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Year 4 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the major endocrine glands and what hormones do they produce?

A
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2
Q

What are the 3 functions of thyroid hormone?

A
  • Thyroid hormone is critical to
    • brain and somatic development in fetus and
      infants
    • metabolic activity in adults
    • function of virtually every organ system.
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3
Q

What are the primary and secondary causes of hypercholesterolaemia?

A
  • Primary:
    • Familial hypercholesterolaemia
    • Polygenic hypercholesterolaemia:
      • Most common, asymptomatic until vascular disease develops.
  • Secondary:
    • Endocrine: hypothyroidism
    • renal: nephrotic syndrome
    • immunological: monoclonal gammopathy
    • hepatic: cholestatic liver disease (e.g. primary biliary cirrhosis)
    • nutritional: diet, anorexia nervosa
    • drugs: cyclosporin, anabolic steroids, carbamazepine
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4
Q

What are the primary and secondary causes of hypertriglyceridaemia?

A
  • Primary:
    • Familial lipoprotein lipase deficiency
    • Familial hypertriglyceridaemia
  • Secondary:
    • endocrine: obesity/metabolic syndrome, hypothyroidism (more for high LDL, not TG), acromegaly, Cushing’s syndrome, DM
    • renal: chronic renal failure, polyclonal and monoclonal hypergammaglobulinemia
    • hepatic: chronic liver disease, hepatitis, glycogen storage disease
    • drugs: alcohol, corticosteroids, estrogen, hydrochlorothiazide, retinoic acid, β-blockers without intrinsic sympathomimetic action (ISA), anti-retroviral drugs, atypical antipsychotics, oral contraceptive pills
    • other: pregnancy
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5
Q

What are the common causes of low HDL?

A
  • Obesity
  • Physical inactivity
  • Cigarette smoking
  • Metabolic syndrome, type 2 DM
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6
Q

What are the side effects of atypical antipsychotics?

Endocrine only

A
  • Increased risk of
    • Dyslipidaemia
    • HTN
    • Metabolic syndrome
    • Hyperglycaemia
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7
Q

Describe the formation of atherosclerosis over time.

A
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8
Q

What is the treatment for hypercholesterolaemia and hypertriglyceridaemia?

A
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9
Q

Where do the different antihyperglycaemia agent act on the glucose metabolism?

A
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10
Q

Describe what pre-diabetes is (imparied glucose tolerance/imparied fasting glucose)?

A
  • 1-5% per yr go on to develop DM
  • 50-80% revert to normal glucose tolerance
  • weight loss may improve glucose tolerance
  • increased risk of developing macrovascular complications
  • lifestyle modifications decrease progression to DM by 58%
  • Diagnostic Criteria
    • impaired fasting glucose (IFG): fasting blood glucose (FBG) 6.1-6.9 mmol/L
    • impaired glucose tolerance (IGT): 2h 75 g oral glucose tolerance test (OGTT) 7.8-11.0 mmol/L
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11
Q

What is the definition of diabetes mellitus?

A

Syndrome of disordered metabolism and inappropriate hyperglycemia secondary to an absolute/relative deficiency of insulin, or a reduction in biological effectiveness of insulin, or both.

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12
Q

What is the diagnostic criteria ofdiabetes mellitus?

A
  • any one of the following is diagnostic
    • presence of classic symptoms of DM (polyuria, polydipsia, polyphagia, weight loss, blurry vision, nocturia, ketonuria) PLUS random blood glucose (BG) ≥ 11.1 mmol/L
    • on at least two separate occasions
      • FPG ≥ 7.0 mmol/L (fasting = no caloric intake for at least 8 h) OR
      • 2 h 75 g OGTT ≥11.1 mmol/L OR
      • random PG ≥11.1 mmol/L OR
      • HbA1c ≥6.5%
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13
Q

What are the aetiologies of DM?

A
  • Type 1 DM (immune-mediated β cell destruction, usually leading to absolute insulin deficiency)
  • Type 2 DM (ranges from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance 2 o to β cell dysfunction)
  • Other specific causes of DM:
    • Genetic defects of β cell function (e.g. MODY – Maturity-Onset Diabetes of the Young) or insulin action
    • Diseases of the exocrine pancreas:
      • Pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis (“bronze diabetes”)
    • Endocrinopathies:
      • Acromegaly, Cushing’s syndrome, glucagonoma, pheochromocytoma, hyperthyroidism
    • Drug-induced:
      • Glucocorticoids, thyroid hormone, β-adrenergic agonists, thiazides, phenytoin, clozapine
    • Infections:
      • Congenital rubella, CMV, coxsackie
    • Genetic syndromes associated with DM:
      • Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome
  • Gestational Diabetes Mellitus
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14
Q

Describe the difference between type I and type II DM with regards to.

Onset, epidemiology, aetilogy, genetics, pathophysiology, natural Hx and circulating autoantibodies?

A
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15
Q

Describe the difference between type I and type II DM with regards to.

Risk factors, body habitus, treatment, acute complications and screening.

A
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16
Q

What are the glycaemic targets in DM?

A

HbA1c 7.0%

More intensive glucose control with those who are young and have not had for long time, less intensive for older/limited life expectancy

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17
Q

What are the aims of diet control in DM?

A
  • daily carbohydrate intake 45-60% of energy, protein 15-20% of energy, and fat <35% of energy
  • intake of saturated fats <7% and polyunsaturated fats <10% of total calories each
  • limit sodium, alcohol, and caffeine intake
  • type 1: carbohydrate counting is used to titrate insulin regimen
  • type 2: weight reduction
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18
Q

WHat are the lifestyle aims of DM?

A
  • regular physical exercise to improve insulin sensitivity, lower lipid concentrations and control blood pressure
  • smoking cessation
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19
Q

When are medical DM treatment indicated?

Oral antihyperglycaemics

A
  • initiate oral antihyperglycemic therapy and/or incretin therapy within 2-3 mo if lifestyle management does not result in glycemic control
  • if HbA1c >8.5%, initiate pharmacologic therapy immediately and consider combination oral therapy or insulin immediately
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20
Q

When is Insulin treatment indicated in DM?

And what are the main catagories of insulins?

A
  • used for type 1 DM at onset, may be used in type 2 DM at any point in treatment
  • routes of administration: subcutaneous injections, continuous subcutaneous insulin infusion pump, IV infusion (regular insulin only)
  • bolus insulins: short-acting (Insulin regular), rapid-acting analogue (Insulin aspart, Insulin lispro, Insulin glulisine)
  • basal insulins: intermediate-acting (Insulin NPH), long-acting analogue (Insulin detemir, Insulin glargine)
  • premixed insulins (% Humulin R and % NPH) 30/70; premixed insulin analogues (Biphasic Insulin aspart, Insulin lispro/lispro protamine)
  • estimated total daily insulin requirement: 0.5-0.7 units/kg (often start with 0.3-0.5 units/kg/day)
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21
Q

What are some approaches to treatment of hyperglycaemia in type 2 DM?

A
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22
Q

What are the different types of insulins available and what is there onset, peak and duration?

A
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23
Q

What are some common insulin regimes used in both TIDM and TIIDM?

