in medullary carcinoma

laryngoscopy: check vocal cords pre and post op

158
Q

complications of thyroid surgery?

A

Early

  • reactionary haemorrhage -> haematoma -> can cause airway obstruction
  • laryngeal oedema can -> airway obstruction

recurrent laryngeal n palsy -> hoarse voice (R more common due to oblique ascent)

  • hypoPTH -> low Ca
  • thyroid storm

late:

hypothyroidism

recurrent hyperthyroidism

Keloid scar

159
Q

mx of haematoma from thyroid surgery?

A

call anaesthetist and remove wound clips

evacuate haematoma and re explore wound

160
Q

which laryngeal n is most likely damaged in thyroid surgery?

A

R due to oblique ascent

damage to one -> hoarse voice

damage to both -> obstruciton needing trache

161
Q

features of primary hyperaldosteronism?

A

excess aldosterone

HTN

HypoK: muscle weakness, hypotonia, hyporeflexia, cramps

alkalosis

162
Q

causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia (70%)

Adrenocortical adenoma: conns (30%)

163
Q

Ix of primary hyperaldosteronism?

A

1st line: Aldosterone/ renin ratio (high)

High resolution CT abdomen and adrenal vein sampling used to differentiate between unilateral and bilateral sources

U+Es, high Na, low K, alkalosis

ECG: signs of hypoK (flat inverted T waves)

164
Q

mx of primary hyperaldosteronism?

A

adrenal adenoma: surgery

bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone or eplerenone

165
Q
A

CT Abdo showing right sided adrenal adenoma

seen below liver

166
Q

what is secondary hyperaldosteronism?

A

high aldosterone due to high renin from decreased renal perfusion

causes:

Renal artery stenosis

diuretics

CCF

hepatic failure

nephrotic syndrome

(Aldosterone; renin ratio is normal)

167
Q

what is Bartter’s syndrome?

A

auto recess

blockage of NaCl reabsorption in loop of Henle (as if taking frusemide)

congenital salt wasting -> RAS activation -> hypoK and metabolic alkalosis

normal BP

168
Q

What does PTH do?

A

secreted in response to low Calcium

  • increases osteoclast activity
  • increases Ca and decreases PO4 reabsorption in kidney

increases 1a-hydroxylation in 25OH-VitD3

169
Q

features of high Calcium?

A

stones; renal stones, polyuria and dipsia (nephrogenic DI), nephrocalcinosis

Bones: bone pain, pathological #s

moans: depression

groans; abo pain, constipation, pancreatitis

170
Q

causes of primary hyperPTH?

A

80%: solitary adenoma

15%: hyperplasia

4%: multiple adenoma

1%: carcinoma

171
Q

Primary HyperPTH is assoc w?

A

high Ca

HTN

MEN 1 and II

172
Q

Ix of Primary HyperPTH?

A

raised calcium, low phosphate

PTH may be raised or normal (inappropriately), Alk phos raised

technetium-MIBI subtraction scan

Xray: osteitis fibrosa cystica, pepperpot skull, phalangeal erosions

DEXA: osteoporosis

ECG: shortened QT interval, bradycardia, 1st degree block

173
Q

Mx of primary HyperPTH?

A

General: increase fluid intake, avoid dietary calcium and thiazides (increase serum Ca)

definitive tx: total parathyroidectomy / excision of adenoma

conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage

calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery

174
Q

what is secondary hyperPTH?

A

Caused: chronic renal failure, Vit D deficiency

Low Ca-> secondary hyper PTH

Low, Ca, high PTH, high PO4, high Alk phos, low Vit D

175
Q

Mx of secondary hyperPTH?

A

tx cause

phosphate binders: e.g. calcichew (w ca)

Vit D: alfacalcidol

Cinacalcet: increases PTH Ca sensitivity

176
Q

what is tertiary hyperPTH?

A

prolonged secondary hyperPTH -> autonomous PTH secretion

high Ca, high PTH, low PO4, high alk phos

177
Q

Causes of hypoPTH?

A

Autoimmune

Congenital: DiGeorge’s

  • CATCH 22 (cardiac abnormality Fallots, abnormal facies, thymic aplasia, cleft palate, hypoCa, chr22)
    iatrogenic: surgery, radiation
178
Q

Mx of hypoPTH

A

Ca supplements

calcitriol (alcalcidol)

179
Q

What is pseudohypoPTH?

A

failure of target organ response to PTH

symptoms of hypoca

short 4 and 5th metacarpals, short stature

IX: low Ca, high PTH

Tx: Ca, calcitriol

180
Q

phaeochromocytoma rules of 10s?

