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MCCQE1 > Medicine - endocrine > Flashcards

Medicine - endocrine Flashcards

1
Q

Treat all diabetic patients aged 40-75 with what regardless of any investigations

A

A statin

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2
Q

Statin indicated conditions

A
  1. Clinical atherosclerosis (MI, ACS, stroke, TIA, carotid disease, peripheral artery disease)
  2. Abdominal aortic aneurysm (>3 cm) or prev AAA surgery
  3. DM >40 yr -15 yr duration for age >30 yr (T1DM) -Microvascular disease
  4. Chronic kidney disease (age 50 yr) -eGFR <60 mL/min/1.73m2 or -ACR >3 mg/mmol 5. LDL-C 5.0 mmol/L
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3
Q

Diagnosis of diabetes (Diabetes Canada 2018 Clinical Practice Guidelines)

A

Any one of the following

FPG 7.0 mmol/L (Fasting = no caloric intake for at least 8 hours) or

HbA1C 6.5% (in adults) (Not for diagnosis of suspected T1DM, children, adolescents, or pregnant women) or

2hPG in a 75g OGTT 11.1mmol/L or Random PG 11.1 mmol/L

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4
Q

Mechanism of action of sulfonylureas

A

Increase endogenous insulin

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5
Q

In whom is Metformin contraindicated?

A
  • >80
  • Renal insufficiency
  • Hepatic failure
  • Heart failure
  • Alcoholics
  • Past history of lactic acidosis on metformin therapy
  • Lactation
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6
Q

Tight glucose control in Type 1 DM decreases risk for micro or macrovascular complications?

A

Micro. The effect on macro (CVA/ MI) is unknown

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7
Q

What type of antibodies may be present in type 1 DM?

A
  • Anti-islet cell
  • Anti-GAD glutamic aid decarboxylase
  • Anti-insulin
  • Anti-Zn transporter
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8
Q

What may a type II with a glucose over 33 mmol/L present with

A

Hyperosmolar Hyperglycaemic state HHS

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9
Q

What is seen on kidney biopsy of diabetic nephropathy?

A

Kimmelstiel-Wilson nodules

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10
Q

Diagnostic HbA1c level for diabetes

A

>6.5%

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11
Q

Diagnostic criteria for metabolic syndrome

A

3 of 5

  1. Abdominal obesity > 40 inches (102cm) in men and 35 inches (88cm) in women
  2. Triglycerides >150mg/gL
  3. BP > 130/85 or a requirement for antihypertensives
  4. Fasting glucose > 100mg/dL
  5. HDL <40mg/dL in men and <50 in women
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12
Q

The single best test for screening of thyroid disease

A

TSH

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13
Q

Preferred screening test for thyroid hormone levels

A

Free T4

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14
Q

Purpose of a radioactive iodine uptake (RAIU) test and scan

A

To determine of a nodule is functioning or nonfunctioning and requires a biopsy for malignancy workup.

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15
Q

Three signs that are specific for Graves disease

A
  • Exopthalmus
  • Pretibial myxedema
  • Thyroid bruits
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16
Q

Antibodies found in patients with Graves disease

A

TSH receptor stimulating antibodies

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17
Q

What to do when screening for TSH if it is a) normal b) high and c) low

A

a) normal- no further tests b) high- measure free T4 c) low- measure free T4 + T3

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18
Q

TSH, T4 and T3 in primary hypothyroidism

A

TSH ⬆︎ T4 ⬇︎ T3 ⬇︎

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19
Q

TSH, T4 and T3 in primary hyperthyroidism

A

TSH ⬇︎ T4 ⬆︎ T3 ⬆︎

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20
Q

TSH, T4 and T3 in secondary hypothyroidism

A

TSH ⬇︎ T4 ⬇︎ T3 ⬇︎

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21
Q

What happens to thyroid levels in pregnancy?