A
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24
Q

First thought.

Treatment for DKA/HHS?

A
  • Fluids
  • Insulin
  • K+
  • Search for and treat precipitant
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25
Q

What are the 8 Is precipitating DKA?

A
  • Infection
  • Ischemia or Infarction
  • Iatrogenic (glucocorticoids)
  • Intoxication
  • Insulin missed
  • Initial presentation
  • Intra-abdominal process (e.g. pancreatitis, cholecystitis)
  • Intraoperative/perioperative stress
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26
Q

Describe the pathophysiology of diabetic ketoacidosis?

A
  • Usually occurs in T1DM
  • Insulin deficiency with ↑ counterregulatory hormones
    (glucagon, cortisol, catecholamines, GH)
  • Can occur with lack of insulin (non-adherence, inadequate dosage, 1st presentation) or increased stress (surgery, infection, exercise)
  • Unrestricted hepatic glucose production → hyperglycemia →
    osmotic diuresis → dehydration and electrolyte disturbance →
    ↓ Na + (water shift to ECF causing pseudohyponatremia)
  • Fat mobilization → ↑ FFA → ketoacids → metabolic acidosis
  • Severe hyperglycemia exceeds the renal threshold for glucose and ketone reabsorption → glucosuria and ketonuria
  • Total body K+ depletion but serum K+ may be normal or elevated 2º to shift from ICF to ECF due to lack of insulin, ↑ plasma osmolality
  • Total body PO43- depletion
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27
Q

What are the clinical features of DKA?

A
  • Polyuria, polydipsia, polyphagia with marked fatigue, N/V
  • Dehydration (orthostatic changes)
  • LOC may be ↓ with ketoacidosis or with high serum osmolality
    (osm >330 mmol/L)
  • Abdominal pain
  • Fruity smelling breath
  • Kussmaul’s respiration
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28
Q

What is seen on bloods in a pt with DKA?

A
  • ↑ BG (typically11-55 mmol/L), ↓ Na+ (2º to
    hyperglycemia → for every ↑ in BG by 10 mmol/L
    there is a ↓ in Na+ by 3 mEq/L)
    • Normal or ↑ K+ , ↓ HCO3– , ↑ BUN, ↑ Cr, ketonemia, ↓ PO43-
    • ↑ osmolality
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29
Q

What in seen on ABG in DKA?

A
  • Metabolic acidosis with ↑ AG, possible 2º respiratory alkalosis
  • If severe vomiting/dehydration there may be a metabolic alkalosis
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30
Q

What is seen in hte urine in DKA?

A

+ve for glucose and ketones

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31
Q

What is the treatment for DKA

A
  • ABCs if patient is stuporous or comatose
  • Monitor degree of ketoacidosis with Anion Gap, not Blood Glucose or serum ketone level
  • Rehydration:
    • 1 L/h NS in first 2 h
    • after 1st 2 L, 300-400 mL/h 0.45% NaCl (continue NS if
      corrected sodium is falling faster than 3 mosm/kg water/h)
    • once BG reaches 13.9 mmol/L then switch to D5W
    • to maintain BG in the range of 13.9-16.6 mmol/L
  • Insulin therapy:
    • critical to resolve acidosis, not hyperglycemia
    • do not use with hypokalemia, until serum K+ is corrected to >3.3 mEq/L
    • use only regular insulin (R)
    • maintain on 0.1 U/kg/h insulin R infusion
    • check serum glucose hourly
  • K+ replacement:
    • with insulin administration, hypokalemia may develop
    • if serum K+ <3.3 mEq/L, hold insulin and give 40 mEq/L K+ replacement
    • when K+ 3.5-5.0 mEq/L add KCL 20-40 mEq/L IV fluid to keep K+ in the range of 3.5-5 mEq/L
  • HCO3–:
    • if pH <7.0 or if hypotension, arrhythmia, or coma is present
      with a pH of <7.1 give HCO3– in 0.45% NaCl
    • do not give if pH >7.1 (risk of metabolic alkalosis)
    • can give in case of life-threatening hyperkalemia
  • ± mannitol (for cerebral edema)
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32
Q

What is the prognosis of DKA?

A
  • 2-5% mortality in developed countries
  • Serious morbidity from sepsis, hypokalemia, respiratory
    complications, thromboembolic complications, and cerebral oedema (the latter in children)
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33
Q

Describe the pathophysiology of hyperosmolar hyperglycaemic state (HHS)?

A
  • Occurs in type 2 DM
  • Often precipitated by sepsis, stroke, MI, CHF, renal failure, trauma, drugs (glucocorticoids, immunosuppressants, phenytoin, diuretics), dialysis, recent surgery, burns
  • Partial or relative insulin deficiency decreases glucose utilization in muscle, fat, and liver while inducing hyperglucagonemia and hepatic glucose production
  • Presence of a small amount of insulin prevents the development of ketosis by inhibiting lipolysis
  • Characterized by hyperglycemia, hyperosmolality, and dehydration without ketosis
  • More severe dehydration compared to DKA due to more gradual onset and ↑duration of metabolic decompensation plus impaired fluid intake which is common in bedridden or elderly
  • Volume contraction → renal insufficiency → ↑ hyperglycemia, ↑ osmolality → shift of fluid from neurons to ECF → mental obtundation and coma
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34
Q

What are the clinical features of HHS?

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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35
Q

What is seen on bloods in HHS?

A
  • ↑ BG (typically 44.4-133.2 mmol/L)
  • In mild dehydration, may have hyponatremia (spurious 2º to hyperglycemia → for every ↑ in BG by 10 mmol/L there is a ↓ in Na + by 3 mEq/L)
    • if dehydration progresses, may get hypernatremia
  • Ketosis usually absent or mild if starvation occurs
  • ↑ osmolality
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36
Q

What is seen on ABG in HHS?

A
  • -ve for ketones unless there is starvation ketosis
  • Glycosuria
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37
Q

WHat is the treatment for HHS?

A
  • ABCs if patient is stuporous or comatose
  • Rehydration:
    • IV fluids: 1 L/h NS initially
    • evaluate corrected serum Na+
    • if corrected serum Na+ high or normal, switch to 0.45% NaCl (4-14 mL/kg/h)
    • if corrected serum Na+ low, maintain NS (4-14 mL/kg/h)
    • when serum BG reaches 13.9 mmol/L switch to D5W
  • K+ replacement:
    • less severe K+ depletion compared to DKA
    • if serum K+ <3.3 mEq/L, hold insulin and give 40 mEq/L K+ replacement
    • if K+ is 3.3-5.0, give KCl 20-30 mEq/L IV fluid
    • if serum K+ ≥5.5 mEq/L, check K + every 2 h
  • Search for precipitating event
  • Insulin therapy:
    • use only regular insulin (R)
    • initially load 0.1 U/kg body weight insulin R bolus
    • maintenance 0.1 U/kg/h insulin R infusion or IM
    • check serum glucose hourly
    • in general lower insulin requirement compared to DKA
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38
Q

What is the prognosis of HHS?

A

Overall mortality approaches 50% primarily because of the older patient population and underlying etiology/precipitant

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39
Q

What are some DDx for ketonaemia in diabetics?

