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
Target blood pressure Diabetes Canada 2018 Clinical Practice Guidelines
130/80
26
Target Fasting plasma glucose Diabetes Canada 2018 Clinical Practice Guidelines
4-7 mmol/L (72-126 mg/dL)
27
Target 2h post-prandial glucose Diabetes Canada 2018 Clinical Practice Guidelines
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
28
Pathology of Type I DM
Pancreatic cells are **infiltrated with lymphocytes** resulting in islet cell destruction 80% of cell mass is destroyed before features of DM present
29
Target HbA1c Diabetes Canada 2018 Clinical Practice Guidelines
\<7%
30
Risk factors Type II DM
* 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)
31
HbA1c reflects what?
Reflects glycemic control over 3 mo and is a measure of patient’s long-term glycemic control
32
LDL-C cholesterol target for diabetics
LDL-C \<2.0 mmol/L
33
Macro ratios for a diabetic diet
Daily carbohydrate intake 45-60% of energy Protein 15-20% of energy Fat \<35% of energy
34
Continue lifestyle modifications in NIDDM for how long before treating?
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
35
Clinical features of HHS Hyperosmolar Hyperglycaemic state
* 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
36
Clinical features DKA
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)
37
Serum abnormalities DKA
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)]
38
What is the best way to monitor the degree of ketoacidosis in DKA?
Anion gap is the most important endpoint used to monitor the resolution of the metabolic acidosis
39
Rehydration in DKA
-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
40
Insulin therapy in DKA
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
41
Risk of MI in those with DM compared to age-matched controls
3-5x higher
42
HbA1c level is a significant and independent predictor of the risk of what in DM?
Stroke
43
Clinical features of diabetic retinopathy
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
44
Percentage of diabetics who progress to neuropathy
Approximately 50% of patients within 10 yr of onset of T1DM and T2DM
45
Classical features of peripheral sensory neuropathy in DM
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
46
Candidates for bariatric surgery in Canada
BMI \>35 and risk factors or BMI \>40 Failing behavioural modication
47
For whom should free T3 be measured?
Free T should only be measured in the small subset of patients with hyperthyroidism and suspected thyrotoxicosis.
48
The first line tool for identification of thyroid nodules that require FNAB
Ultrasound
49
Investigation of choice for hyperthyroid patients with thyroid nodules
Radioisotope thyroid scan and RAIU
50
Indication for a radioisotope thyroid scan (Technetium-99)
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)
51
What is the chance of malignancy in a hot nodule in a hyperthyroid patient?
Very low. Treat the hyperthyroidism Cold nodules require a workup
52
Epidemiology of thyrotoxicosis
Epidemiology • 1% of general population have hyperthyroidism • F:M = 5:1
53
Graves Disease- genetic associations
Association with HLA-B8 and DR3
54
Pathophysiology of Graves
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
55
Graves Disease investigation findings
* 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
56
Treatment for Graves
Thionamides, radiodine (RAI), or surgery.
57
Name two thionamides and their mechanism of action
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
58
Major side effects antithyroid meds
Hepatotoxicity (cholestasis, hepatitis), agranulocytosis, vasculitis Note they are also **teratogens**
59
Symptomatic Rx hyperthyroidism
Beta-blockers
60
Risks of thyroidectomy
Hypoparathyroidism and vocal cord palsy
61
Painful Thyroiditis (DeQuervain's, granulomatous) is strongly associated with what genetically?
Strongly associated with HLA-D35
62
Painful Thyroiditis (DeQuervain's, granulomatous): presentation clinically
**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)
63
Painful Thyroiditis (DeQuervain's, granulomatous): Treatment options
-**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
64
Toxic Adenoma/Toxic Multinodular Goitre: Clinical features, and who tends to present with it
_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
65
Toxic Adenoma/Toxic Multinodular Goitre: Treatment
* 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
Thyrotoxic crisis clinical features
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
Thyrotoxic crisis bloods
* increased free T4 and T3, undetectable TSH * ± anemia, leukocytosis, hyperglycemia, hypercalcemia, elevated LFTs
68
Thyrotoxic crisis Rx
* **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
Foods that reduce absorption of thyroxine
Soybeans and coffee
70
Secondary hypothyroidism is caused by what?