A

TBG increases resulting in reduced free T3/T4 levels and increased TSH

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22
Q

What is the natural history of impaired glucose tolerance (pre-diabetes)? ie in terms of progression

A
  • 1-5% per yr go on to develop DM
  • 50-80% revert to normal glucose tolerance
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23
Q

Genetic syndromes associated with DM

A
  • Down’s syndrome
  • Klinefelter’s syndrome
  • Turner’s syndrome
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24
Q

Infections associated with DM

A
  • Congenital rubella
  • CMV
  • Coxsackie
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25
Q

Target blood pressure Diabetes Canada 2018 Clinical Practice Guidelines

A

130/80

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26
Q

Target Fasting plasma glucose Diabetes Canada 2018 Clinical Practice Guidelines

A

4-7 mmol/L (72-126 mg/dL)

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27
Q

Target 2h post-prandial glucose Diabetes Canada 2018 Clinical Practice Guidelines

A

5-10 mmol/L (90-180 mg/dL) or 5-8 mmol/L (90-144 mg/dL) if not meeting target A1c and can be safely achieved

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28
Q

Pathology of Type I DM

A

Pancreatic cells are infiltrated with lymphocytes resulting in islet cell destruction 80% of cell mass is destroyed before features of DM present

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29
Q

Target HbA1c Diabetes Canada 2018 Clinical Practice Guidelines

A

<7%

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30
Q

Risk factors Type II DM

A
  • Age >40 yr
  • Schizophrenia
  • Abdominal obesity/overweight
  • Fatty liver
  • First-degree relative with DM
  • Hyperuricemia
  • Race/ethnicity (Black, Aboriginal, Hispanic, Asian-American, Pacific Islander)
  • Hx of impaired glucose tolerance or impaired fasting glucose
  • HTN
  • Dyslipidemia
  • Medications e.g. 2nd generation antipsychotics
  • PCOS
  • Hx of gestational DM or macrosomic baby (>9 lb or >4 kg)
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31
Q

HbA1c reflects what?

A

Reflects glycemic control over 3 mo and is a measure of patient’s long-term glycemic control

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32
Q

LDL-C cholesterol target for diabetics

A

LDL-C <2.0 mmol/L

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33
Q

Macro ratios for a diabetic diet

A

Daily carbohydrate intake 45-60% of energy Protein 15-20% of energy Fat <35% of energy

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34
Q

Continue lifestyle modifications in NIDDM for how long before treating?

A

2-3 months

Unless initial HbA1c >8.5% at the time of diagnosis, in which case initiate pharmacologic therapy with metformin immediately, and consider combination of therapies or insulin immediately

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35
Q

Clinical features of HHS Hyperosmolar Hyperglycaemic state

A
  • Onset is insidious, preceded by weakness, polyuria, polydipsia
  • History of decreased fluid intake
  • History of ingesting large amounts of glucose containing fluids
  • Dehydration (orthostatic changes)
  • ⇣ LOC ⇢ lethargy, confusion, comatose due to high serum osmolality
  • Kussmaul’s respiration is absent unless the underlying precipitant has also caused a metabolic acidosis
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36
Q

Clinical features DKA

A

Hyperglycemia (polyuria, polydipsia, weakness) • Acidosis (air hunger, nausea, vomiting, abdominal pain, Kussmaul’s respiration, acetone-odoured breath) • Precipitating conditions (insulin omission, new diagnosis of diabetes, infection, MI, thyrotoxicosis, drugs)

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37
Q

Serum abnormalities DKA

A

Serum • ⇡ BG (typically 11-55 mmol/L, ⇣ Na+ (2º to hyperglycemia - for every ⇡ in BG by 10 mmol/L there is a ⇣ in Na+ by 3 mmol/L)

  • Normal or ⇡ K+, ⇣HCO3–, ⇡ BUN, ⇡ Cr, ketonemia, ⇣ PO43-
  • ⇡ osmolality
  • corrected sodium = current sodium + [0.3 x (current glucose -5)]
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38
Q

What is the best way to monitor the degree of ketoacidosis in DKA?

A

Anion gap is the most important endpoint used to monitor the resolution of the metabolic acidosis

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39
Q

Rehydration in DKA

A

-500 mL/h x4 h, then 250 mL/h x4 h NS if mild-moderate deficit, 1-2 L/h NS if severe deficit (shock)

– Switch to 0.45% NaCl once euvolemic (continue NS if corrected [Na+] is low or rate of fall of plasma osmolality 3 mosm/kg/h)

– once BG reaches 14.0 mmol/L add Dextrose 5% in water or D10W to maintain BG of 12-14 mmol/L

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40
Q

Insulin therapy in DKA

A

Critical to resolve acidosis, not hyperglycemia

  • do not use with hypokalemia (see below), until serum K+ is corrected to >3.3 mmol/L
  • use only regular insulin (R)
  • maintain on 0.1 U/kg/h insulin R infusion
  • check serum glucose hourly
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41
Q

Risk of MI in those with DM compared to age-matched controls

A

3-5x higher

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42
Q

HbA1c level is a significant and independent predictor of the risk of what in DM?