A

Starvation or alcohol ketosis

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40
Q

Describe the macrovascular complications in DM and there likelyhood and there treatment.

Bloody important shit to know LONGCASE!

A
  • increased risk of CAD, ischemic stroke, and peripheral arterial disease secondary to accelerated atherosclerosis
  • CAD - coronary artery disease
    • risk of MI is 3-5x higher in those with DM compared to age-matched controls
    • CAD is the leading cause of death in type 2 DM
    • most patients with DM are considered “high risk” under the risk stratification for CAD
  • ischemic stroke
    • risk of stroke is approximately 2.5x higher in those with DM
    • level of glycemia is both a risk factor for stroke and a predictor of a poorer outcome in patients who suffer a stroke
    • HbA1c level is a significant and independent predictor of the risk of stroke
  • peripheral arterial disease
    • manifested by intermittent claudication in lower extremities, intestinal angina, foot ulceration
    • risk of foot gangrene is 30x higher in those with DM compared to age-matched controls
    • risk of lower extremity amputation is 15x higher in those with DM
  • treatment
    • tight blood pressure control (<130/80 mmHg); especially for stroke prevention
    • tight glycemic control in early DM without established CVD
    • tight low density lipoprotein (LDL) cholesterol control (LDL 77 mg/dL [<2.0 mmol/L])
    • ACEI or angiotensin receptor blocker in high-risk patients
    • smoking cessation
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41
Q

What is the average fluid loss in DKA and HHS?

A

Average fluid loss runs at 3-6 L in DKA, and 8-10 L in HHS

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42
Q

What are the microvascular complications of DM?

A
  • Diabetic retinopathy
  • Diabetic nephropathy
  • Diabetic neuropathy
    • Peripheral sensory neuropathy
    • Motor neuropathy
    • Autonomic neuropathu
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43
Q

Describe the epidemiology of diabetic retinopathy?

A
  • type 1 DM: 25% affected at 5 yr, 100% at 20 yr
  • type 2 DM: 25% affected at diagnosis, 60% at 20 yr
  • leading cause of blindness in North America between the ages of 20-74
  • most important factor is disease duration
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44
Q

Describe the clinical features of diabetic retinopathy?

A
  • nonproliferative
    • asymptomatic but if macular involvement occurs vision may be impaired
    • microaneurysms, hard exudates, dot-blot and flame hemorrhages
  • preproliferative
    • macular edema, cotton wool spots, venous shunts and beading, intra-retinal microvascular abnormalities (IRMA)
  • proliferative
    • with neovascularization and fibrous scarring; great risk for loss of vision secondary to vitreous hemorrhage (floaters) and/or retinal detachment
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45
Q

Describe the treatment and prevention of diabetic retunopathy.

A
  • tight glycemic control (delays onset, decreases progression), tight lipid control, manage HTN,
  • smoking cessation
  • pan-retinal laser photocoagulation for treatment of neovascularization
  • vitrectomy
  • annual follow-up visits with an optometrist or ophthalmologist examination through dilated pupils whether symptomatic or not (immediate referral after diagnosis of type 2 DM; 5 yr after diagnosis of type 1 DM)
  • interval for follow-up should be tailored to severity of retinopathy
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46
Q

Describe the epidemiology of diabetic nephropathy?

A
  • DM-induced renal failure is the most common cause of renal failure in North America
  • 20-40% of persons with type 1 DM (after 5-10 yr) and 4-20% with type 2 DM have progressive nephropathy
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47
Q

Describe the pathophysiology of diabetic nephropathy?

A
  • thickening of capillary basement membrane and glomerular mesangium resulting in glomerulosclerosis and renal insufficiency
  • diffuse glomerulosclerosis is more common than nodular intercapillary glomerulosclerosis (Kimmelstiel-Wilson lesions)
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48
Q

How is diabetic nephropathy screened?

A
  • serum creatinine
  • random urine test for albumin to creatinine ratio (ACR) plus urine dipstick test for all type 2 DM patients at diagnosis, then annually, and for postpubertal type 1 DM patients with ≥5 yr duration of DM
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49
Q

What are the clinical features of diabetic nephropathy?

A
  • initial changes include microalbuminuria, increased GFR (up to 140%) from hyperfiltration, enlarged kidneys
  • microalbuminuria: 30 μg/mg
  • macroalbuminuria: 300 μg/mg
  • progression over 15 yr to cause HTN, persistent proteinuria (macroalbuminuria), nephrotic syndrome, and renal failure
  • elevated HbA1c is an independent risk factor for progression to microalbuminuria
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50
Q

What is the treatment and prevention of diabetic nephropathy?

A
  • tight glycemic control
  • tight blood pressure control (<130/80 mmHg): can use either ACEI or ARB (often used first line for their CVD protection)
  • even in the absence of glycemic control ACEIs or ARBs reduce the level of albuminuria and the rate of progression of renal disease in normotensive and hypertensive patients with type 1 or type 2 DM
  • type 1 DM → CKD with either HTN or albuminuria → ACEIs 1st line; ARBs 2nd line
  • type 2 DM → CKD with HTN and albuminuria → ACEIs or ARBs (dose adjust if creatinine clearance (CrCl) <60 mL/min)
  • consider use of non-dihydropyridine calcium channel blocker (e.g. diltiazem) in those unable to tolerate both ACEIs and ARBs
  • limit use of nephrotoxic drugs and dyes
  • renal failure may necessitate hemodialysis and renal transplant
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51
Q

Describe the epidemiology of diabetic neuropathy?

A

Approximately 50% of patients within 10 yr of onset of type 1 DM and type 2 DM

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52
Q

Describe the apthophysiology of diabetic neuropathy?

A
  • can have peripheral sensory neuropathy, motor neuropathy, or autonomic neuropathy
  • mechanism poorly understood
  • acute cranial nerve palsies and diabetic amyotrophy are thought to be due to ischemic infarction of peripheral nerve
  • the more common motor and sensory neuropathies are thought to be related to metabolic or osmotic toxicity secondary to increased sorbitol and/or decreased myoinositol (possible mechanisms include accumulation of advanced glycation endproducts [AGE], oxidative stress, protein kinase C, nerve growth factor deficiency)
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53
Q

Describe the screening done for diabetic neuropathy?

A

128 Hz tuning fork or 10 g monofilament at diagnosis and annually in people with type 2 DM and after 5 yr duration of type 1 DM

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54
Q

Describe the clinical presentation of diabetic peripheral sensory neuropathy?

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
  • Symptoms may first occur in entrapment syndromes
    • e.g. carpal tunnel
  • May result in neuropathic ulceration of foot
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55
Q

Describe the clinical presentation of diabetic motor neuropathy?

A
  • Less common than sensory neuropathy
  • Delayed motor nerve conduction and muscle weakness/atrophy
  • May involve one nerve trunk (mononeuropathy) or more (mononeuritis multiplex)
  • Some of the motor neuropathies spontaneously resolve after 6-8 wk
  • Reversible CN palsies: III (ptosis/ophthalmoplegia, pupil sparing), VI (inability to laterally deviate eye), and VII (Bell’s palsy)
  • Diabetic amyotrophy: refers to pain, weakness, and wasting of hip flexors or extensors
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56
Q

Describe the clincial presentation of diabetic autonomic neuropathy?