Insufficiency of pituitary TSH
71
Neurological signs of hypothyroidism
* Paresthesia * Slow speech * Muscle cramps * Delay in relaxation phase of deep tendon reflexes (“hung reflexes”) -Carpal tunnel syndrome * Asymptomatic increase in CK * Seizures
72
Myxedema Coma: mortality rate
40%
73
Myxedema Coma: what is it?
medical emergency – severe hypothyroidism complicated by trauma, sepsis, cold exposure, MI, inadvertent administration of hypnotics or narcotics, and other stressful events
74
Myxedema Coma: Clinical Features
* hallmark symptoms of decreased mental status and hypothermia * hyponatremia, hypotension, hypoglycemia, bradycardia, hypoventilation, and generalized non-pitting edema often present
75
Goitrogens- name some
• iodine deciency or excess • rogens: brassica vegetables (e.g. turnip, cassava) • drugs: iodine, lithium, para-aminosalicylic acid
76
Which layer of the adrenal cortex produces mineralocorticoids (aldosterone)?
Zona glomerulosa
77
Which layer of the adrenal cortex produces glucocorticoids (cortisol)?
Zona Fasciculata
78
Which layer of the adrenal cortex produces androgens (DHEA, androstenedione)
Zona Reticularis
79
Principle action of aldosterone
* 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
Gold standard test used to diagnose adrenal insufficiency
Insulin tolerance test
81
Dexamethasone (DXM) Suppression Test assesses what?
HPA axis. Principle: DXM suppresses pituitary ACTH, plasma cortisol should be lowered if HPA axis is normal
82
Overnight DXM Suppression Test: method
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
Core features of primary hyperaldosteronism
Hypertension and Hypokalemia
84
Usual cause of hyperaldosteronism
Bilateral adrenocortical hyperplasia (60-70%) Sometimes unilateral adrenal adenoma (Conn syndrome)
85
Hyperaldosteronism treatment
Adenoma: surgical resection Bilateral hyperplasia: Aldosterone receptor antagonist
86
Pheochromocytoma is most commonly associated with which neoplastic syndromes?
MEN 2A and 2B
87
What type of tissue is a pheochromocytoma a tumour of?
Chromaffin tissue - secretes catecholamines)
88
Presenting features of pheochromocytoma
* 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
Best initial test for pheochromocytoma
24-urine catecholamines After that do a CT
90
Most common cause of Cushing's syndrome
Iatrogenic due to prolonged steroid therapy
91
Most common endogenous cause of Cushing's syndrome
Hypersecretion of ACTH from a pituitary adenoma (Cushing's Disease)
92
Diagnostic tests for Cushing's (4)
- 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
Acromegaly lab tests 1. to establish abnormality 2. to confirm Dx
1) **IGF-1 levels** (not growth hormone) 2) **OGTT** - GH levels will remain high despite glucose administration
94
Surgery for acromegaly
Transphenoidal surgical resection
95
Medical therapy for acromegaly
Ocreotide
96
Complications of acromegaly
- **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
Clinical features of acromegaly
* Skull enlargement * frontal bossing * wide spaced teeth * Coarsening of facial features * Large tongue * Skin tags
98
Diabetes insipidus- essential problem
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
Diagnosis of diabetes insipidus
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
What are the three peaks of occurrence of physiologic gynecomastia?
Neonates Puberty Old age
101
Percentage of gynecomastia that is idiopathic
58%
102
Pathological causes of gynecomastia
* Hepatic **cirrhosis** * Testicular carcinoma (not commonly though) * Chronic kidney disease * **Lung cancers** * Klinefelter's * Certain meds * Pituitary adenoma
103
ADH works where to do what?
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
What happens to plasma osmolality in SIADH?
Decreases
105
Best initial management of SIADH
**Restrict fluid**. This is the cornerstone of managing SIADH
106
Why do you have to correct hyponatremia slowly in SIADH?
To prevent osmotic demyelination syndrome
107
Management of persistent or symptomatic hyponatremia in SIADH
IV hypertonic saline therapy
108
ADH secretion does what to urine volume
Reduces it, producing concentrated urine
109
Some complications of Pagets Disease of Bone (PDB)
**Nerve root compression** Spinal stenosis Deafness **Pathological fractures** Secondary osteoarthritis **Osteosarcoma** High output cardiac failure
110
Classic radiologic findings of PDB
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
The most sensitive way to differentiate primary from secondary causes of hyperaldosteronism?
Aldosterone to renin ratio You can do the test with random sodium intake
112
Best test for adrenal function eg Addison's
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
First line treatment PDB. And what supplements also need to be administered?