A

Stroke

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43
Q

Clinical features of diabetic retinopathy

A

macular edema: diffuse or focal vascular leakage at the macula

  • non-proliferative (microaneurysms, intraretinal hemorrhage, vascular tortuosity, vascular malformation)
  • proliferative (abnormal vessel growth) • retinal capillary closure
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44
Q

Percentage of diabetics who progress to neuropathy

A

Approximately 50% of patients within 10 yr of onset of T1DM and T2DM

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45
Q

Classical features of peripheral sensory neuropathy in DM

A

Paresthesias (tingling, itching), neuropathic pain, radicular pain, numbness, decreased tactile sensation

Bilateral and symmetric with decreased perception of vibration and pain/ temperature; especially true in the lower extremities but may also be present in the hands

Decreased ankle reflex

Distal-predominant – longest nerves affected first

Classic stocking-glove distribution

May result in neuropathic ulceration of foot

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46
Q

Candidates for bariatric surgery in Canada

A

BMI >35 and risk factors or BMI >40 Failing behavioural modication

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47
Q

For whom should free T3 be measured?

A

Free T should only be measured in the small subset of patients with hyperthyroidism and suspected thyrotoxicosis.

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48
Q

The first line tool for identification of thyroid nodules that require FNAB

A

Ultrasound

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49
Q

Investigation of choice for hyperthyroid patients with thyroid nodules

A

Radioisotope thyroid scan and RAIU

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50
Q

Indication for a radioisotope thyroid scan (Technetium-99)

A

if 1) one or more thyroid nodule(s) and 2) patient is hyperthyroid to determine whether nodules are hot (functioning excess thyroid hormone production) or cold (non-functioning)

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51
Q

What is the chance of malignancy in a hot nodule in a hyperthyroid patient?

A

Very low. Treat the hyperthyroidism

Cold nodules require a workup

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52
Q

Epidemiology of thyrotoxicosis

A

Epidemiology • 1% of general population have hyperthyroidism • F:M = 5:1

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53
Q

Graves Disease- genetic associations

A

Association with HLA-B8 and DR3

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54
Q

Pathophysiology of Graves

A

Autoimmune disorder due to breakdown in thyroid tolerance likely due to a combination of factors including autoreactive B lymphocytes and an imbalance favouring a 2 vs 1 immune response

• B lymphocytes produce thyroid-stimulating immunoglobulin (TSI) that binds and stimulates the TSH receptor and stimulates the thyroid gland

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55
Q

Graves Disease investigation findings

A
  • low TSH
  • increased free T4 (and/or increased T3)
  • positive for TRAb (sensitivity and specicity of third gen TRAb tests that are available currently is > 98% allowing use for determining etiology of hyperthyroidism)
  • increased radioactive iodine (I-131) uptake
  • homogeneous uptake on thyroid scan
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56
Q

Treatment for Graves

A

Thionamides, radiodine (RAI), or surgery.

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57
Q

Name two thionamides and their mechanism of action

A

Thionamides (antithyroid medications): propylthiouracil (PTU) or methimazole (MMI) Inhibit TH synthesis by inhibiting peroxidase-catalyzed reactions, thereby inhibiting organification of iodide, blocking the coupling of iodotyrosines

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58
Q

Major side effects antithyroid meds

A

Hepatotoxicity (cholestasis, hepatitis), agranulocytosis, vasculitis

Note they are also teratogens

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59
Q

Symptomatic Rx hyperthyroidism

A

Beta-blockers

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60
Q

Risks of thyroidectomy

A

Hypoparathyroidism and vocal cord palsy

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61
Q

Painful Thyroiditis (DeQuervain’s, granulomatous) is strongly associated with what genetically?