A
  • Postural hypotension, tachycardia, decreased cardiovascular response to Valsalva maneuver
  • Gastroparesis and alternating diarrhea and constipation
  • Urinary retention and erectile dysfunction
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57
Q

What is the treatment and prevention of diabetic neuropathy?

A
  • tight glycemic control
  • for neuropathic pain syndromes: tricyclic antidepressants (e.g. amitriptyline), pregabalin, duloxetine, anti-epileptics (e.g. carbamazepine, gabapentin), and capsaicin
  • foot care education
  • Jobst® fitted stocking and tilting of head of bed may decrease symptoms of orthostatic hypotension
  • treat gastroparesis with domperidone and/or metoclopramide (dopamine antagonists), erythromycin (stimulates motilin receptors)
  • medical, mechanical, and surgical treatment for erectile dysfunction
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58
Q

What are some other complications (not macro or microvascular) of diabetes?

A
  • Dermatologic
    • diabetic dermopathy: atrophic brown spots commonly in pretibial region known as “shin spots”, secondary to increased glycosylation of tissue proteins or vasculopathy
    • eruptive xanthomas secondary to increased triglycerides
    • necrobiosis lipoidica diabeticorum: rare complication characterized by thinning skin over the shins allowing visualization of subcutaneous vessels
  • Bone and Joint Disease
    • juvenile cheiroarthropathy: chronic stiffness of hand caused by contracture of skin over joints secondary to glycosylated collagen and other connective tissue proteins
    • Dupuytren’s contracture
    • bone demineralization: bone density 10-20% below normal
    • adhesive capsulitis (“frozen shoulder”)
  • Cataracts
    • subcapsular and senile cataracts secondary to glycosylated lens protein or increased sorbitol causing osmotic change and fibrosis
  • Infections: foot infections
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59
Q

What are the common causes of hypoglycaemia?

A
60
Q

How is exogenous and endogenous source of hyperinsulinaemia differentiated?

A

C-peptide

Increased = endogenous

Decreased or normal = exogenous

61
Q

What is C-peptide?

A

A short peptide released into the circulation when proinsulin is cleaved to insulin

62
Q

What are the clinical features of hypoglycaemia?

A
  • Whipple’s triad
    • serum glucose 45 mg/dL (<2.5 mmol/L) in males and 40 mg/dL (<2.2 mmol/L) in females
    • neuroglycopenic symptoms
    • rapid relief provided by administration of glucose
  • adrenergic symptoms (typically occur first; caused by autonomic nervous system activity)
    • palpitations, sweating, anxiety, tremor, tachycardia
  • neuroglycopenic symptoms (caused by decreased activity of CNS)
    • dizziness, headache, clouding of vision, mental dullness, fatigue, confusion, seizures, coma
63
Q

What Ix need to be ordered in someone who is hypoglycaemic?

A
  • UEC, LFTs, drugs/toxins, cortisol
  • if concerned about possible insulinoma:
    • blood work to be drawn when patient is hypoglycemic (e.g. during hospitalized 72 h fast) for glucose, serum ketones, insulin, pro-insulin, C-peptide, insulin antibodies
64
Q

What is the treatment for hypoglycaemia?

A
  • for fasting hypoglycemia, must treat underlying cause
  • for post-prandial (reactive) hypoglycemia, frequent small feeds
  • treatment of hypoglycemic episode in the unconscious patient or patient NPO
    • D50W 50 mL (1 ampule) IV or 1 mg glucagon SC (if no IV available)
    • may need ongoing glucose infusion once BG > 90 mg/dL (5 mmol/L)
65
Q

What is the definition of metabolic syndrome?

A
  • Elevated waist circumference
  • Elevated triglyceride levels: ≥1.7 mmol/L or on medical therapy
  • Reduced HDL:<1.0 mmol/L in men, <1.3 mmol/L in women OR on drug treatment
  • Elevated blood pressure: ≥130 systolic or ≥85 diastolic OR on medical therapy for HTN
  • Elevated fasting glucose: >5.5 mmol/L or on medical therapy
66
Q

What is normal total serum Ca2+ levels?

A

2.2 - 2.6 mmol/L

67
Q

How is parathyroid hormone regulated and what is its net effect?

A
  • Stimulated by low serum Ca2+ and high serum PO43-; inhibited by chronic low serum Mg2+, high serum Ca2+, and calcitriol.
  • Net effect: ↑ Ca2+, ↑Cacitriol, ↓PO43-
68
Q

How is calcitriol (1,25-(OH)2D3) regulated, its net effect and its source?

A
  • Source:
    • Dietary intake
    • Synthesized from cholesterol: UV on skin makes cholecalciferol (vitD3) → liver makes calcidiol (25-(OH)D3) → kidneys make calcitriol
  • Regulation:
    • Renal calcitriol production is stimulated by low serum PO43- and PTH; inhibited by high serum PO43- and calcitriol in negative feedback
  • Net effect: ↑Ca2+, ↑PO43-
69
Q

How is calcitonin regulated, its net effect and its source?

A
  • Source: Thyroid C cells
  • Regulation:
    • Stimulated by pentagastrin (GI hormone) and high serum Ca2+; inhibited by low serum Ca2+
  • ​Net effect: ↓Ca2+ (in pharmacologic doses), ↓PO43-
70
Q

Describe how parathyroid hormone is regulated?

A
71
Q

What is the definition of hypercalcaemia?

A

Serum Ca2+ level >2.6 mmol/L after correction for albumin.

72
Q

How do you correct Ca2+ for albumin?

A
73
Q

How do you approach a patient who has hypercalcaemia?

A
  1. Is the patient hypercalcemic? (correct for albumin)
  2. Is the PTH high/normal or low?
  3. If PTH is low, is phosphate high/normal or low? If phosphate is high/normal is the level of vitamin D metabolites high or low?
74
Q

What is the cause of primary hyperparathyroidism?

A
  • Increased PTH secretion commonly due to:
    • parathyroid adenoma (81%)
    • lithium therapy
    • less often parathyroid carcinoma (4%) or parathyroid hyperplasia (15%)
75
Q

What is the cause of secondary hyperparathyroidism?

A

Partial resistance to PTH action leads to parathyroid gland hyperplasia and increased PTH secretion, often in patients with renal failure and osteomalacia (due to low or low normal
serum calcium levels)

76
Q

What is the cause of tertiary hyperparathyroidism?

A

Irreversible clonal outgrowth of parathyroid glands, usually in long-standing inadequately treated chronic renal failure on dialysis

77
Q

What is the criteria for surgical referral for primary hyperparathyroidism?

A
  • Surgical excision acts as a definitive treatment and is recommended for patients who are symptomatic.
  • For mild asymptomatic disease medical surveillance may be appropriate with annual serum calcium, creatinine, and
    BMD.
  • For asymptomatic patients surgery is recommended for those who meet ≥1 of the following criteria:
    • Serum calcium concentration more than 0.25 mmol/L above the upper limit of normal
    • Creatinine clearance <60 mL/min
    • BMD T-score <-2.5 at hip, spine, or distal radius, and/or previous fragility fracture
    • Age <50 yr
78
Q

First thought:

Hypercalcaemia.