Bisphosphonates are first line Also calcium and vitamin D
114
Signs of zinc deficiency
* Leukonychia * Night blindness * Impaired taste * Impaired growth * Alopecia * Impaired immunity * Anemia lethargy * Poor wound healing * Delayed puberty
115
Which substance can worsen Graves orbitopathy?
Radioactive iodine
116
Elevated parathyroid hormone levels are usually caused by what?
Single parathyroid adenoma in 80% cases
117
Calcium reference range
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
Best screening test for diabetic nephropathy
Detection of microalbuminuria
119
HbA1c target
7%
120
Laboratory features of pheochromocytoma
**Hyperglycemia** **Hypercalcemia** Erythrocytosis
121
Renoprotective drugs for diabetic nephropathy
ACE inhibitors Angiotensin receptor blockers They delay the progression of chronic kidney disease in DMs with Microalbuminuria
122
In addition to the treatment of diabetes, insulin can also be used to manage severe what?
Hyperkalemia
123
Drugs that can cause SIADH
* Amiodarone * Carbamazepine * SSRIs * Chlorpromazine
124
First line of management for severe hypercalcemia
**Saline infusion** Hypercalcemia causes dehydration from vomiting and renal insufficiency. Hydration alone may lower calcium levels.
125
How do you monitor thyroxine overreplacement?
With TSH levels
126
Omega 3 fish oils have been shown to do what to reduce the risk of stroke after MI
Reduce triglycerides
127
Absolute contraindication to radio iodine Rx for Graves disease
Pregnancy
128
What do you have to do to antithyroid medication before radio iodine therapy?
Stop it
129
The most common cause of death in Marfan Syndrome
Dissecting aortic aneurysm
130
The screening tool of choice for Cushing's
24-hour urinary cortisol
131
The most specific test for acromegaly
Measuring serum GH during OGTT
132
What is the WHO definition for 'impaired fasting glucose' (IFG)?
Fasting glucose 5.6-7 mmol/l.
133
Which tumours are associated with MEN2A (multiple endocrine neoplasia)?
Mnemonic TAP 1. Thyroid (medullary carcinoma). 2. Adrenal (phaeochromocytoma). 3. Parathyroid.
134
What is the function of parathyroid hormone (PTH)?
To increase serum Ca levels NOTES Acts at the bone (osteoclast stimulation) and kidneys (Ca absorption and PO4 excretion, calcitriol synthesis).
135
What is the mechanism of action of metformin?
1. Decreases hepatic glucose production. 2. Decreases intestinal glucose absorption. 3. Increases insulin sensitivity.
136
Most serious side effect of metformin
Lactic acidosis
137
List 2 examples of rapid-acting insulin
1. Humalog 2. Novorapid NOTES Usually taken just before a meal. Usually prescribed in type 1 diabetes. Increased risk of hypoglycaemic episodes.
138
List 2 examples of long-acting insulin
1. Lantus (glargine). 2. Levemir (determir). 3. Hypurin bovine lente.
139
What is Kallman syndrome?
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
"What is the treatment for asymptomatic SIADH?"
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
What is the treatment for hypocalcaemia?
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
First line treatment for acromegaly
Surgery
143
What are the clinical features of hypercalcaemia?
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
What is Chvostek's sign?
Contraction of ipsilateral facial muscles on tapping the facial nerve anterior to the ear.
145
What is Trousseau's sign?
Carpopedal spasm after application of a tourniqet to occlude the pulse for 3 min. NOTES A sign of hypocalcaemia.
146
What is the treatment for Graves eye disease?
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
Hypertension and hypokalemia together
Primary hyperaldosteronism \*\*\*
148
Pretibial myxoedema Graves disease
149
Acromegaly
150
Cushing's syndrome
151
Chvostek sign Hypocalcemia
152
Paget's disease with cotton wool appearance
153
Myxoedema
154
155
Causes of hyperprolactinaemia
* _Pituitary or hypothalamic tumour_ compressing stalk infiltration * Pregnancy or breast feeding * Co-secretion of prolactin in acromegaly * _Hypothyroidism_ * Stress * _Renal failure_ * Drugs
156
Pheochromocytoma investigations
Plasma-free metanephrines and normetanephrines Abdominal CT
157
Pheochromocytoma complications
* **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
Biggest cause of Addison's disease in the developing world
TB
159
Signs of primary adrenal insufficiency
* Gradual onset * Hypotension * Hyperpigmentation * Fatigue * Musce weakness * Weight loss
160
**What might this be?** ## Footnote 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
An Addisonian crisis