A

Strongly associated with HLA-D35

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62
Q

Painful Thyroiditis (DeQuervain’s, granulomatous): presentation clinically

A

Painful swelling of the thyroid (may radiate to jaw and ears)

Transient vocal cord paresis

Malaise, Fatigue, myalgia, fever

Often preceded by URTI Painful condition lasts for a week to few months

Signs of hyperthyroidism during hyperthyroid phase (palpitations, tachycardia, stare)

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63
Q

Painful Thyroiditis (DeQuervain’s, granulomatous): Treatment options

A

-NSAID/prednisone for pain

𝝱-adrenergic blockage is usually effective in reversing most of the hypermetabolic and cardiac symptoms

If symptomatically hypothyoid, may treat short-term with thyroxine

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64
Q

Toxic Adenoma/Toxic Multinodular Goitre: Clinical features, and who tends to present with it

A

Clinical Features

  • multinodular goitre
  • tachycardia, heart failure, arrhythmia, weight loss, nervousness, weakness, tremor, and sweats
  • seen most frequently in elderly people as opposed to Graves’ disease which is more common in younger ppl
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65
Q

Toxic Adenoma/Toxic Multinodular Goitre: Treatment

A
  • use high dose radioactive iodine (I-131) to ablate hyperfunctioning nodules
  • 𝜷-blockers often necessary for symptomatic treatment prior to definitive therapy
  • surgical excision may also be used as 1st line treatment
66
Q

Thyrotoxic crisis clinical features

A

hyperthyroidism

  • Extreme hyperthermia (40°C), tachycardia, vomiting, diarrhea, hepatic failure with jaundice, AF, congestive heart failure
  • CNS manifestations including agitation, delirium, psychosis, lethargy, seizures, coma
67
Q

Thyrotoxic crisis bloods

A
  • increased free T4 and T3, undetectable TSH
  • ± anemia, leukocytosis, hyperglycemia, hypercalcemia, elevated LFTs
68
Q

Thyrotoxic crisis Rx

A
  • PTU is the anti-thyroid drug of choice and is used in high doses (200 mg q4h)
  • Give iodide, which acutely inhibits release of thyroid hormone, 1 h after first dose of PTU is given
  • Hydrocortisone 100 mg IV q8h or dexamethasone 2-4 mg IV q6h for the rst 24-48 h; inhibits peripheral conversion of T4 to T3
69
Q

Foods that reduce absorption of thyroxine

A

Soybeans and coffee

70
Q

Secondary hypothyroidism is caused by what?

A

Insufficiency of pituitary TSH

71
Q

Neurological signs of hypothyroidism

A
  • Paresthesia
  • Slow speech
  • Muscle cramps
  • Delay in relaxation phase of deep tendon reflexes (“hung reflexes”) -Carpal tunnel syndrome
  • Asymptomatic increase in CK
  • Seizures
72
Q

Myxedema Coma: mortality rate

A

40%

73
Q

Myxedema Coma: what is it?

A

medical emergency – severe hypothyroidism complicated by trauma, sepsis, cold exposure, MI, inadvertent administration of hypnotics or narcotics, and other stressful events

74
Q

Myxedema Coma: Clinical Features

A
  • hallmark symptoms of decreased mental status and hypothermia
  • hyponatremia, hypotension, hypoglycemia, bradycardia, hypoventilation, and generalized non-pitting edema often present
75
Q

Goitrogens- name some

A

• iodine deciency or excess • rogens: brassica vegetables (e.g. turnip, cassava) • drugs: iodine, lithium, para-aminosalicylic acid

76
Q

Which layer of the adrenal cortex produces mineralocorticoids (aldosterone)?

A

Zona glomerulosa

77
Q

Which layer of the adrenal cortex produces glucocorticoids (cortisol)?

A

Zona Fasciculata

78
Q

Which layer of the adrenal cortex produces androgens (DHEA, androstenedione)

A

Zona Reticularis

79
Q

Principle action of aldosterone

A
  • a mineralocorticoid which regulates extracellular fluid volume through Na+ (and Cl–) retention and K+ (and H+) excretion (stimulates distal tubule Na+/K+ ATPase)
  • regulated by the renin-angiotensin-aldosterone system and by hyperkalemia
80
Q

Gold standard test used to diagnose adrenal insufficiency

A

Insulin tolerance test

81
Q

Dexamethasone (DXM) Suppression Test assesses what?

A

HPA axis.