A

Bones, stones, groans, and psychic moans.

79
Q

What are the symptoms of hypercalcaemia?

Hint: CVS, GI, Renal, Rheum, MSK, Psych, neuro.

A
80
Q

What is the most common cause of hypercalcaemia in hospital?

A

Malignancy-associated hypercalcemia

  • Usually occurs in the later stages of disease
  • Most commonly seen in lung, renal, breast, ovarian, and squamous tumors, as well as lymphoma and multiple myeloma
  • Mechanisms:
    • Secretion of parathyroid hormone-related protein (PTHrP) which mimics PTH action by preventing renal calcium excretion and activating osteoclast-induced bone resorption
    • Cytokines in multiple myeloma
    • Calcitriol production by lymphoma
    • Osteolytic bone metastases direct effect
    • Excess PTH in parathyroid cancer
81
Q

What are the DDx for hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Malignancy: hematologic, humoral, skeletal metastases (>90% from 1 or 2)
  • Renal disease: tertiary hyperparathyroidism
  • Drugs: calcium carbonate, milk alkali syndrome, thiazide, lithium, theophylline, vitamin A/D intoxication
  • Familial hypocalciuric hypercalcemia
  • Granulomatous disease: sarcoidosis, TB, Hodgkin’s lymphoma
  • Thyroid disease: thyrotoxicosis
  • Adrenal disease: adrenal insufficiency, pheochromocytoma
  • Immobilisation
82
Q

How do you manage a patient with acute hypercalcaemia?

Ix and RX

A
  • ABCs: Insert large bore IV cannula and send blood for FBC, UEC, LFTs, calcium, lipase and TFT.
  • ECG monitor:
    • Bradycardia
    • Short GT interval with a widened QRS
    • Flattened T waves, atrioventricular block and cardiac arres
  • CXR: may show underlying cause.
  • Rehydrate: 0.9% NS 500ml/h
  • Frusemide 20-40 mg IV once urine output is established to maintain diuresis
  • Refer to medical team.
    • Bisphosphonates (diminishes bone resorption): max effect at 7 days
    • Corticosteroids in hypervitaminosis D and haematological malignancies (anti-tumour effect): acts in 5-10 days
    • Dialysis: last resort treatment
83
Q

WHat are the clinical features of hypocalcaemia?
Acute vs chronic.

A
84
Q

First thought.

Signs and symtpoms of acute hypocalcaemia?

A
  • Paresthesias: perioral, hands, and feet
  • Chvostek’s sign: percussion of the facial nerve just anterior to the
    external auditory meatus elicits ipsilateral spasm of the orbicularis oculi or orbicularis oris muscles
  • Trousseau’s sign: inflation of a blood pressure cuff above systolic pressure for 3 min elicits carpal spasm and paresthesia
85
Q

DDx for tetany.

A
  • Hypocalcemia
  • Metabolic alkalosis (with hyperventilation)
  • Hypokalemia
  • Hypomagnesemia
86
Q

What are the causes of hypocalcaemia?

A
  • Chronic renal failure, acute pancreatitis
  • Rhadbomyolysis, tumour lysis syndrome, whole blood transfusion and toxic shock syndrome
  • primary respiratory alkolosis (hyperventilation)
  • Post-parathyroidectomy or thyroid surgery; autoimmune hypoparathyroidism
87
Q

What are the complications of hypocalcaemia?

A
  • Bone disease
  • Cardio: cardiovascular collapse, hypotesion unresponsive to fluids and vasopressors and dysrhythmias.
  • Neuro: acute seizures or tetany, basal ganglia calcification, parkinsonism, hemiballismus and choreathetosis.
88
Q

How is hypocalcaemia managed?

A
  • correct underlying disorder:
    • FBC, UEC, LFTs, creatine kinase, magnesium and lipase
    • ECG:
      • Qt interval prolongation, T wave inversion
      • AV block, torsade de point (cardiad arrest may ensue)
  • mild/asymptomatic (ionized Ca2+ >0.8 mmol/L)
    • treat by increasing dietary Ca2+ by 1000 mg/d
    • calcitriol 0.25 µg/d
  • acute/symptomatic hypocalcemia (ionized Ca2+ <0.7 mmol/L)
    • immediate treatment required - IV 0.9% NS 250ml/h
    • IV 10% calcium chloride 10-40 mL
    • goal is to raise Ca2+ to low normal range (2.0-2.1 mmol/L) to prevent symptoms but allow maximum stimulation of PTH secretion
  • if PTH recovery not expected, requires long-term therapy with calcitriol and calcium
  • do not correct hypocalcemia if asymptomatic and suspected to be transient
89
Q

Sketch the pathway involved in hormonal regulation of gonadal function in men?

A
90
Q

Sketch the pathway involved in hormonal regulation of gonadal function in female?

A
91
Q

What is the definition of hypergonadotropic hypogonadism (primary hypogonadism)?

A
  • Primary testicular failure:
    • ↑LH and FSH, ↑FSH:LH ratio
    • ↓testosterone and sperm count
92
Q

What is the aetiology of hypergonadotropic hypogonadism (primary hypogonadism)?

A
  • Congenital:
    • Chromosomal defects (Klinefelter’s, Noonan)
    • Cryptorchidism
    • Disorders of sexual development (DSD)
    • Bilateral anorchia (vanishing testicle syndrome)
    • Myotonic dystrophy
    • Mutation of FSH or LH receptor gene
    • Disorders of androgen synthesis
  • Germ cell defects
    • Sertoli cell only syndrome
    • Leydig cell aplasia/failure
  • Infection/Inflammation
    • Orchitis – TB, lymphoma, mumps, leprosy
    • Genital tract infection
  • Physical factors
    • Trauma, heat, irradiation, testicular torsion, varicocele
  • Drugs
    • Marijuana, alcohol, chemotherapy, ketoconazole, glucocorticoid, spironolactone
  • Autoimmune (antisperm antibodies)
  • Chronic systemic diseases (AIDS)
  • Idiopathic
93
Q

How is hypergonadotropic hypogonadism (primary hypogonadism) diagnosed?

A
  • Testicular size and consistency (soft/firm)
  • Sperm count
  • LH, FSH, total, and/or bioavailable testosterone hCG stimulation
  • Karyotype
94
Q

Define hypogonadotropic hypogonadism (secondary hypogonadism)?

A
  • Hypothalamic-pituitary axis failure:
    • ↓ LH + FSH
    • ↓ testosterone and sperm count
95
Q

What is the aetiology of hypogonadotropic hypogonadism (secondary hypogonadism)?