A

bilateral in 10%

malignant in 10%

extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

10% familial and assoc w MEN II, neurofibromatosis and von Hippel Lindau

181
Q

features of phaeochromocytoma?

A

typically episodic

hypertension (around 90% of cases, may be sustained)

headaches

palpitations

sweating

anxiety

182
Q

Ix of phaeochromocytoma?

A

24h Urinary collection of metanephrines

(also vanillylmandelic acid)

Abdo CT/MRI

183
Q

Mx of phaeo?

A

Medical:

if malignant

chemo or radiolabelled MIBG (mete-iodobenzylguanide)

Surgery:

adrenalectomy is definitive

use Alpha blocker (phenoxybenzamine) first, then BB (propranolol) preop

-monitor BP post op

184
Q

features of hypertensive crisis?

A

pallor

pulsating headache

feeling of impending doom

V high BP

Tachycardic and cardiogenic shock

185
Q

mx of hypertensive crisis?

A

Phentolamine 2-5mg IV (a blocker) or labetalol 50mg IV

  • repeat to safe BP

phenoxybenzamine 10mg/d PO when BP controlled

elective surgery after 4-6 wks to allow full alpha blockade and volume expansion

186
Q

features of cushings syndrome?

A

catabolic effects:

proximal myopathy

striae

bruising

osteoporosis

glucocorticoid effects:

obesity

DM

mineralocorticoid effects:

HTN

hypoK

appearance:

moon face

thin skin

centripetal obesity, thin limbs

acne and hirsutism

interscapular and supraclaviciular fat pads

187
Q

Causes of high ACTH causing CUshings?

A

Cushings disease:

  • bilateral adrenal hyperplasia due to ACTH- secreting pituitary tumour
  • cortisol suppression w high dose dex

Ectopic ACTH:

  • SCLC
  • carcinoid tumour
  • skin pigmentation, metabolic alkalosis, weight loss, hyperglycaemia
  • no suppression w any dose of dex
188
Q

causes of ACTH independent Cushings?

ie. no suppression w any dose of dexamethasone

A

iatrogenic steroids: commonest cause

adrenal adenoma/ ca

Carney complex: LAME syndrome

McCune Albright

189
Q

Ix of Cushings?

A

1st line: 24h urinary free cortisol

Dexamethasone suppression test

  • High dose dexamethasone suppresses Cushings Disease
  • CT/MRI brain/ adrenals
  • DEXA scan: osteoporosis
190
Q

Mx of Cushings’ Syndrome?

A

treat underlying cause

Cushings disease: transsphenoidal excision

Adrenal Adenoma/Ca: adrenalectomy

Ectopic ACTH: tumour excision, metyrapone (inhibits cortisol synthesis)

191
Q

Symptoms of Diabetes Insipidus?

A

polyuria

polydipsia

dehydration

hyperNa: lethargy, thirst, confusion, coma

192
Q

causes of Diabetes Insipidus?

A

Cranial:

idiopathic 50%

congenital

tumours

trauma

vascular - sheehans syndrome

infection - meningoencephalitis

infiltration: sarcoidosis

nephrogenic:

  • congenital
    metabolic: low K, high Ca
    drugs: lithium, vaptans, demecleocycline

post obstructive uropathy

193
Q

Ix of Diabetes Insipidus?

A

Bloods: U+E, Ca, glucose

Urine and plasma osmolality: urine fails to concentrate w water deprivation

Diagnosis via water deprivation test w desmopressin trial

194
Q

Mx of cranial DI?

A

Find cause: MRI brain

Desmopressin PO

195
Q

Mx of nephrogenic DI?

A

treat cause

196
Q

causes of erectile dysfunction?

A

Smoking

Alcohol

DM

endo: hypogonadism, hyperthyroid, high prolactin
neuro: MS, autonomic neuropathy, cord lesion

Pelvic surgery: bladder, prostate

penile abnormalities: peyronies disease

197
Q

How do thiazolidinediones work in DM?

A

agonists to PPAR-gamma receptor and REDUCE peripheral insulin resistance

e.g. pioglitazone

adverse effects: weight gain, liver impairment, fluid retention, increased risk of #s and bladder Ca

198
Q

Pioglitazone SE profile?

A

weight gain

liver impairment (monitor LFTs)

fluid retention - contraindicated in HF

Increased risk of #s and bladder cancer

199
Q

causes of hirsutism?

A

familial

idiopathic

increased androgens: PCOS, Cushings, Adrenal Ca, drugs- steroids

200
Q

features of PCOS?

A

secondary oligo/amenorrhoea -> infertility

obesity

acne, hirsutism

201
Q

Ix of PCOS?