Principle: DXM suppresses pituitary ACTH, plasma cortisol should be lowered if HPA axis is normal

82
Q

Overnight DXM Suppression Test: method

A

Oral administration of 1 mg DXM at midnight, then measure plasma cortisol levels the following day at 8 AM

Physiologic response: plasma cortisol <50 nmol (<1.8 μg/dL) Inappropriate response: failure to suppress plasma cortisol

83
Q

Core features of primary hyperaldosteronism

A

Hypertension and Hypokalemia

84
Q

Usual cause of hyperaldosteronism

A

Bilateral adrenocortical hyperplasia (60-70%)

Sometimes unilateral adrenal adenoma (Conn syndrome)

85
Q

Hyperaldosteronism treatment

A

Adenoma: surgical resection

Bilateral hyperplasia: Aldosterone receptor antagonist

86
Q

Pheochromocytoma is most commonly associated with which neoplastic syndromes?

A

MEN 2A and 2B

87
Q

What type of tissue is a pheochromocytoma a tumour of?

A

Chromaffin tissue - secretes catecholamines)

88
Q

Presenting features of pheochromocytoma

A
  • 50% suffer from paroxysmal HTN; the rest have sustained HTN
  • classic triad (not found in most patients): episodic “pounding” headache, palpitations/tachycardia, diaphoresis
  • other symptoms: tremor, anxiety, chest or abdominal pain, nausea and vomiting, visual blurring, weight loss, polyuria, polydipsia
89
Q

Best initial test for pheochromocytoma

A

24-urine catecholamines

After that do a CT

90
Q

Most common cause of Cushing’s syndrome

A

Iatrogenic due to prolonged steroid therapy

91
Q

Most common endogenous cause of Cushing’s syndrome

A

Hypersecretion of ACTH from a pituitary adenoma (Cushing’s Disease)

92
Q

Diagnostic tests for Cushing’s (4)

A
  • 24hr free cortisol (↑)
  • Salivary cortisol - late night (↑)
  • ACTH (↑)
  • Dex suppression test morning cortisol level (low dose ↑ high dose ↓)- suppression is normal (no Cushing’s)
93
Q

Acromegaly lab tests 1. to establish abnormality 2. to confirm Dx

A

1) IGF-1 levels (not growth hormone)
2) OGTT - GH levels will remain high despite glucose administration

94
Q

Surgery for acromegaly

A

Transphenoidal surgical resection

95
Q

Medical therapy for acromegaly

A

Ocreotide

96
Q

Complications of acromegaly

A
  • Diabetes from glucose intolerance dt XS GH secretion.
  • Cardiomyopathy
  • Carpal tunnel syndrome
  • Bitemporal hemianopsia (optic chiasm/ pituitary adenoma)
  • Sleep apnea
  • Heart disease

Leading cause of death is cardiovascular

  • congestive heart failure
97
Q

Clinical features of acromegaly

A
  • Skull enlargement
  • frontal bossing
  • wide spaced teeth
  • Coarsening of facial features
  • Large tongue
  • Skin tags
98
Q

Diabetes insipidus- essential problem

A

Inability to produce concentrated urine due to ADH dysfunction.

Central DI- posterior pituitary fails to secrete ADH, or

_Nephrogenic D_I- kidneys fail to respond to ADH

99
Q

Diagnosis of diabetes insipidus

A

1) serum osmolality > urine osmolality, reduced urinary sodium, possible hypernatremia
2) water deprivation test - patients continue to excite high volume of dilute urine
3) desmopressin acetate suppression test (DDAVP) - DDAVP is synthetic analog of ADH. In Central DI it shows reduced urine output and increased urine osmolarity. _In nephrogenic DI there is no effec_t on urine output or osmolarity.

100
Q

What are the three peaks of occurrence of physiologic gynecomastia?

A

Neonates Puberty Old age

101
Q

Percentage of gynecomastia that is idiopathic

A

58%

102
Q

Pathological causes of gynecomastia

A
  • Hepatic cirrhosis
  • Testicular carcinoma (not commonly though)
  • Chronic kidney disease
  • Lung cancers
  • Klinefelter’s
  • Certain meds
  • Pituitary adenoma
103
Q

ADH works where to do what?

A

At the collecting ducts of the nephron to bring back water from urine to the bloodstream therefore to dilute the serum. Serum osmolality and serum sodium drop.

104
Q

What happens to plasma osmolality in SIADH?

A

Decreases

105
Q

Best initial management of SIADH

A

Restrict fluid. This is the cornerstone of managing SIADH

106
Q

Why do you have to correct hyponatremia slowly in SIADH?