A
  • Congenital
    • Kallman’s syndrome
    • Prader-Willi syndrome
    • Abnormal subunit of LH or FSH
  • Infection
    • Tuberculosis, meningitis
  • Endocrine
    • Adrenal androgen excess
    • Cushing’s syndrome
    • Hypo or hyperthyroidism
    • Hypothalamic-pituitary disease (tumor, hyperprolactinemia, hypopituitarism)
  • Drugs
    • Alcohol, marijuana, spironolactone, ketoconazole, GnRH agonists, androgen/oestrogen/progestin use, chronic narcotic use
  • Chronic illness
    • Cirrhosis, chronic renal failure, AIDS
    • Sarcoidosis, Langerhan’s cell histiocytosis haemochromatosis
  • Critical illness
    • Surgery, MI, head trauma
  • Obesity
  • Idiopathic
96
Q

What is the karyotypic diagnosis of Klinefelter’s syndrome?

A
  • 47,XXY (most common)
  • 48,XXXY, 49,XXXXY
97
Q

What are the clinical features of Klinefelters syndrome?

A
  • Tall, slim, underweight
  • No features prepuberty
  • Postpuberty: male may suffer from developmental delay, long
    limbs, gynecomastia, lack of facial hair
  • Mild intellectual disability
  • Behavioral or psychiatric disorders – anxiety, shyness, aggressive behavior, antisocial acts
98
Q

Describe the clinical features of Turners syndrome?

A
  • Short stature, short webbed neck, low posterior hair line, wide carrying angle
  • Broad chest, widely spaced nipples
  • Lymphedema of hands and/or feet, cystic hygroma in newborn with polyhydramnios, lung hypoplasia
  • Coarctation of aorta, bicuspid aortic valve
  • Renal and cardiovascular abnormalities, increased risk of HTN
  • Less severe spectrum with mosaic
  • Mildly deficient to normal intelligence
99
Q

What is the karyotype of Turners syndrome?

A

45,X (most common)

100
Q

What are the two distinct features of primary hypogonadism?

A
  • The decrease in sperm count is affected to a greater extent than the decrease in serum testosterone level
  • Likely to be associated with gynecomastia
101
Q

What are the two features of secondary hypogonadism?

A
  • Associated with an equivalent decrease in sperm count and serum testosterone
  • Less likely to be associated with gynecomastia
102
Q

What are the aetiologies of hyperprolactinaemia?

A
  • pregnancy and breastfeeding
  • prolactinoma: most common pituitary adenoma (prolactin-secreting tumors may be induced by oestrogens and grow during pregnancy)
  • pituitary masses with pituitary stalk compression causing reduced dopamine inhibition of prolactin release
  • primary hypothyroidism (increased TRH)
  • decreased clearance due to chronic renal failure or severe liver disease (prolactin is metabolized by both the kidney and liver)
  • medications with anti-dopaminergic properties are a common cause of high prolactin levels: antipsychotics (common), antidepressants, antihypertensives, anti-migraine agents (triptans/ergotamines), bowel motility agents (metoclopramide/domperidone), H2-blockers (ranitidine)
  • macroprolactinemia (high molecular weight prolactin also known as big big prolactin)
103
Q

What is the treatment of hyperprolactinemia?

A
  • long-acting dopamine agonist: bromocriptine, cabergoline, or quinagolide (Norprolac®)
  • surgery ± radiation (rare)
  • prolactin-secreting tumors are very slow-growing and sometimes require no treatment
  • if medication-induced, consider stopping medication if possible
  • in certain cases if microprolactinoma and not planning on becoming pregnant, may consider OCP
104
Q

What is your approach to male infertility?

A
  • Infertility: failure of a couple to conceive after 12 mo of regular intercourse without use of contraception in women <35 yr of age; and after 6 mo of regular
    intercourse without use of contraception in women ≥35 yr
  • History
    • Partner status re: infertility
    • Length of time for attempt to conceive
    • Prior successes with other partners
    • Ejaculation problems
    • Frequency of intercourse
    • Prev Surg, Med Hx, STD Hx
    • Hx orchitis? Cryptorchidism?
    • Hx toxic exposure?
    • Medications
    • Alcohol and illicit drug use
    • Heat exposure: bath, sauna, whirlpool
    • Smoking
  • P/E
    • General (height, weight, gynecomastia, masculine)
    • Testicular size and consistency
    • Varicocele?
    • Pituitary disease?
    • Thyroid disease?
  • Investigations
    • Should be considered for couples unable to conceive after 12 mo of unprotected and frequent intercourse; consider earlier evaluation if suggestive medical hx and physical, and in women ≥35 yr of age
    • Semen analysis x 2 (sperm count, morphology, motility)
    • Scrotal/testicular U/S (look for varicocele)
    • Blood work: LH, FSH, testosterone, prolactin, thyroid function tests, DNA fragmentation of sperm, karyotype, Y chromosome deletion
    • Test female partner
  • Treatment
    • No specific therapy for majority of cases
    • Treat specific causes
    • Consider: intrauterine insemination, IVF, therapeutic donor insemination, testicular aspiration of sperm, adoption
105
Q

What are the causes of primary amenorrhea without secondary sexual development?

A
  • High FSH (hypergonadotropic hypogonadism)
    • Gonadal dysgenesis
      • Abnormal sex chromosome (Turner’s XO)
      • Normal sex chromosome (46XX, 46XY)
  • Low FSH (hypogonadotropic hypogonadism)
    • Constitutional delay (most common)
    • Congenital abnormalities
      • Isolated GnRH deficiency
      • Pituitary failure (Kallman syndrome, head injury, pituitary adenoma, etc.)
    • Acquired
      • Endocrine disorders (type 1 DM)
      • Pituitary tumors
      • Systemic disorders (IBD, JRA, chronic infections, etc.)
106
Q

What are the causes of secondary amenorrhea with and without hyperandrogenism?

A
  • With hyperandrogenism:
    • PCOS
    • Autonomous hyperandrogenism (androgen secretion independent of the HPO axis)
      • Ovarian: tumor, hyperthecosis
      • Adrenal androgen-secreting tumor
    • Late onset or mild congenital adrenal hyperplasia (rare)
  • Without hyperandrogenism:
    • Hypergonadotropic hypogonadism (i.e. premature ovarian failure: high FSH, low estradiol)
      • Idiopathic
      • Autoimmune: type 1 DM, autoimmune thyroid disease, Addison’s disease
      • Iatrogenic: cyclophosphamide drugs, radiation
    • Hyperprolactinemia
    • Endocrinopathies: most commonly hyper or hypothyroidism
    • Hypogonadotropic hypogonadism (low FSH):
      • Pituitary compression or destruction: pituitary adenoma, craniopharyngioma, lymphocytic hypophysitis, infiltration (sarcoidosis), head injury, Sheehan’s syndrome
    • Functional hypothalamic amenorrhea (often related to stress, excessive exercise and/or anorexia)
107
Q

What is the definition of primary amenorrhea?

A

No menses by age 13 in absence of 2ºvsexual characteristics or no menses byvage 15 with 2º sexual characteristics or no menses 2 yr after thelarche

108
Q

What is the definition of secondary amenorrhea?

A

No menses for >6 mo or 3 cycles after documented menarche

109
Q

What is the definition of oligomenorrhea?

A

Episodic vaginal bleeding occurring at intervals >35 d

110
Q

What investigations need to be ordered in a female with hypogonadism?