A

US ovaries: bilateral polycystic ovaries

Hormones: high testosterone, low SHBG, high LH:FSH ratio

202
Q

Mx of PCOS?

A

metformin

COCP

clomifene for infertility

203
Q

causes of gynaecomastia?

A

liver cirrhosis

hypogonadism

hyperthyroidism

oestrogen producing tumours

drugs: spironolactone, cimetidine, digoxin, oestrogen

204
Q

symptoms of hyperprolactinaemia?

A

amenorrhoea

infertility

galactorrhoea

decreased libido

Erectile dysfunction

mass effects from prolactinoma

205
Q

Ix of Acromegaly?

A

raised IGF-1

high glucose, Ca, PO4

glucose tolerance test: GH not suppressed

visual fields and acuity

MRI brain

206
Q

Causes of hyperprolactinoma?

A

Dopamine antagonists (commonest cause):

antiemetics: metoclopramide
antipsychotics: haloperidol, risperidone

disinhibition by compression of pituitary stalk:

pituitary adenoma

craniopharyngioma

excess pituitary production:

pregnancy, breastfeeding

prolactinoma (PRL >5000)

hypothyroidism (high TRH-> increased prolactin)

207
Q

Ix of prolactinoma?

A

basal prolactin (>5000 - prolactinoma)

pregnancy test

TFTs

MRI brain

208
Q

Mx of hyperprolactinoma?

A

1st line: dopamine agonists

cabergoline, bromocriptine

  • to decrease prolactin secretion and tumour size

2nd line; transsphenoidal excision

  • if visual or pressure symptoms not managed by medical tx
209
Q

what rate should insulin be given at initially in DKA?

A

0.1 u/kg/ hour

210
Q

micro vs macroadenoma?

A

micro <1 cm

macro >1 cm

211
Q

most common hormone secreted by a pituitary tumour

A

prolactin 50%

212
Q

features of pituitary adenoma?

A

headache

visual field defect: bitemporal hemianopia (superior)

CN palsies: 3, 4, 5, 6 (pressure on cavernous sinus)

Diabetes insipidus

CSF rhinorrhoea

213
Q

Ix of pituitary adenoma?

A

MRI pituitary

Visual field testing

hormones: Prolactin, IGF (GH), ACTH, cortisol, TFTs, LH/FSH

suppression tests

214
Q

Craniopharyngioma features?

A

superior to optic chiasm -> inferior bitemporal hemianopia

commonest childhood intracranial tumour -> Growth failure

Calcification seen on CT/MRI

215
Q

What is pituitary apoplexy?

A

rapid pituitary enlargement due to bleed into a tumour

mass effects: headache, meningism, low GCS, bitemporal hemianopia

cardiovascular collapse due to acute hypopituitarism

216
Q

mx of pituitary apoplexy?

A

urgent hydrocortisone 100mg IV

217
Q

Mx of pituitary adenoma?

A

medical:

replace hormones

treat hormone excess

surgery: trans sphenoidal excision
- pre op hydrocortisone
- post op dynamic pituitary tests

radiotherapy

218
Q

what drug is given pre op to trans sphenoidal excision of pituitary?

A

Hydrocortisone

219
Q

Causes of hypopituitarism?

A

Hypothalamic:

Kallmann’s (anosmia + GnRH deficiency)

Tumour

Inflam, infection, ischaemia

Pituitary stalk:

trauma, surgery, craniopharyngioma

Pituitary:

irradiation

ischaemia- apoplexy, sheehans

tumour

infiltration: hereditary haemochromatosis, amyloid

220
Q

commnest causes of panhypopituitarism?

A

surgery

tumour

irradiation

221
Q

features of hypopituitarism?

A

Hormone deficiency:

GH = central obesity, atherosclerosis, decreased strength/ CO

LH/FSH: low libido, erectile dysfunction, amenorrhoea, breast atrophy

TSH; hypothyroidism

ACTH: secondary adrenal failure

222
Q

Ix of hypopituitarism?

A

basal hormone tests

dynamic pituitary function test:

insulin -> should raise cortisol + GH

GnRH -> LH/FSH

TRH -> T4 + prolactin

MRI brain

223
Q

Tx of hypopituitarism?

A

hormone replacement

tx underlying cause

224
Q

What is MEN1?

A

auto dom

3 Ps

Pituitary adenoma: prolactin or GH

Pancreatic tumour: insulinoma/ gastrinoma

Parathyroid adenoma/ hyperplasia

225
Q

What is MEN 2a?

A

auto dom

functioning hormone tumours in multiple organs

2 Ps 1M

Phaeochromocytoma

Parathyroid hyperplasia/ adenoma

Medullary thyroid Ca

226
Q

What is MEN 2b?