A

To prevent osmotic demyelination syndrome

107
Q

Management of persistent or symptomatic hyponatremia in SIADH

A

IV hypertonic saline therapy

108
Q

ADH secretion does what to urine volume

A

Reduces it, producing concentrated urine

109
Q

Some complications of Pagets Disease of Bone (PDB)

A

Nerve root compression

Spinal stenosis

Deafness

Pathological fractures

Secondary osteoarthritis

Osteosarcoma

High output cardiac failure

110
Q

Classic radiologic findings of PDB

A

Thickening of the cortex

Accentuation of the trabecular pattern

Increased bone density

Skull X-Rays described as having ‘cotton wool’ appearance

X-Rays are diagnostic

111
Q

The most sensitive way to differentiate primary from secondary causes of hyperaldosteronism?

A

Aldosterone to renin ratio

You can do the test with random sodium intake

112
Q

Best test for adrenal function eg Addison’s

A

Cosyntropin stimulation test (inject cosyntropin iv and measure cortisol 60mins later)

aka the ACTH Test/ The Synacthen test

ACTH is injected and cortsol is measured

It is 97% sensitive and 95% specific for primary adrenal insufficiency

113
Q

First line treatment PDB. And what supplements also need to be administered?

A

Bisphosphonates are first line

Also calcium and vitamin D

114
Q

Signs of zinc deficiency

A
  • Leukonychia
  • Night blindness
  • Impaired taste
  • Impaired growth
  • Alopecia
  • Impaired immunity
  • Anemia lethargy
  • Poor wound healing
  • Delayed puberty
115
Q

Which substance can worsen Graves orbitopathy?

A

Radioactive iodine

116
Q

Elevated parathyroid hormone levels are usually caused by what?

A

Single parathyroid adenoma in 80% cases

117
Q

Calcium reference range

A

Calcium is maintained within a fairly narrow range from 8.5 to 10.5 mg/dl (4.3 to 5.3 mEq/L or 2.2 to 2.7 mmol/L).

118
Q

Best screening test for diabetic nephropathy

A

Detection of microalbuminuria

119
Q

HbA1c target

A

7%

120
Q

Laboratory features of pheochromocytoma

A

Hyperglycemia

Hypercalcemia

Erythrocytosis

121
Q

Renoprotective drugs for diabetic nephropathy

A

ACE inhibitors

Angiotensin receptor blockers

They delay the progression of chronic kidney disease in DMs with Microalbuminuria

122
Q

In addition to the treatment of diabetes, insulin can also be used to manage severe what?

A

Hyperkalemia

123
Q

Drugs that can cause SIADH

A
  • Amiodarone
  • Carbamazepine
  • SSRIs
  • Chlorpromazine
124
Q

First line of management for severe hypercalcemia

A

Saline infusion

Hypercalcemia causes dehydration from vomiting and renal insufficiency. Hydration alone may lower calcium levels.

125
Q

How do you monitor thyroxine overreplacement?

A

With TSH levels

126
Q

Omega 3 fish oils have been shown to do what to reduce the risk of stroke after MI

A

Reduce triglycerides

127
Q

Absolute contraindication to radio iodine Rx for Graves disease

A

Pregnancy

128
Q

What do you have to do to antithyroid medication before radio iodine therapy?

A

Stop it

129
Q

The most common cause of death in Marfan Syndrome

A

Dissecting aortic aneurysm

130
Q

The screening tool of choice for Cushing’s

A

24-hour urinary cortisol

131
Q

The most specific test for acromegaly

A

Measuring serum GH during OGTT

132
Q

What is the WHO definition for ‘impaired fasting glucose’ (IFG)?

A

Fasting glucose 5.6-7 mmol/l.

133
Q

Which tumours are associated with MEN2A (multiple endocrine neoplasia)?

A

Mnemonic TAP 1. Thyroid (medullary carcinoma). 2. Adrenal (phaeochromocytoma). 3. Parathyroid.

134
Q

What is the function of parathyroid hormone (PTH)?

A

To increase serum Ca levels NOTES Acts at the bone (osteoclast stimulation) and kidneys (Ca absorption and PO4 excretion, calcitriol synthesis).

135
Q

What is the mechanism of action of metformin?