HINT: thought to have due to amenorrhea

A
  • β-hCG, hormonal workup (TSH, prolactin, FSH, LH, androgens, estradiol)
  • progesterone challenge to assess estrogen status
    • medroxyprogesterone acetate (Provera®) 10 mg PO OD for 10-14 d
    • any uterine bleed within 2-7 d after completion of Provera® is considered to be a positive test/withdrawal bleed
      • withdrawal bleed suggests presence of adequate estrogen to thicken the endometrium; thus withdrawal of progresterone results in bleeding
      • if no bleeding occurs, there may be inadequate estrogen (hypoestrogenism) or excessive androgens or progesterones (decidualization)
  • karyotype: indicated if premature ovarian failure or absent puberty
  • U/S to confirm normal anatomy, identify PCOS
111
Q

Sketch the hypothalamic-pituitary hormonal axis for all the hormones of the pituitary gland.

A
112
Q

What are the visual field defects attributed to pituitary tumours?

A
113
Q

First though

Acromegaly

HINT: ABCDEF

A
  • Arthralgia/Arthritis
  • Blood pressure raised
  • Carpal tunnel syndrome
  • Diabetes
  • Enlarged organs
  • Field defect (visual)
114
Q

What happens when you have an excess of growth hormones?

A
  • in children (before epiphyseal fusion) leads to gigantism
  • in adults (after epiphyiseal fusion) leads to acromegaly
115
Q

What are the clinical features of acromegally?

A
  • Dermatological:
    • thickening of skin
    • increased sebum production, acne, sebaceous cysts,
    • sweating
    • fibromata mollusca, acanthosis nigricans,
  • MSK
    • arthralgia, carpal tunnel syndrome, degenerative
      osteoarthritis
    • enlargement of hands and feet
    • coarsening of facial features
    • thickening of calvarium
    • prognathism (growth of jaw)
  • Endo:
    • thyromegaly
    • DM
  • Renal:
    • renal calculi
  • Cardioresp:
    • HTN
    • cardiomyopathy
    • obstructive sleep apnea,
  • GIT
    • colonic polyps
116
Q

Describe the apthophysiology of acromegally?

A
  • normally GH is a catabolic hormone that acts to increase blood glucose levels
  • in growth hormone excess states secretion remains pulsatile but there is loss of hypoglycemic stimulation, glucose suppression, and the nocturnal surge
  • proliferation of bone, cartilage, soft tissues, organomegaly
  • insulin resistance and IGT
117
Q

What Ix should be done on a pt with ?acromegally?

A
  • glucose suppression test is the most specific test (75 g of glucose PO suppresses GH levels in healthy individuals but not in patients with acromegaly)
  • elevated serum insulin-like growth factor-1 (IGF-1) is usually first line diagnostic test
118
Q

What are the clinical features of Cushing’s syndrome?

A
  • symptoms: weakness, insomnia, mood disorders, impaired cognition, easy bruising, oligo-/amenorrhea, hirsutism, and acne (ACTH dependent)
  • signs: central obesity, round face, supraclavicular and dorsal fat pads, facial plethora, proximal muscle wasting, purple abdominal striae, skin atrophy, acanthosis nigricans, HTN, hyperglycemia, osteoporosis, pathologic fractures, hyperpigmentation, hyperandrogenism if ACTH-dependent
119
Q

What Ix need to be done for Cushing’s syndrome?

A
  • Dexamethasone suppression test-overnight
  • Cortisol urine
  • ACTCH
  • UECs
120
Q

Interpret these thyroid function tests.

A
121
Q

What is the aetiology of a toxic nodule/multinodular goiter?

A
  • autonomous thyroid hormone production from a functioning adenoma that is hypersecreting T3 and T4
  • may be singular (toxic adenoma) or multiple (toxic multinodular goiter [Plummer’s disease])
122
Q

What are the clinical features of a toxic nodule/multinodular goiter?

A
  • goiter with adenomatous changes
  • tachycardia, heart failure, arrhythmia, weight loss, nervousness, weakness, tremor, and sweats
  • seen most frequently in elderly people, often with presentation of atrial fibrillation
123
Q

What are the clinical outcomes for the different types of thyroid cancer?

A
124
Q

What are the indications for a neck US?

A
  • Symptoms suggestive of neck mass
  • Clinical lump in neck (including goitre or large nodule)
  • Nodule on other imaging modality
  • Cold nodules on nuclear scan (not necessarily high risk)
  • Suspicion of thyroid cancer
125
Q

WHat is the treatment for a toxic thyroid nodule?

A
  • If small - no treatment necessary
  • If large and causing mediastinal compression – surgery indicated
  • For multinodular goitre – radioactive iodine
    • Ablates hyperactive nodule without affecting ‘cold’ areas
    • Hypothyroidism uncommon
    • Safe, convenient, single dose
    • Long-term control without medication requirement
126
Q

Describe the causes, Ix and treatment of thyroiditis.

A
  • Inflammation of the thyroid gland
  • Causes – Post-partum, post-viral, drugs (amiodarone, interferons, tyrosine kinase inhibitors), autoimmune (Hashimoto’s, may be preceded by thyrotoxicosis), radiation, idiopathic
  • Signs – if chronic see hypothyroid signs, if acute see hyperthyroid signs
  • Investigation
    • CRP/ESR, elevated thyroglobulin levels and depressed radioactive iodine intake
    • Determine the type of thyroiditis – test TSH and thyroid antibodies
  • Treatment – correct underlying cause, in the meantime beta-blockers can help lower heart rate and reduce tremors, and steroids to reduce inflammation if painful
  • Course – spontaneous resolution, may progress to hypothyroidism (transient or permanent)
127
Q

What is the treatment for hyperthyroidism?

A
  • Depends on cause:
    • thionamides: PTU or MMI; MMI recommended (except in first trimester pregnancy)
    • β-blockers for symptom control
    • radioactive iodine thyroid ablation for Graves’ disease
    • surgery in the form of hemi, sub-total, or complete thyroidectomy
128
Q

What is the treatment of hypothyroidism?

A
  • L-thyroxine (dose range: 0.05-0.2 mg PO OD ~1.6 µg/kg/d)
  • elderly patients and those with CAD: start at 0.025 mg daily and increase gradually every 6 wk (start low, go slow)
  • after initiating L-thyroxine, TSH needs to be evaluated in 6 wk; dose is adjusted until TSH returns to normal reference range
  • once maintenance dose achieved, follow-up TSH with patient annually
  • secondary/tertiary hypothyroidism
    • monitor via measurement of free T4 (TSH is unreliable in this setting)
129
Q

Palmar creae xanthoma are associated with which disease?

A

Remnant hyperlipidaemia (Type III hyperlipidaemia)

130
Q

Describe the renin-angiotensin-aldosterone system.

A
131
Q

Define Addison’s disease.

A

a state of inadequate cortisol and aldosterone production by the adrenal glands

132
Q

What are the aetiologies of primary adrenocortical insufficiency?