A

auto dom

functioning hormone tumours in multiple organs

3Ms + 1 P

phaeochromocytoma

marfanoid habitus

Medullary thyroid Ca

Multiple mucosal neuromas

227
Q

What is Carney Complex/ LAME syndrome?

A

LAME Syndrome

auto dom

Lentigenes: spotty skin pigmentation
Atrial Myxoma

Endocrine tumours: pituitary, adrenal hyperplasia

Schwannomas

228
Q

what is Von Hippel Lindau?

A

Renal cysts

bilat RCC

haemangioblastomas - often in cerebellum

phaeochromocytoma

pancreatic endocrine tumours

229
Q

what is the most severe of Grave’s eye disease?

A

from most severe:

sight loss due to optic n involvement

corneal involvement

extra ocular muscle involvement

proptosis

230
Q

Autoimmune polyendocrine syndrome type 1 consists of?

A

Auto recessive

Addisons

Candidiasis

HypoPTH

231
Q

Autoimmune polyendocrine Syndrome Type 2 consists of?

A

polygenic

addisons

thyroid disease: Graves, hypothyroid

T1DM

232
Q

Causes of Addison’s disease?

A

destruction of adrenal cortex -> glucocorticoid and mineralocorticoid deficiency

Autoimmune destruction 80% in UK

TB: commonest worldwide

Mets: lung

Haemorrhage; waterhouse-friedrichson

congenital: CAH

233
Q

features of addisons?

A

hyperpigmentation: buccal mucosa, palmar creases

vitiligo

weight loss

lethargy

postural hypotension-> dizziness, faints

hypoglycaemia

addisonian crisis

234
Q

Ix of addisons disease?

A

Bloods: low Na, high K, low glucose, Ca, anaemia

Short SynACTHen test to diagnose

21-hydroxylase Abs: +ve in 80% of autoimmune disease

plasma renin and aldosterone

CXR: TB?

AXR: adrenal calcification

235
Q

Mx of Addisons?

A

Replace: Hydrocotrisone, fludrocortisone

Advice:

dont stop steroids suddenly, increase steroid dose during illness, injury

wear medic alert bracelet

236
Q

Causes of secondary adrenal insufficiency?

ie. hypothalamic or pituitary failure

A

chronic steroid use -> suppression of HPA axis

pituitary apoplexy/ Sheehans

pituitary microadenoma

features: no pigmentation (ACTH low)

237
Q

Addisonian crisis features?

A

shocked: confused, low BP, high HR, oliguria

hypoglycaemia

precipitated by:

infection, trauma, surgery, stopping long term steroids,

adrenal haemorrhage (Waterhouse-Friedrichson)

238
Q

Mx of Addisonian Crisis?

A

hydrocortisone 100 mg im or iv 6hrly until pt stable

1L normal saline infused over 30-60 mins or with dextrose if hypoglycaemic

Tx underlying cause

oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

239
Q

Mx of Addisons disease pt w intercurrent illness?

what to change for doses of hydrocortisone and fludrocortisone

A

double dose of hydrocort

keep same dose fludrocort

240
Q

which mx has the lowest glucocorticoid activity and highest mineralocorticoid?

A

fludrocortisone

241
Q

which mx has the highest glucocorticoid activity and lowest mineralocorticoid?

A

dexamethasone

betamethasone

242
Q

what mx has high glucocorticoid and mineralocorticoid activity?

A

Hydrocortisone

243
Q

features of neuroblastoma?

A

tumour arises from neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.

abdominal mass

pallor, weight loss

bone pain, limp

hepatomegaly

paraplegia

proptosis

244
Q

Ix of neuroblastoma?

A

raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels

calcification may be seen on abdominal x-ray

biopsy

245
Q

Mx of subclinical hypothyroidism in < 65 years with symptoms suggestive of hypothyroidism?

A

trial of levothyroxine

If there is no improvement in symptoms, stop levothyroxine

246
Q

Mx of subclinical hypothyroidism in asymptomatic ppl?

A

observe and repeat thyroid fn in 6mo

247
Q

mx of subclinical hypothyroidism in older ppl?

A

follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’

esp if over 80

248
Q

what electrolyte is extremely important for Calcium levels in the body?

A

Magnesium

required for both PTH secretion and its action on target tissues. Hypomagnesaemia may both cause hypocalcaemia and render patients unresponsive to treatment with calcium and vitamin D supplementation.

Magnesium and calcium interact at a cellular level also and as a result decreased magnesium will tend to affect the permeability of cellular membranes to calcium, resulting in hyperexcitability.

Medicine (16 decks)

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