A
  1. Decreases hepatic glucose production.
  2. Decreases intestinal glucose absorption.
  3. Increases insulin sensitivity.
136
Q

Most serious side effect of metformin

A

Lactic acidosis

137
Q

List 2 examples of rapid-acting insulin

A
  1. Humalog
  2. Novorapid

NOTES Usually taken just before a meal. Usually prescribed in type 1 diabetes. Increased risk of hypoglycaemic episodes.

138
Q

List 2 examples of long-acting insulin

A
  1. Lantus (glargine).
  2. Levemir (determir).
  3. Hypurin bovine lente.
139
Q

What is Kallman syndrome?

A

Hypogonadotropic hypogonadism with anosmia

NOTES

A genetic disorder, due to failure of migration of hypothalamic GnRH-secreting neurons. Represents a type of tertiary hypogonadism.

140
Q

“What is the treatment for asymptomatic SIADH?”

A

Must consider and address the underlying cause, in the meantime:

  1. Conservative - Patient education. Fluid restriction e.g. 1500ml/day.
  2. Meds e.g. IV saline in severe hyponatraemia (consider).

NOTES SIADH = syndrome of inappropriate antidiuretic hormone. Slow correction of hyponatraemia minimises the risk of osmotic demyelination syndrome.

141
Q

What is the treatment for hypocalcaemia?

A

Must consider and address underlying cause, in the meantime:

  1. Resus A+B - consider airway support and O2. C - IV access.
  2. Meds 20ml of 10% calcium gluconate IV.
142
Q

First line treatment for acromegaly

A

Surgery

143
Q

What are the clinical features of hypercalcaemia?

A

History

Neuro: tiredness, acute confusion.

Urinary: polyuria, polydipsia, may be renal stones.

GIT: constipation, nausea.

Skeletal: pathological fractures (demineralisation).

Examination: signs of delirium, dehydration. Palpation: may be abdo tenderness.

NOTES Mnemonic for features of hypercalcaemia: ““stones, bones, and groans””.

144
Q

What is Chvostek’s sign?

A

Contraction of ipsilateral facial muscles on tapping the facial nerve anterior to the ear.

145
Q

What is Trousseau’s sign?

A

Carpopedal spasm after application of a tourniqet to occlude the pulse for 3 min.

NOTES A sign of hypocalcaemia.

146
Q

What is the treatment for Graves eye disease?

A
  1. Conservative e.g. smoking cessation; dark glasses; artificial tears.
  2. Meds e.g. prednisolone, consider rituximab.
  3. Radiotherapy (uncertain benefit).
  4. Surgery (orbital decompression).
147
Q

Hypertension and hypokalemia together

A

Primary hyperaldosteronism ***

148
Q
A

Pretibial myxoedema

Graves disease

149
Q
A

Acromegaly

150
Q
A

Cushing’s syndrome

151
Q
A

Chvostek sign

Hypocalcemia

152
Q
A

Paget’s disease with cotton wool appearance

153
Q
A

Myxoedema

154
Q
A
155
Q

Causes of hyperprolactinaemia

A
  • Pituitary or hypothalamic tumour compressing stalk infiltration
  • Pregnancy or breast feeding
  • Co-secretion of prolactin in acromegaly
  • Hypothyroidism
  • Stress
  • Renal failure
  • Drugs
156
Q

Pheochromocytoma investigations

A

Plasma-free metanephrines and normetanephrines

Abdominal CT

157
Q

Pheochromocytoma complications

A
  • Hypertensive crisis- elevated systolic blood pressure (> 200 mmHg) that is unresponsive to traditional treatment and threatens end-organ damage
  • Myocardial Ischemia/Infarction
  • Toxic myocarditis
  • Cardiomyopathy
  • Stroke
  • Headache
158
Q

Biggest cause of Addison’s disease in the developing world

A

TB

159
Q

Signs of primary adrenal insufficiency

A
  • Gradual onset
  • Hypotension
  • Hyperpigmentation
  • Fatigue
  • Musce weakness
  • Weight loss
160
Q

What might this be?

Sudden penetrating pain in the legs, lower back, or abdomen

Severe vomiting and diarrhea, resulting in dehydration

Low blood pressure

Syncope

Hypoglycemia

Confusion, psychosis, slurred speech

Severe lethargy

Hyponatremia

Hyperkalemia

Hypercalcemia

Convulsions

Fever

A

An Addisonian crisis

MCCQE1 (20 decks)

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