A
  • Autoimmune (70-90%)
    • Isolated adrenal insufficiency
    • Polyglandular autoimmune syndrome type I and II
    • Antibodies often directed against adrenal enzymes and 3 cortical zones
  • Infection:
    • TB (7-20%) (most common in developing world)
    • Fungal: histoplasmosis, paracoccidioidomycosis
    • HIV, CMV
    • Syphilis
  • Infiltrative:
    • Metastatic cancer (lung>stomach>esophagus>colon>breast); lymphoma
    • Sarcoidosis, amyloidosis, hemochromatosis
  • Vascular:
    • Bilateral adrenal hemorrhage
    • Sepsis (meningococcal, Pseudomonas)
    • Coagulopathy in adults or Waterhouse-Friderichsen syndrome in children
    • Thrombosis, embolism, adrenal infarction
  • Drugs:
    • Inhibit cortisol: ketoconazole, megestrol acetate
    • Increase cortisol metabolism: rifampin, phenytoin, barbiturates, heparin, coumadin
  • Others:
    • Adrenoleukodystrophy
    • Congenital adrenal hypoplasia (impaired steroidogenesis)
    • Familial glucocorticoid deficiency or resistance
133
Q

What is the cause of secondary adrenocortical insufficiency?

A
  • inadequate pituitary ACTH secretion
  • multiple etiologies (see Hypopituitarism), including withdrawal of exogenous steroids
134
Q

What are the clinical features of primary and secondary adrenal insufficiency?

A
135
Q

What is the Rx for adrenocortical insufficiency?

A
  • acute condition – can be life-threatening
    • IV NS in large volumes (2-3 L); add D5W if hypoglycemic from adrenal insufficiency
    • hydrocortisone 50-100 mg IV q6-8h for 24h, then gradual tapering
    • identify and correct precipitating factors
  • maintenance
    • hydrocortisone 15-20 mg total daily dose, in 2-3 divided doses, highest dose in the AM
    • Florinef® (fludrocortisone, synthetic mineralocorticoid) 0.05-0.2 mg PO daily if mineralocorticoid deficient increase dose of steroids 2-3 fold for a few days during moderate-severe illness (e.g. with vomiting, fever)
    • major stress (e.g. surgery, trauma) requires 150-300 hydrocortisone IV daily divided into 3 doses
    • medical alert bracelet and instructions for emergency hydrocortisone/dexamethasone IM/SC injection
136
Q

What are the clinical features of hypothyroidism?

A
  • Tiredness
  • Weight gain
  • Feeling cold
  • Constipation
  • Brady cardia
  • Goitre
  • Slow relaxation of the tendon reflexes
  • Hoarse voice
  • A puffy facial appearance.
137
Q

What are the signs and symptoms of an Addisonian crisis?

A
  • Sudden penetrating pain in the legs, lower back or abdomen
  • Confusion, psychosis, slurred speech
  • Severe lethargy
  • Convulsions
  • Fever
  • Hyperkalemia
  • Hypercalcemia
  • Hypoglycemia
  • Hyponatremia
  • Hypotension
  • Hypothyroid
  • Severe vomiting and diarrhea, resulting in dehydration
  • Syncope
138
Q

Define multiple endocrine neoplasm?

A
  • neoplastic syndromes involving multiple endocrine glands
  • tumors of neuroectodermal origin
  • autosomal dominant inheritance with variable penetrance
  • genetic screening for RET proto-oncogene on chromosome 10 has long-term benefit in MEN II
    • early cure and prevention of medullary thyroid cancer
139
Q

Which tissues are involved in MEN I?

A
  • Pituitary - anterior pituitary adenoma
  • Parathyroid
  • Entero-pancreatic endocrine
    • Pancreatic islet cell tumors
    • Gastrinoma
    • Insulinomas
    • Vasoactive intestinal peptide
    • (VIP)-omas
    • Glucagonoma
    • Carcinoid syndrome
140
Q

What are the signs and symptoms of MEN I?

A
  • From pituitary:
    • Headache, visual field defects. Often non-secreting but may
      secrete GH (acromegaly) and PRL (galactorrhea, erectile
      dysfunction, decreased libido, amenorrhea)
  • From parathyroid:
    • Nephrolithiasis, bone abnormalities, MSK complaints,
      symptoms of hypercalcemia
  • From pancreas:
    • Epigastric pain (peptic ulcers and esophagitis), Hypoglycemia Secretory diarrhea
    • Rash, anorexia, anemia, diarrhea, glossitis, Flushing, diarrhea, bronchospasm
141
Q

Which tissues are involved in MEN IIa?

A
  • Thyroid (>90%)
    • Medullary thyroid cancer (MTC)
  • Adrenal medulla (40-50%)
    • Pheochromocytoma
  • Parathyroid (10-20%)
    • 1o parathyroid hyperplasia
142
Q

Which tissues are involved in MEN IIb?

A
  • Thyroid
    • MTC
  • Adrenal medulla
    • Pheochromocytoma
  • Neurons
    • Mucosal neuroma, intestinal
    • ganglioneuromas
143
Q

Define gynaecomastia?

A
  • true gynecomastia refers to benign proliferation of the glandular component of the male breast, resulting in the formation of a concentric, rubbery, firm mass extending from the nipple(s)
  • pseudogynecomastia or lipomastia refers to enlargement of soft adipose tissue, especially seen in obese individuals and does not warrant further evaluation
144
Q

What are the causes of gynaecomastia?

A
  • Physiologic
    • puberty
    • elderly (involutional)
    • neonatal (maternal hormone)
  • Pathologic
    • endocrinopathies: primary or secondary hypogonadism, hyperthyroidism, extreme hyperprolactinemia, adrenal disease
    • tumors: pituitary, adrenal, testicular, breast, ectopic production of hCG
    • chronic diseases: cirrhosis, renal, malnutrition (with refeeding)
    • drugs: estrogens and estrogen agonists, spironolactone, ketoconazole, cimetidine, digoxin, chemotherapy, marijuana, alcohol
    • congenital/genetic: Klinefelter’s syndrome, androgen insensitivity
    • other: idiopathic, familial
145
Q

Describe the pathophysiology of gynaecomastia?

A

hormonal imbalance due to increased oestrogen activity (increased production, or increased availability of oestrogen precursors for peripheral conversion to oestrogen) or decreased androgen activity (decreased androgen production, binding of androgen to sex hormone binding globulin (SHBG), or androgen receptor blockage)

146
Q

What Ix need to be done on a pt with gynaecomastia?

A
  • laboratory: serum TSH, PRL, LH, FSH, testosterone, estradiol, LFTs, creatinine, hCG (if hCG is elevated need to locate the primary tumor)
  • CXR and CT of chest/abdomen/pelvis (to locate neoplasm)
  • testicular U/S to rule out testicular mass
  • MRI of hypothalamic-pituitary region if pituitary adenoma suspected
147
Q

What is the treatment for gynaecomastia?

A
  • initial observation for most men with gynecomastia
  • medical
    • correct the underlying disorder, discontinue responsible drug
    • androgens for hypogonadism
    • anti-estrogens: tamoxifen, clomiphene
  • surgical
    • usually required for macromastia; gynecomastia present for >1 yr (fibrosis is unresponsive to medication); or failed medical treatment and for cosmetic purposes

Year 4 (25 decks)

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